what diseases are c section babies more prone to colic

  • Periodical List
  • HHS Author Manuscripts
  • PMC3110651

Clin Perinatol. Author manuscript; available in PMC 2012 Jun 1.

Published in terminal edited grade as:

PMCID: PMC3110651

NIHMSID: NIHMS284291

Cesarean versus Vaginal Commitment: Long term infant outcomes and the Hygiene Hypothesis

Josef Neu

a Professor of Pediatrics, Division of Neonatology, University of Florida; Gainesville, Florida

b Manager, Neonatology Fellowship Training Programme, University of Florida, Gainesville, Florida

Jona Rushing

c Fellow, Section of Obstetrics and Gynecology, Partitioning of Maternal Fetal Medicine, Academy of Florida, Gainesville, Florida

Keywords: microbiota, mode of commitment, hygiene hypothesis

INTRODUCTION

In the United States the rate of cesarean delivery (CD) has risen 48% since 1996, reaching a level of 31.8% in 2007. 1 This tendency is reflected in many parts of the world, with the almost populous country in the world, China, approaching l%2 and some individual clinics in Brazil approaching 80% 3. While a meaning number of CD are preformed for obstetrical indications, some are simply due to maternal request and may incur several risks for the child. Well known amongst these risks are neonatal low due to general anesthesia, fetal injury during hysterotomy and/or commitment, increased likelihood of respiratory distress even at term, and breastfeeding complications. Concurrent with the trend of increasing CD, in that location has been an epidemic of both autoimmune diseases such as type 1 diabetes, Crohn's illness, and multiple sclerosis and allergic diseases, such equally asthma, allergic rhinitis, and atopic dermatitisiv , 5. The occurrence of these diseases is higher in more flush, Western, industrialized countries. Several theories have emerged that suggest environmental influences are contributing to this phenomenon. Well-nigh notably, the "hygiene hypothesis" suggests that an overly make clean environs, peculiarly in early babyhood, may contribute to the development of several babyhood diseases. It was first proposed past Strachan, who observed an changed correlation between hay fever and the number of older siblings. half dozen This was subsequently extended by others from the allergies to autoimmune diseases such every bit type 1 diabetes. 5 Whether the increment in CD incidence is also causally related will be addressed in this review.

The interplay between the emerging microbial ecology of the gastrointestinal tract and the developing mucosal immune organization serves every bit a backdrop for a relationship between CD and the emergence of some of these diseases. With the highly immunoreactive intestine serving as the largest surface expanse of the body that is exposed to the environs, particularly a vast array of luminal microbes and antigens, it is intriguing to speculate that the intestinal environmental interaction during early development of the immune organization may relate to these diseases. One intriguing component of this relates to the early evolution of the intestinal microbiota, the developing immune system and the early influence of cesarean versus vaginal commitment (VD) on these phenomena. The immune system undergoes major development during infancy and is highly related to the microbes that colonize the intestinal tract.7 - 9 It has been suggested that dissimilar initial exposures depend on mode of delivery (VD vs. CD). The microbes that "seed' the intestine during either CD or VD may lead to changes in long term colonization and subsequent altering of immune evolution (Fig. one). Hither nosotros will provide background about the human microbiota, its relationship to the developing immune organisation, and the relationship of manner of delivery on the colonization of the infant intestine, development of the immune organisation, and subsequent childhood allergies, asthma and autoimmune diseases.

An external file that holds a picture, illustration, etc.  Object name is nihms-284291-f0001.jpg

THE HUMAN MICROBIOTA

The human body, consisting of about 100 trillion cells, carries about ten times as many microorganisms in the intestines. ten - 12 It is estimated that these gut flora have around 100 times as many genes in amass every bit there are in the human being genome.thirteen The metabolic activities performed by these bacteria resemble those of an organ, leading some to liken gut leaner to a "forgotten" organ. 12 Microorganisms perform a host of useful functions, such as fermenting unused energy substrates, preparation the immune arrangement, preventing growth of harmful, pathogenic bacteria, regulating the development of the gut, and producing vitamins for the host (such as biotin and vitamin Thousand). 14 Excitement near the potential of harnessing the intestinal microbiota for therapeutic purposes and health is reflected by the popularity of pro- and prebiotics and even such seemingly esoteric therapies as human being fecal transplantation. 15

Not all the species in the gut have been identified because about cannot be cultured, 10 and identification is difficult. An try to better describe the microflora of the gut and other body locations using newly adult non-culture based technologies16 has been initiated and termed the "Homo Microbiome Project"17. This project has a mission of generating resources enabling comprehensive label of the human microbiota and analysis of its part in human health and disease. Although the homo intestine is the site where most studies are being focused, other sites such every bit the pare, float, mouth and vagina harbor singled-out microbial populations and are probable to also play major roles in health and illness16.

Intestinal MICROECOLOGY OF THE FETUS AND NEWBORN

Nearly current literature suggests that the gastrointestinal tract of a normal fetus is sterile. During nativity and chop-chop thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. It is obvious that exposure at birth would differ by way of commitment. What long term sequelae or affect this deviation in exposure may accept on the kid has yet to exist determined.

Some recent research piece of work suggests colonization may begin even before. While the epitome has been that babies' intestines are sterile until birth, contempo work constitute a microbial community already dwelling in the meconium of some babies born prematurely.18 It has also been shown that amniotic fluid of mothers with preterm labor contains a large and various spectrum of bacterial rDNA. 20 While a babe is in utero, information technology typically swallows 400 to 500 milliliters of amniotic fluid per day at term, and the hypothesis that intra-amniotic infection is the driving force backside preterm labor is ane beingness widely studied in obstetrics.19 Whether the microbes or microbial components swallowed in the amniotic fluid stimulate an inflammatory response driving preterm birth remains to be evaluated. The result these organisms accept on the developing immune system, aside from their role in preterm labor, also raises interesting questions.

Currently, very few studies accept investigated the development of the human microbiota later nascence using non-culture based techniques. In a step toward greater systematic investigation of babies born at term, Palmer et al.21 evaluated the developing microbiota of infants during the showtime year after nativity using microarray techniques to detect and quantify the minor subunit ribosomal RNA (SSU rRNA) gene sequences of most currently recognized species and taxonomic groups of bacteria; this was done along with sequencing of cloned libraries of PCR-amplified SSU rDNAto contour the microbial communities in xiv good for you full-term infants during the get-go year later birth. To investigate possible origins of the babe microbiota, the researchers also profiled vaginal and milk samples from most of the mothers every bit well as stool samples from all of the mothers, most of the fathers, and two siblings. The investigators found that the composition and temporal patterns of the microbial communities varied widely from baby to baby, but the distinct features of each infant's microbial community were recognizable for intervals of weeks to months. The strikingly parallel temporal patterns from a set of dizygotic twins suggested that incidental environmental exposures play a major function in determining the distinctive characteristics of the microbial customs in each baby. By the finish of the outset twelvemonth of life, microbial ecosystems in each babe, although still distinct, had converged toward a profile feature of the adult alimentary canal. Of involvement, Bifidobacteria were non found in these infants using these techniques. This could be highly meaning in that it may debunk the large corporeality of attention this microbe has received as a potentially important microbe that may exist harnessed as a probiotic. On the other hand, this could be a technical problem that nevertheless needs to be solved using these newly adult methodologies.

Although a few studies accept monitored the bacterial communities in preterm infants, our picture of the intestinal microbiota still remains limited. To determine whether noncultured bacteria stand for an important part of the customs in premature babies' abdominal ecosystems, Magne et al.22 used 16S rRNA genes and PCR-based electrophoretic profiling of 288 clones obtained from the fecal samples of 16 preterm infants. These were classified into 25 molecular species. The hateful number of molecular species per infant was iii.25 and ranged from one to eight. The researchers found high interindividual variability. The main bacterial groups encountered belonged to the Enterobacteriaceae family unit and the genera Enterococcus, Streptococcus, and Staphylococcus. The preterm infants were colonized by anaerobes and only iv bifidobacteria (once more seeming to minimize these taxa during development). The researchers did non make up one's mind the relative impacts of delivery manner, sex, gestational age, birth weight, age at sampling, feeding modes, and antibiotic therapies. They ended that species diversity was depression and interindividual variability was loftier in the carrion of preterm infants, as revealed by sequences of 16S rRNA genes and PCR-temporal temperature gradient gel electrophoresis profiles (TGGE). The abdominal ecosystem of these preterm infants had no typical characteristic.

In summary, whether the fetal intestinal ecosystem is sterile at the time of birth remains a question. This may exist the case in some infants, merely not necessarily in others, particularly preterms. This may in plow play a function in the initiation of preterm labor. Nevertheless, the species diversity does appear to be depression in virtually infants before long later on birth, but this increases with environmental exposure. Very little is currently known about the specific emergence of the microbial ecology of infants during the first year after birth and how this specifically relates to development of immunity and subsequent wellness and affliction.

FUNCTIONS OF THE INTESTINAL MICROBIOTA

A comprehensive review of the functions of the intestinal microbiota is beyond the scope of this review, just here nosotros wish to focus on the immunologic functions because of their importance in development of the immune system and possible pathogenesis of several known allergic and autoimmune diseases. Abdominal bacteria are central in promoting the early development of the gut's mucosal allowed system, both in terms of its physical components and part and continue to play a role later in life in its operation. The bacteria stimulate the lymphoid tissue associated with the gut mucosa to produce antibodies to pathogens. The allowed system recognizes and fights harmful bacteria, just leaves the helpful species lonely, a tolerance developed in infancy, and sometimes termed the "old friends" hypothesis. 23 (Effigy 2) This hypothesis appears to be a synthesis of the hygiene hypothesis that proposes that the role of these microorganisms that have evolve with humans provide an essential role in the institution of the immune system wherein the microorganisms and the host have evolved a co-dependence: the near relevant organisms are those that co-evolved with mammals. These microorganisms are interacting with other modernistic environmental changes that also lead to enhanced inflammatory responses such as inappropriate diet, obesity, psychological stress, vitamin D deficiency, pollution (dioxins), and perhaps even cesarean delivery. The range of chronic inflammatory disorders that is afflicted is potentially larger than usually assumed and include allergies, autoimmunity, inflammatory bowel disease, but besides vascular affliction, some cancers, depression/feet and perhaps neurodegenerative disorders and type two diabetes.

An external file that holds a picture, illustration, etc.  Object name is nihms-284291-f0002.jpg

"The Old Friends Hypothesis"

Common organisms interact with dendritic cells in the GI tract, leading to increased maturation of dendritic cells. When in that location is interaction with these organisms again, the dendritic cells increment Treg maturation; not Th1 or Th2. This increases the baseline amount of anti-inflammatory cytokines, producing a Eyewitness Suppression. Some other consequence of the increased number of mature dendritic cells is as they interact with cocky antigens, they increase the number Treg specific to these antigens. This is referred to as Specific Suppression. Together these two arms atomic number 82 to tolerance of both self antigens as well as those of helpful gut organisms.

Bones laboratory based research is supplementing the epidemiologic studies. Recent findings have shown that gut bacteria play a role in the expression of Toll-like receptors (TLRs) in the intestines. TLRs are one of the two classes of blueprint recognition receptors (PRR) that provide the intestine the power to discriminate between pathogenic and commensal leaner. These PRRs identify the pathogens that have crossed the mucosal barrier and trigger a set of responses that take action confronting the pathogen, involving 3 master immunosensory cells: surface enterocytes, Yard cells and dendritic cells.24 The other class of PRRs are known as the nucleotide-binding oligomerization domain/caspase recruitment domain isoforms (NOD/CARD), which are cytoplasmic proteins that recognize endogenous or microbial molecules or stress responses and form oligomers that activate inflammatory caspases. This would result in the cleavage and activation of important inflammatory cytokines and/or activate the NF-κB signaling pathway to induce the production of inflammatory molecules. 24

Bacteria tin can influence the phenomenon known equally oral tolerance, in which the immune arrangement is less sensitive to an antigen (including those produced past gut leaner) once it has been ingested. This tolerance, mediated in part by the gastrointestinal immune system and in part by the liver, can reduce overreactive immune responses like those found in allergies and auto-allowed disease.25

There are several antenatal and perinatal events that might also bear on the development of the intestinal microbial ecology. Therapy with broad-spectrum antibiotics is a mutual do for mothers who go into premature labor or who take a CD. This treatment can reduce the biodiversity of the fecal microbiota and may be a factor in the crusade of necrotizing enterocolitis. 26 , 27 Studies in mice show that intestinal commensal microbiota accept an influence on early on postnatal allowed development via interactions with abdominal Toll like receptors, which in turn are likely to influence the evolution of the mucosal immune system and mucosal-related diseases.28 Other studies suggest that specific microbes may induce regulatory T-prison cell development. For example, a prominent human commensal, Bacteroides fragilis, directs the development of Foxp3(+) regulatory T cells (Tregs) with a unique "inducible" genetic signature. 29 Monocolonization of germ-gratuitous animals with B. fragilis increases the suppressive chapters of Tregs and induces anti-inflammatory cytokine product exclusively from Foxp3(+) T cells in the gut. This outcome appears to be mediated by an immunomodulatory molecule, polysaccharide A (PSA), of B. fragilis, which mediates the conversion of CD4(+) T cells into Foxp3(+) Treg cells that produce IL-10 during commensal colonization. Functional Foxp3(+) Treg cells are also produced by PSA during intestinal inflammation, and Toll-like receptor two signaling is required for both Treg induction and IL-10 expression. These studies as well evidence that PSA is not only able to prevent, merely also cure experimental colitis in animals and therefore demonstrate that B. fragilis Treg lineage differentiation pathway in the gut to actively induce mucosal tolerance.29

VAGINAL VS. CESAREAN Commitment

During vaginal delivery, the contact with the maternal vaginal and intestinal flora is an important source for the start of the infant'southward colonization. During CD, this direct contact is absent, and non-maternally derived environmental leaner play an important role for infants' intestinal colonization.31 Some authors have suggested that the limerick of the very first human microbiota could have long lasting furnishings on the intestine in breast fed infants. For example, Gronlund, et al 32 showed that the primary gut flora in infants born by cesarean commitment may be disturbed for up to six months subsequently birth. Another study using culture based techniques showed that the mode of delivery was associated with differences in abdominal microbes 7 years after delivery. 33 The clinical relevance of these changes is unknown, and even longer follow-up is needed to plant how long-lasting these alterations of the primary gut flora tin can be.

Nonetheless, in that location is accumulating prove that intestinal bacteria play an important role in the postnatal development of the immune system. 30 Thus, if the intestinal flora develops differently depending on the style of delivery, the postnatal development of the allowed system might also be different. Available epidemiological data show that atopic diseases appear more than often in infants later cesarean delivery than after vaginal delivery.34 - 37 The composition of enteric microbiota in early days of life seems, therefore, to be a very important factor for achieving and maintaining skilful health in the years to come. It follows that it is fundamental to identify more thoroughly the intestinal ecosystem of the newborn.

Although in that location is an increasing torso of evidence that the intestinal microbiota play an essential role in the postnatal development of the immune arrangement, the mechanisms remain poorly understood. Malamitsi-Puchner et al.38 found that only vaginal commitment promotes the production of various cytokines implicated in neonatal immunity. Hallstrom et al. 39 found a link between cesarean commitment, disturbed intestinal colonization, and, maybe, occurrence of necrotizing enterocolitis (NEC) in preterm infants. Although the epidemiological studies demonstrated that elective cesarean delivery provides an increased risk for allergic diseases in after babyhood, confounding factors could also play intermediate roles. Data available from several studies indicate a delayed onset of lactation with cesarean department.twoscore , 41 Thus, many infants born past cesarean delivery too lacked the early back up of chest milk as stimulator for a physiological intestinal flora. Both the nonphysiological showtime of colonization and the missing early dietary back up past delayed start of lactation might result in these long-lasting effects.

Babies are built-in with immunological tolerance that is instructed by the female parent by preferential induction of regulatory T lymphocytes42, which might allow the baby to become colonized by this get-go inoculum. The mechanism is via substantial numbers of maternal cells crossing the placenta to reside in fetal lymph nodes, inducing the development of CD4+CD25highFoxP3+ Tregs that suppress fetal anti-maternal amnesty and persist at least until early machismo. However, only a subset (if whatever) of the microbes to which the newborn is initially exposed will permanently colonize bachelor niches and contribute to the distinctive microbiota harbored by the body habitats of adults. 21 Every bit more than and more deliveries bypass the vagina, babies may not exist exposed to these microbes at birth. Differences in delivery mode have been linked with differences in the intestinal microbiota of babies.31 , 32 , 43 , 44 Initial communities may serve as a direct source of protective or pathogenic bacteria very early on in life.

Another recent study45, offers a detailed look at the early stages of the body's colonization by microbes. Babies built-in vaginally were colonized predominantly by Lactobacillus, whereas cesarean delivery babies were colonized past a mixture of potentially pathogenic bacteria typically found on the pare and in hospitals, such as Staphylococcus and Acinetobacter, southwarduggesting babies born past CD were colonized with skin flora in lieu of traditionally vaginal type of bacterium.

The outcome of mode of commitment on development of childhood disease has but recently begun to be explored (Table 1). The effect appears to be most robust in the area of immune mediated diseases. CD has been associated with a pregnant increased rate of asthma, especially in females, and allergic rhinitis, merely not atopic dermatitis.46 This increase was even more credible when accounting for the factors surrounding the CD. The risk of asthma was increased by lx% in females who underwent a repeat cesarean without ruptured membranes versus those babies with ruptured membranes and/or labor prior to CD.46

Table 1

Cesarean Delivery Associated Childhood Diseases1 , ii
Allergic Rhinitis
All Cesareans 1.37 (1.xiv-1.63)
Echo Cesareans Only 1.78 (1.34-2.37)
Asthma
All Cesareans 1.24 (1.01-1.53)
Female ane.53 (1.10-two.10)
Female & Repeat Cesarean 3 1.83 (ane.13-ii.97)
Celiac Disease 1.80 (1.13-two.88)
Diabetes Mellitus (Type 1) 1.19 (one.04-1.36)
Gastroenteritis 4 1.31 (ane.24-ane.38)
Gastroenteritis AND Asthma 1.74 (ane.36-2.23)

Children born by CD are as well significantly more than likely to endure from celiac disease and to be hospitalized for gastroenteritis.47 No clan has been found between CD and Crohn's illness or ulcerative colitis. Withal, while preterm birth has been implicated in the evolution of inflammatory bowel illness, mode of delivery has not 48

Type I Diabetes Mellitus has been on the rise in recent decades, mirroring the rise in CD.49 Meta-analysis plant a xix% increase in Type I DM in cesarean children when controlling for confounders such as gestational age, maternal historic period, and birth weight. 50 A recent retrospective study of children in Scotland failed to show such an clan. 51 However, information technology is important to betoken out that the Scotland report had a very small number of subjects (n=361) compared to the meta-assay (n=9938) and the charge per unit of CD was only 14% in the Scottish study (much beneath the US average).

SUMMARY AND CONCLUSIONS

While CD is necessary in modern obstetrics, the procedure appears to shift a babe's outset bacterial community. A meliorate understanding of this early on colonization, which is also influenced by events such as breast-feeding, may lead to medical practices for establishing salubrious bacterial colonization. The causal relationship between CD, the shift in microbiota and many childhood diseases continues to be studied. However, at that place are several problems with the studies we have reviewed here.

Information technology is impossible to lump CD into ane category without delineating the indication for CD. It stands to reason that a fetus delivered after abort at 8 centimeters dilation after a long labor would be exposed to a much unlike microbial surround than a fetus that undergoes CD for maternal request prior to rupture of membranes. It is naïve to think that the fetus is only exposed to microbes every bit the head passes through the vaginal introitus onto the perineum and to ignore the constant exposure to vaginal flora afterwards rupture of membranes. Sonntag et al 48 failed to testify a human relationship between manner of delivery and inflammatory bowel illness. Notwithstanding, the boilerplate age of a subject in this study was 42 years old. Indication for CD in the late 1960'due south, prior to common use of external fetal monitoring, is strikingly dissimilar than modern obstetrical indications. The intrapartum exposures of these subjects is about likely vastly different than a more than contemporary cohort. Hereafter studies must be more than meticulous in categorizing CD to fully understand the consequence of CD on colonization and babyhood disease.

The function of antepartum and intrapartum antibiotics must too be accounted for in future studies. What result, if any, these accept on the microbiota of the fetus and/or subsequent development of illness is unknown. Nearly 20% of women in the U.s.a. are colonized with Grouping B Streptococcus and will subsequently receive intrapartum antibiotics. Standard of care likewise dictates that antibiotics be administered prior to cesarean commitment and to mothers in preterm labor and/or with premature prolonged rupture of membranes. Given all of this, the exposure to antenatal antibiotics is pregnant. Dominguez-Bello 45 noted a difference in fetal colonization based on mode of delivery. However, none of their vaginally delivered patients received antibiotics and the cesarean cases received cephalosporin "several hours" prior to incision which is not the recommended course in the U.s.. Whether this exposure accounts for the divergence, or if fetuses who receive antibiotics per standard guidelines in the US show a different colonization pattern, is an of import enquiry surface area to explore.

The link betwixt mode of commitment and subsequent childhood pathology is an important one. This becomes even more of import as maternal desire for primary cesarean delivery is on the ascent and rates of vaginal nascence after cesarean (VBAC) are failing in this state. This new data almost colonization differences with differing modes of delivery seems to exist taking the hygiene hypothesis to an entirely new level.

Footnotes

Publisher'due south Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its terminal citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that utilise to the journal pertain.

Dr. Neu is an Advisory Board Member for Mead Johnson and Medela.

~ The journey of a thousand miles begins with i step. ~

Lao Tsu

REFERENCES

1. Hamilton BE, Martin JA, Ventura SJ. Births: Preliminary Information for 2007. National Vital Statistics Reports. 2009;57(12):1–21. [PubMed] [Google Scholar]

2. Lumbiganon P, Laopaiboon M, Gülmezoglu M, et al. Method of delivery and pregnancy outcomes in Asia: the WHO global survey on maternal and perinatal health 2007—08. The Lancet. 2010;375(9713):490–9. [PubMed] [Google Scholar]

3. Rebelo F, da Rocha CM, Cortes TR, et al. High cesarean prevalence in a national population-based study in Brazil: the part of private practise. Acta Obstet Gynecol Scand. 2010;89(7):903–8. [PubMed] [Google Scholar]

4. Okada H, Kuhn C, Feillet H, et al. The 'hygiene hypothesis' for autoimmune and allergic diseases: an update. Clin Exp Immunol. 2010;160(1):1–9. [PMC costless article] [PubMed] [Google Scholar]

5. Bach JF. The issue of infections on susceptibility to autoimmune and allergic diseases. N Engl J Med. 2002;347(12):911–20. [PubMed] [Google Scholar]

7. Caicedo RA, Schanler RJ, Li N, Neu J. The developing intestinal ecosystem: implications for the neonate. Pediatr Res. 2005;58(4):625–8. [PubMed] [Google Scholar]

8. Rautava Due south, Walker WA. Commensal bacteria and epithelial cross talk in the developing intestine. Curr Gastroenterol Rep. 2007;9(v):385–92. [PMC complimentary article] [PubMed] [Google Scholar]

9. Eberl G, Lochner Chiliad. The development of intestinal lymphoid tissues at the interface of self and microbiota. Mucosal Immunol. 2009;ii(six):478–85. [PubMed] [Google Scholar]

10. Sears CL. A dynamic partnership: celebrating our gut flora. Anaerobe. 2005;11(5):247–51. [PubMed] [Google Scholar]

11. Steinhoff U. Who controls the crowd? New findings and old questions nearly the abdominal microflora. Immunol Lett. 2006;99(1):12–6. [PubMed] [Google Scholar]

13. Qin J, Li R, Raes J, et al. A human being gut microbial factor catalogue established by metagenomic sequencing. Nature. 2010;464(7285):59–65. [PMC free commodity] [PubMed] [Google Scholar]

14. Guarner F, Malagelada JR. Gut flora in health and disease. Lancet. 2003;361(9356):512–9. [PubMed] [Google Scholar]

15. Khoruts A, Dicksved J, Jansson JK, et al. Changes in the limerick of the human fecal microbiome after bacteriotherapy for recurrent Clostridium difficile-associated diarrhea. J Clin Gastroenterol. 2010;44(5):354–60. [PubMed] [Google Scholar]

xvi. Dethlefsen L, McFall-Ngai K, Relman DA. An ecological and evolutionary perspective on human being-microbe mutualism and disease. Nature. 2007;449(7164):811–8. [PubMed] [Google Scholar]

17. Group NHW, Peterson J, Garges S, et al. The NIH Human Microbiome Project. Genome Res. 2009;xix(12):2317–23. [PMC free article] [PubMed] [Google Scholar]

18. Mshvildadze Chiliad, Neu J, Schuster J, et al. Intestinal microbial ecology in premature infants assessed with non-civilisation-based techniques. J Pediatr. 2010;156(1):20–five. [PMC free article] [PubMed] [Google Scholar]

19. Goldenberg RL, Culhane JF, Iams JD, et al. Epidemiology and causes of preterm nativity. Lancet. 2008;371(9606):75–84. [PMC free article] [PubMed] [Google Scholar]

20. DiGiulio DB, Romero R, Amogan HP, et al. Microbial prevalence, multifariousness and affluence in amniotic fluid during preterm labor: a molecular and civilization-based investigation. PLoS 1. 2008;3(eight):e3056. [PMC gratis commodity] [PubMed] [Google Scholar]

21. Palmer C, Bik EM, Digiulio DB, et al. Development of the Human being Infant Intestinal Microbiota. PLoS Biol. 2007;v(seven):e177. [PMC free article] [PubMed] [Google Scholar]

22. Magne F, Abély M, Boyer F, et al. Low species diversity and high interindividual variability in faeces of preterm infants as revealed past sequences of 16S rRNA genes and PCR-temporal temperature gradient gel electrophoresis profiles. FEMS Microbiol Ecol. 2006;57(ane):128–38. [PubMed] [Google Scholar]

23. Rook GA. 99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: darwinian medicine and the 'hygiene' or 'erstwhile friends' hypothesis. Clin Exp Immunol. 2010;160(1):70–xc. [PMC complimentary article] [PubMed] [Google Scholar]

25. Round JL, O'Connell RM, Mazmanian SK. Coordination of tolerogenic immune responses by the commensal microbiota. J Autoimmun. 2010;34(3):J220–five. [PMC free commodity] [PubMed] [Google Scholar]

26. Cotten CM, Taylor S, Stoll B, et al. Prolonged elapsing of initial empirical antibiotic treatment is associated with increased rates of necrotizing enterocolitis and death for extremely low birth weight infants. Pediatrics. 2009;123(ane):58–66. [PMC free article] [PubMed] [Google Scholar]

27. Wang Y, Hoenig JD, Malin KJ, et al. 16S rRNA gene-based assay of fecal microbiota from preterm infants with and without necrotizing enterocolitis. ISME J. 2009;3(8):944–54. [PMC free article] [PubMed] [Google Scholar]

28. Dimmitt RA, Staley EM, Chuang G, et al. Part of Postnatal Acquisition of the Intestinal Microbiome in the Early Development of Immune Function. J Pediatr Gastroenterol Nutr. 2010 [PMC complimentary commodity] [PubMed] [Google Scholar]

29. Round JL, Mazmanian SK. Inducible Foxp3+ regulatory T-jail cell development by a commensal bacterium of the abdominal microbiota. Proc Natl Acad Sci U South A. 2010;107(21):12204–nine. [PMC gratuitous commodity] [PubMed] [Google Scholar]

30. Björkstén B. Effects of intestinal microflora and the environment on the development of asthma and allergy. Springer Semin Immunopathol. 2004;25(3-iv):257–70. [PubMed] [Google Scholar]

31. Biasucci Yard, Benenati B, Morelli Fifty, et al. Cesarean delivery may affect the early biodiversity of intestinal bacteria. J Nutr. 2008;138(9):1796S–800S. [PubMed] [Google Scholar]

32. Grönlund MM, Lehtonen OP, Eerola E, et al. Fecal microflora in healthy infants born by unlike methods of delivery: permanent changes in intestinal flora afterward cesarean delivery. J Pediatr Gastroenterol Nutr. 1999;28(1):nineteen–25. [PubMed] [Google Scholar]

33. Salminen South, Gibson GR, McCartney AL, et al. Influence of mode of commitment on gut microbiota composition in seven year old children. Gut. 2004;53(9):1388–9. [PMC complimentary article] [PubMed] [Google Scholar]

34. Negele K, Heinrich J, Borte M, et al. Mode of delivery and development of atopic disease during the beginning 2 years of life. Pediatr Allergy Immunol. 2004;15(1):48–54. [PubMed] [Google Scholar]

35. Debley JS, Smith JM, Redding GJ, et al. Childhood asthma hospitalization risk after cesarean delivery in former term and premature infants. Ann Allergy Asthma Immunol. 2005;94(two):228–33. [PubMed] [Google Scholar]

36. Laubereau B, Filipiak-Pittroff B, von Berg A, et al. Caesarean section and gastrointestinal symptoms, atopic dermatitis, and sensitisation during the first year of life. Arch Dis Child. 2004;89(11):993–7. [PMC free commodity] [PubMed] [Google Scholar]

37. Eggesbø Thou, Botten M, Stigum H, et al. Is delivery by cesarean section a risk gene for food allergy? J Allergy Clin Immunol. 2003;112(2):420–6. [PubMed] [Google Scholar]

38. Malamitsi-Puchner A, Protonotariou Due east, Boutsikou T, et al. The influence of the mode of delivery on circulating cytokine concentrations in the perinatal period. Early on Hum Dev. 2005;81(iv):387–92. [PubMed] [Google Scholar]

39. Hällström M, Eerola E, Vuento R, et al. Effects of mode of delivery and necrotising enterocolitis on the intestinal microflora in preterm infants. Eur J Clin Microbiol Infect Dis. 2004;23(6):463–70. [PubMed] [Google Scholar]

40. Dewey KG, Nommsen-Rivers LA, Heinig MJ, et al. Take a chance factors for suboptimal infant breastfeeding behavior, delayed onset of lactation, and excess neonatal weight loss. Pediatrics. 2003;112(3Pt1):607–19. [PubMed] [Google Scholar]

41. Evans KC, Evans RG, Royal R, et al. Result of caesarean section on breast milk transfer to the normal term newborn over the beginning week of life. Arch Dis Kid Fetal Neonatal Ed. 2003;88(5):F380–2. [PMC free article] [PubMed] [Google Scholar]

42. Mold JE, Michaëlsson J, Burt TD, et al. Maternal alloantigens promote the evolution of tolerogenic fetal regulatory T cells in utero. Science. 2008;322(5907):1562–5. [PMC costless article] [PubMed] [Google Scholar]

43. Mackie RI, Sghir A, Gaskins Hr. Developmental microbial ecology of the neonatal gastrointestinal tract. Am J Clin Nutr. 1999;69(five):1035S–45S. [PubMed] [Google Scholar]

44. Penders J, Thijs C, Vink C, et al. Factors influencing the composition of the abdominal microbiota in early on infancy. Pediatrics. 2006;118(2):511–2. [PubMed] [Google Scholar]

45. Dominguez-Bello MG, Costello EK, Contreras M, et al. Commitment way shapes the conquering and structure of the initial microbiota across multiple body habitats in newborns. Proc Natl Acad Sci U S A. 2010;107(26):11971–5. [PMC free article] [PubMed] [Google Scholar]

46. Renz-Polster H, David MR, Buist AS, et al. Caesarean section delivery and the chance of allergic disorders in childhood. Clin Exp Allergy. 2005;35(eleven):1466–72. [PubMed] [Google Scholar]

47. Decker E, Engelmann M, Findeisen A, et al. Cesarean delivery is associated with celiac affliction but non inflammatory bowel illness in children. Pediatrics. 2010;125(6):e1433–40. [PubMed] [Google Scholar]

48. Sonntag B, Stolze B, Heinecke A, et al. Preterm nativity simply not fashion of delivery is associated with an increased run a risk of developing inflammatory bowel disease later in life. Inflamm Bowel Dis. 2007;13(11):1385–ninety. [PubMed] [Google Scholar]

49. Onkamo P, Vaananen South, Karvonen M, et al. Worldwide increment in incidence of Blazon I diabetes--the assay of the data on published incidence trends. Diabetologia. 1999;42(12):1395–403. [PubMed] [Google Scholar]

50. Cardwell CR, Stene LC, Joner G, et al. Caesarean section is associated with an increased risk of childhood-onset blazon 1 diabetes mellitus: a meta-analysis of observational studies. Diabetologia. 2008;51(5):726–35. [PubMed] [Google Scholar]

51. Robertson L, Harrild K. Maternal and neonatal gamble factors for childhood blazon 1 diabetes: a matched example-control written report. BMC Public Wellness. 2010;27(10):281. [PMC costless commodity] [PubMed] [Google Scholar]

hillprideaught.blogspot.com

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110651/

0 Response to "what diseases are c section babies more prone to colic"

Post a Comment

Iklan Atas Artikel

Iklan Tengah Artikel 1

Iklan Tengah Artikel 2

Iklan Bawah Artikel