Published online Nov 8, 2013. doi: 10.5409/wjcp.v2.i4.46
Revised: August 7, 2013
Accepted: September 18, 2013
Published online: November 8, 2013
Processing time: 127 Days and 18.8 Hours
The intestinal tract is colonized soon after birth with a variety of ingested environmental and maternal microflora. This process is influenced by many factors including mode of delivery, diet, environment, and the use of antibiotics. Normal intestinal microflora provides protection against infection, ensures tolerance to foods, and contributes to nutrient digestion and energy harvest. In addition, enteral feeding and colonization with the normal commensal flora are necessary for the maintenance of intestinal barrier function and play a vital role in the regulation of intestinal barrier function. Intestinal commensal microorganisms also provide signals that foster normal immune system development and influence the ensuing immune responses. There is increasingly recognition that alterations of the microbial gut flora and associated changes in intestinal barrier function may be related to certain diseases of the gastrointestinal tract. This review summarizes recent advances in understanding the complex ecosystem of intestinal microbiota and its role in regulating intestinal barrier function and a few common pediatric diseases. Disruption in the establishment of a stable normal gut microflora may contribute to the pathogenesis of diseases including inflammatory bowel disease, nosocomial infection, and neonatal necrotizing enterocolitis.
Core tip: This review summarizes recent advances in understanding the complex ecosystem of intestinal microbiota and its role in regulating intestinal barrier function and a few common pediatric diseases. There is increasingly recognition that the stimulation of initial intestinal microbial colonization is important for proper maturation of the innate immune system and continued regulation and maintenance of intestinal barrier function. Disruption of the establishment of a stable normal gut microflora may contribute to the pathogenesis of diseases including inflammatory bowel disease, nosocomial infection, and neonatal necrotizing enterocolitis in premature infants.