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Necrotizing enterocolitis (NEC) is a serious disease that affects the bowel of premature infants in the first few weeks of life.
This review is available through the The Cochrane Library, which contains more than 5,300 research reviews produced by an international network of over 28,000 research experts and consumer representatives from 120 countries. We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. The field of genomics has expanded into subspecialties such as metagenomics over the course of the last decade and a half.
The purpose of this brief review is to introduce the reader to the concept of the human microbiome and to summarize recent literature specifically regarding the neonatal gut microbiome, from its establishment at birth through its evolution during early infancy.
The first, and most important, contribution to the genesis of the microbiome is vertical transmission of maternal microbiota.
As such, the gastrointestinal (GI) tract has the greatest diversity and abundance of microbes and evidence is mounting that it becomes colonized antenatally. Infants born via vaginal delivery have intestinal colonization reflective of maternal vaginal flora such as Lactobacillus and Prevotella species. Further development of the neonatal gut microbiome after birth, regardless of mode of delivery is governed by interaction between the microbiota and the host’s immune system. Once established, the intestinal microbiome engages in a symbiotic relationship with its host. Nutrition, be it breast milk or formula, has been demonstrated to play a major role in early colonization patterns of the neonatal gut microbiota. Live bacteria are also found in human milk, including Staphylococcus, Streptococcus, Bifidobacterium, and Lactobacillus (33). Formula-fed infants are exposed to a different array of carbohydrates, bacteria, and nutrients, which leads to different colonization patterns and immunomodulatory effects on their developing gut microbiota. In breast-fed infants, transmission of sIgA from the mother is reflective of her own microbiota and confers a protective effect against pathogens that could lead to dysbiosis, the disruption of a healthy, functional infant microbiome. This difference in colonization and transmission of immune-modulating factors between breast and formula-fed infants may have far reaching effects over the course of a human’s life as it may impact disease risk.
Preterm infants, particularly VLBW infants, are at a disadvantage when it comes to development of a healthy microbiome. In addition to altered microbial diversity as described above, premature infants are both qualitatively and quantitatively immunodeficient, owing to their underdeveloped immune systems. Even after the microbiome is well established in healthy infants, dysbiosis, or shifts in microbial composition or diversity, can occur in the setting of dietary changes, antibiotic exposure, or infection. Given the relative instability and impressionability of the developing gut microbiome in early life, coupled with its purported disease prediction, detection, and treatment benefits, it seems logical to explore avenues within which evolution and maintenance of a healthy gut milieu can be promoted. Although the cause of NEC is not entirely known, milk feeding and bacterial growth play a positive role.
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This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. The development of massively parallel sequencing capabilities has allowed for increasingly detailed study of the genome of the human microbiome, the microbial super organ that resides symbiotically within the mucosal tissues and integumentary system of the human host.
This burgeoning area of study has resulted in significant advances in whole-genome analysis techniques that have greatly facilitated the study of the human microbiome.
It is an entity that has wide-reaching metabolic, nutritional, and immunological effects on the host, and as such has generated a great deal of interest within the biomedical research community.
We review differences in microbial colonization and immune function of the intestinal tract in healthy full-term newborns compared with their preterm very low birth weight (VLBW) (birth weight <1500 g) counterparts and the implications for development of disease when the microbiome is disrupted (dysbiosis). Colonization of mucosa in the digestive, respiratory, urogenital tracts, as well as the skin begins at, or perhaps even before, the time of birth when a newborn is exposed to a mother’s microbiota. This exceeds the number of self and pathogen-based antigens a human will encounter in their lifetime (12).
Infants born via Cesarean delivery are colonized by epidermal rather than vaginal species, such as Clostridium, Staphylococcus, Propionobacterium, and Corynebacterium and they have a deficiency of anaerobes with lower numbers of Bacteroides and Bifidobacterium when compared to vaginally born infants (14–18). The progression of how this evolves remains incompletely characterized and many questions remain surrounding the true origins of the microbes that colonize the neonatal gut and what factors underlie inter-infant differences in gut microbiota, Palmer et al. The neonatal immune system will rapidly mature secondary to influence of microbiota, diet, exposure to new microbes, xenobiotics, and other environmental exposures (12). Several associated factors influence the dynamic composition of the breast milk microbiota, including maternal health and mode of delivery (34). In contrast to human milk oligosaccharides as mentioned earlier in this section, oligosaccharides currently added to infant formula are structurally different from those naturally found in human milk and, therefore, are unlikely to mimic some of the structure-specific effects on the gut that are seen in breast-fed neonates (32). In particular, it enables digestion of otherwise indigestible carbohydrates and triggers activation of lipoprotein lipase. Factors contributing to this are not limited to their gut immaturity, and also include preterm rupture of membranes, maternal infection, increased incidence of Cesarean delivery, perinatal and postnatal broad-spectrum antibiotic exposure as well as exposure to other gut-modifying medications such as H2 blockers, altered gut motility, periods of fasting, intensive care infection control standards and selection for resistant microbes, and decreased exposure to human milk (17, 25, 29, 50). They have suboptimal gut epithelial cell barrier function at baseline, predisposing them to invasion by pathogens that in turn can trigger exaggerated inflammatory responses by their still-developing immune system that may lead to disease processes such as necrotizing enterocolitis (NEC) (16, 55).
Dysbiotic conditions can favor invasion and growth of pathogenic species and can disrupt the finely tuned regulatory circuits of the immune system that maintain a system of pro- and anti-inflammatory checks and balances.
Probiotics (dietary supplements containing potentially beneficial bacteria or yeast) have been used to prevent NEC.


The gut microbiome, and particularly the study of its origins in neonates, has become subtopics of great interest within the field of genomics. The microbiome evolves within a healthy host from birth to death, constantly fine-tuning it to maintain a homeostatic balance with the host’s immune system.
It was previously thought that the in utero environment was largely sterile and that a fetus was not colonized with bacteria until the time of birth.
Thus, the mode of delivery appears to have an influence on the diversity and function of an infant’s microbiota, which can persists for months and, perhaps longer, after birth.
The organisms that comprise the microbiota benefit from the warm, nutrient-rich environment afforded by the gut.
Oligosaccharides, glycoconjugates, and natural components of human milk are also thought to prevent the attack of enteropathogens and stimulate growth of Bifidobacterium (4, 30, 31). At least some of the bacteria present in the maternal gut is thought to reach the mammary gland through an endogenous route, the so-called enteromammary pathway and likely contributes to the bacterial composition of breast milk (17). It has been demonstrated that term breastfed infants have a gut microbiota dominated by species of Bifidobacterium but decreased Enterobacteria. An increasingly investigated avenue is the relationship between alterations in the gut microbiome and its possible involvement in the development of disease later in life. This leads to glucose absorption and storage of fatty acids and thus to excessive weight gain.
Given these factors, it seems likely, and has indeed been shown to be true that a preterm infant’s gut microbiota has reduced microbial diversity coupled with an increase in colonization with pathogenic organisms (17, 51). This immune dysfunction, coupled with low diversity of gut microbiota and possibly an overall predominance of pathogenic bacteria within the preterm intestinal microbiome has been noted in at-risk preterm neonates with life threatening Enterobacter and coagulase negative Staphylococcus sepsis, and is a prime example of dysbiosis (14, 56, 57). The neonatal microbiome, in healthy full-term infants and especially in preterm infants given its dynamic nature, is fragile and impressionable. A Cochrane updated Review of studies found that the use of probiotics reduces the occurrence of NEC and death in premature infants born less than 1500 grams. This brief review seeks to summarize recent literature regarding the origins and establishment of the neonatal gut microbiome, beginning in utero, and how it is affected by neonatal nutritional status (breastfed versus formula fed) and gestational age (term versus preterm). Continued evolution of the human microbiome after birth is governed by host factors such as both the adaptive and innate immune system, as well as external factors such as diet, medication and toxin exposure, and illness (3, 4). Recent studies suggest the presence of a microbiome within the placenta as well as fetal meconium, suggesting that the colonization process begins well before delivery. Interestingly, each individual’s microbiome is populated by only 15% of the 1000 plus species of intestinal bacteria already described, leading to significant inter-individual variability of the microbiome (4, 12).
They noted an overall earlier appearance of aerobes such as Staphylococcus, Streptococcus, and Enterobacteria; a later appearance of anaerobes such as Eubacteria and Clostridium, and variable timing of the emergence of Bacteroides, which ultimately established a presence in all babies by age 1 year. These human milk oligosaccharides are known to directly interact with the surface of pathogenic bacteria, and various oligosaccharides in milk are believed to inhibit the binding of pathogens and toxins to host cell receptors (32). The composition of breast milk bacteria becomes increasingly less diverse, beginning with typical skin- and enteric-type organisms in colostrum to less diverse flora with greater infant oral and skin microbiota as lactation progresses (35).
This promotes formation of regulatory immune networks that further govern development and function of the gut microbiome (12).
A prime example of this is the obesity epidemic, which may begin as early as the perinatal period.
Increased numbers of Firmicutes and decreased Bacteroidetes in the gut microbiota have also been shown in experimental animal models to predispose toward excess energy storage and obesity (46, 47).
Additionally, the preterm gut microbiome is less stable compared to that of term counterparts and is also thought to be delayed in transition to an adult colonization pattern (3, 14, 25, 29).
As such, the microbiome is extremely susceptible to external influences that can dramatically affect the short- and long-term health of the host. There is insufficient data with regard to the benefits and potential adverse effects in the most at risk infants less than 1000 grams at birth.
We also explore the role of dysbiosis, a perturbation within the fragile ecosystem of the microbiome, and its role in the origin of select pathologic states, specifically, obesity and necrotizing enterocolitis (NEC) in preterm infants. Of particular interest is the study of the gut microbiome, its evolution beginning in utero and across the lifespan, its effect on promotion of health, and its role in the development of disease. Transient colonization was noted at varying time points by other organisms including Prevotella, Acinetobacter, Desulfovibrio, Veillonella, and Clostridium perfringens (21).
The human, in turn, benefits from activities of the microbiota that primarily allow for an increased digestive capacity and an ability to harvest nutrients from food. Other constituents of human milk, such as interleukin-10, epidermal growth factor, transforming growth factor-β1, and erythropoietin, can represent important mediators in the inflammatory response against bacterial pathogens within the gut (4). Non-digestible carbohydrates found in breast milk ferment in the colon and promote further growth of probiotic Bifidobacterium and Bacteroides species (27). Interestingly, even relatively small amounts of formula supplementation of breast-fed infants will result in shifts from a breast-fed to a formula-fed pattern (41, 42).
Production of metabolites such as short chain fatty acids such as butyrate and acetate by early commensal gut microbiota may play a role in epigenetic alteration of gut epithelium and immune function that predispose to diseases like obesity (25, 48).
The development of NEC in the preterm population is a multifactorial, devastating, and as yet poorly understood disease process. We discuss the evidence supporting enteral pre- and pro-biotic supplementation of commensal organisms such as Bifidobacterium and Lactobacillus in the neonatal period, and their role in the prevention and amelioration of NEC in premature infants. Other studies have also shown persistent differences in intestinal microbial colonization between Cesarean-delivered and vaginally delivered children as far as 7 years of age (20). Weaning from breast milk or formula and introducing solid foods causes a shift in composition of the neonatal gut microbiome and leads to increased counts of Bacteroides, Clostridium, and anaerobic species of Streptococcus but decreased numbers of Bifidobacterium.


Interestingly, it has also been noted that during lactation, the cells of the maternal intestinal lymphoid tissue travel via the lymphatic and vascular circulations to the breast, facilitating the transfer of maternal intestinal and mammary skin microbiota to the breast-fed newborn (4, 36). This phenomenon, which can extend to perinatal and postnatal age, is known as disease programing during the development phase (4, 45). A link between NEC and a microbial etiology has been recognized for decades and has been corroborated by outbreaks in NICUs, the presence of pneumatosis intestinalis as a likely byproduct of bacterial fermentation, and the often concomitant presence of bacteremia (58). Finally, we review directions to consider for further research to promote human health within this field. They observed that in the first week of life the full-term neonatal gut microbiome is largely colonized by members of the Actinobacteria, Proteobacteria, Bacteroidetes, and, much less, Firmicutes phyla (Figure 1) (5, 6). This shift in bacterial makeup leads to expression of bacterial genes that are involved both in degradation of xenobiotic compounds, vitamin biosynthesis, and production of other metabolites such as butyrate and acetate (21, 25, 27, 28). They demonstrated that when compared with full-term infants, preterm infants showed increased populations of facultative anaerobes such as Enterococcus, Enterobacter, and Lactobacillus, increased numbers of Staphylococcus, and decreased numbers of anaerobes like Bifidobacterium, Bacteroides, and Atopobium (3, 29, 52). As such, NEC is increasingly thought to be, at least in part, related to a perturbation of intestinal immune homeostasis, and a generalized disturbance of normal colonization patterns within the developing gut, rather than growth of a single pathogen (59, 60).
This is contrasted with the previously described finding that neonates weighing <1200 g have a gut microbiome dominated by members of both Firmicutes and Tenericutes phyla (5, 7, 8). The differences seen between these studies highlights the need for cautious further investigation to best characterize the infant gut microbiome. In addition to these pro-nutrient effects, the intestinal microbiome can limit nutrient resources available to pathogens, specifically by out-competing them for metabolic resources and for physical space (12, 27). This suggests that even in infants not receiving exclusive breast milk, a breast-fed gut microbiota could be achieved, in part at least, by supplementing with a type of formula having a composition similar to breast milk.
The advent of a variety of techniques for metagenomic analysis of the developing human gut microbiome has given way to studies investigating whether there is a signature microbial pattern that predisposes to or heralds the onset of NEC. This evidence of early colonization of the neonatal gut microbiome so close to the time of birth suggests that there may be exposure to an antenatal source of commensal bacteria, such as the placenta, and this seeding may vary by length of gestation (5).
Nevertheless, gut colonization patterns established within the first week of life are thought to have effects on the composition of the individual’s future gut microbiota via a variety of factors (17, 19, 23, 24).
Gut microbiota also aid in development of barrier function, integrity, and systemic immune function. As summarized by Berrington et al., recent analyses of microbiomic data from preterm infants with NEC show great variability in proposed dysbiotic growth patterns (3).
It is well known that as fetuses become more neurologically mature, they begin to swallow large amounts of amniotic fluid, particularly during the third trimester of pregnancy. The term infant’s gut microbiome undergoes rapid maturation over the first year of age and is securely established in an adult form by 3 years of age.
This includes formation of a tolerant state between gut organisms and the immune system and is thought to affect tight junction structure and function (3, 29).
VLBW infants are paradoxically at increased risk for development of obesity later in life possibly due to metabolic programing that predisposes toward energy storage even when nutrients are not in short supply.
Interestingly, they also suggest that there may be gestational age thresholds for colonization with certain microbes – 33 weeks appears to be the milestone for appearance of Bifidobacterium species, the organism most commonly implicated in development and maintenance of a healthy gut microbiome (53).
Some studies implicate increased Proteobacteria and decreased Firmicutes in the development of NEC (61), while others note more than one pattern of dysbiosis within a given neonatal cohort. If the uterine environment is colonized with its own microbiota, as is suggested in recent studies, then the fetal gut may in turn become colonized by these organisms. An individual’s ultimate adult gut microbiome profile is likely governed by an elucidated interplay between initial colonizing microbiota, genes, normal gut development, diet, and environment (14, 21, 25, 26).
Generation of pro-inflammatory or anti-inflammatory responses as a result of exposure to bacteria include activation or deactivation of toll like receptors, T-lymphocyte activation, and triggering secretion of pro- and anti-inflammatory interleukins and cytokines, as well as activation of B-cells within the mesenteric lymph node system (3, 25) – the scope of which is beyond this present review. An alternative hypothesis, which could explain this predisposition toward obesity in this population centers around altered nutrient processing and utilization and immune regulation, has a function of altered gut microbiota (25). Overall, these arms of the innate and adaptive immune system interact with the microbiota to establish normal digestive capabilities, gut motility, immune tolerance to foods and certain microbial antigens, and protection against pathogens (25). To date, little research has been done to evaluate the effect of composition of the neonatal gut microbiota, term or preterm, its relationship to early nutritional status, and its effect on later development of obesity and other pro-inflammatory disease states. The exact role of the neonatal gut microbiome in the development and maturation of the infant immune system, as well as the influence of the neonatal immune system on governance of the fledgling gut microbiome is still poorly understood from a mechanistic standpoint and continues to be a growing area for further research (27). Given obesity’s long-reaching effects across the lifespan, seeking to further understand its origins and metabolic underpinnings, perhaps beginning as early as the neonatal period, remains an important focus of continued investigation. Alternatively, other groups have found no differences in microbiota between NEC-affected patients and healthy controls (63). Of note, mode of delivery, antibiotic exposure, mode of feeding, and age of infants at time of sampling only affected the rate of progression toward an anaerobic-dominated microbiota in the study infants, and not the sequence to achieve it (54).
A 2013 study of longitudinal development of the preterm gut microbiome in twins also demonstrates that they share similar gut microbiome development even within the complex, multiexposure environment of a NICU suggesting that in preterm infants, development of the gut microbiome may also be influenced by genetics (51). While the evolution of the term infant gut microbiome has been somewhat characterized, to date, there are still few prospective studies of the evolution of the preterm, VLBW gut microbiome to assess if there is a characteristic patterned succession and time course of microbial colonization for this group from birth through early childhood.



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