Regulation Of Inflammatory Immune Responses

1181 WordsNov 10, 20155 Pages
Regulation of inflammatory immune responses During pregnancy, there are elevated levels of anti-inflammatory mediators such as IL-10, and lowered levels of pro-inflammatory cytokines such as IL-1β and TNF-α (Wang et al., 1996). Excess prostaglandin F2 (Norwitz et al., 1992a) and macrophage-associated products such as pro-inflammatory cytokine TNF- (Norwitz et al., 1992b) are released when the foetus is fully matured. However, early expulsion of the foetus can be a result of turned on pro-inflammatory cytokine production due to the presence of bacterial products (Nayak et al., 2012). Borges et al. proposes that the presence of TNF- in the lung is able to lead to inflammatory cell recruitment and pro-inflammatory mediator production via the altering of response to phagocytes founded on the fact that pro-inflammatory responses in the lung are a result of TNF- blocking apoptotic cell clearance by alveolar macrophages (Borges et al., 2009). SP-A has the ability to inhibit TNF- production in a CD14-independent manner in lung decidual macrophages and so obstructs the premature activation of the release of the PG pathway thus delaying and regulating the onset of labour (Alcorn and Wright, 2004b). In support of this observation, pro-inflammatory cytokines and chemokines were observed to down regulate when human amnion explants were incubated with SP-A (Lee et al., 2010). IL-1b, CXCL2, and CXCL5 mRNA expressions decreased significantly after treatment with SP-A as shown in Table 2
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