Abstract
Abstract: Bacteria populated the earth two billion years prior to emergence of eukaryotic life. Now, some 400-500 species are estimated to inhabit the human mucosal surfaces, bulk of which reside in the intestinal tract. Traditionally, a newborn gut was considered sterile, but new evidence indicate presence of bacteria in the fetus and meconium. Mode of delivery, feeding type, the environment, and caregivers provide the initial bacterial exposure to the newborn to help develop a healthy colonization pattern. There is ample evidence in favor of simple problems such as feeding intolerance to very severe diseases such as necrotizing enterocolitis resulting in part due to disruption of normal microbiota. However, there is paucity of data on a “true” healthy microbial pattern in neonates. Similarly, most of the work done on neonatal microbiome is from the west and a comparative comparison of microbiota has not been done in babies from different parts of the world. Apart from acting against pathogens and maintaining homeostasis in infectious, inflammatory, and autoimmune diseases, the intestinal microbiota has now been a focus of attention in their role in vaccine response. Maturation of mucosal immune system as a result of colonization by bacteria has been known for some time, and new research in humans and animals provides clear evidence of a bacterial role in the development of both innate and adaptive immune response in the mammalian host. The type, number, and timing of exposure of mucosal and dendritic cells to bacteria and bacterial products and induction of specific T helper and T- regulatory components of the immune system have been examined with some details in different disease models. We will discuss these and other factors currently known to play a role and their mechanism in modulating the infant immune response. Recent results from an Indian probiotic trial in neonatal sepsis using live bacteria in the first week of life will be presented in light of its mucosal effects in blockage of bacterial translocation and possible extra-intestinal impacts via modulation of innate immunity.
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