Gram negative bacteria such as Salmonella & E.coli, on the other hand, has lipopolysccharrides (LPS) as its main cell wall constituent activating TLR4.
Recognition of these MAMPS with a TLR by SIgA attaching to J-chain-containing Ig polymers and transepithelial transport via M, gives rise to induction of memory cells that change rapidly with the microbial environment (shown in Fig1) .
This is in contract to SIgA synergic responses of the immune system where systematic challenge changes memory cells in a slow process. This allows the gut environment to change without an inflammatory response when commensals and probiotics change the environment so that new bacteria can live symbiotically in . Recognition via TLRs on dentricic cells causes signal cascades within the gut to induce cytokines, chemokines and antimicrobial factors (Fig 2). Commensal causes the nuclear factor B(NF-B) to inhibits NF-B kinase and MAPK via TLR4 attaching to lipossacharides on gram negative bacteria . Signals allow for rapid post translational protein modifications. This prohibits tissue damaging immune responses to commensal bacteria and allows their survival and the death of pathogenic bacteria.
A loss in TLR signalling can cause inflammation when the epithelium is infected by pathogenic bacteria. Paneth cells are AMP secretary cells in the crypts of Lieberkuhn, which defend the host . AMPs are the primary interactions with commensals and host cells within the innate immune response and directly kill pathogens and create a feedback loop (Fig3). In humans they are secreted into the blood and provoke defensin production. Ablation of MyD88 in Paneth cells reduces the synthesis of RegIII and creates defects in the epithelial barrier against microbes .This allows the immune system to have direct contact with the bacteria to kill of the infection. This is not done by commensal bacteria as there is no contact with the epithelium and they do not cause damage to it, distinguishing the two immune responses as inflammatory and regulatory.
Nuclear oligomerization domain 1 and 2 (NOD) are receptors like TLR but are intracellular rather than bound to the membrane. They generate local and systemic responses to bacterial fermentation by-products such as short fatty acids and -D-glutamyl-mesodiaminopimelic acid that are usually present in Gram negative bacteria, for example E.colli .to determine environmental shifts in bacteria composition and modulation of neutrophil function. NOD1 signalling causes maturation of B cells that are needed for TLR signalling, IgA production and a pro-inflammatory response.
Acute phase reactant serum amayloid A is expressed when segmented filamentous bacteria (SRBs) are associated in the membranes of ileal cells (of mice). The expression causes dendritic cells to activate and Th17 differentiation, as well as, IL6 secretion from activated CD4+ T cells in the adaptive immune response. Because of this RegIII AMPs are...