| Summary: | There is a critical time-window early in life during which appropriate microbial exposure has to occur in order to induce functional, life-long immune regulation. Actinobacteria and Proteobacteria dominate the GIT microbiota of children. With age, Firmicutes and Bacteroidetes dominate the commensal's landscape. Proteobacteria are most abundant in GIT of elderly people. A critical level of microbial diversity after birth is required to prevent the induction of hyper-IgE during adulthood. The colonisation process induces a change from foetal TH2 to a TH1/TH17 T-cell state. There is a temporal activation of the innate mucosal immunity: TLR2 and TLR4 expressed in the sterile foetal environment are replaced by TLR5, coinciding with the post-natal microbial expansion; as TLR tolerance develops, it attenuates and remain diminished into adulthood. CD5+ B-cells contribute to the first line of defence against bacterial infections. Ageing is associated with an increased inflammatory response via the CD14/TLR4/MD2 receptor complex (monocytes, DC, macrophages, and B-cells), and increased ROS production (neutrophils). Gut flora changes post-mortem, presenting as biphasic pattern of bacterial overgrowth (after 3 and 72 hr post-mortem). Intestinal bacteria translocateto MLN, spleen, liver, kidney, and cardiac blood, as early as 5 min after death. Intestinal tissue destruction is observed within 3 hr post-mortem, whereas proliferative lymphocytes decrease between 3 and 12 hr post-mortem. The stomach microbiota is less diverse than that in mouth, colon, and stool. H. pylori induces chronic inflammation of the stomach mucosa. Colonisation resistance comprises the ability of GIT microbiota to deter pathogens from causing infections. Probiotics (Bifidobacteria and Lactobacilli), prebiotics (DHNA), and dietary supplements (arginine) modulate intestinal commensals, maintaining the homeostasis, and conferring a health benefit on the host.
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