“…Endometrial receptivity is compromised by the presence of pathogenic bacteria and bacterial products such as gram-negative bacterial endotoxin (lipopolysaccharide, LPS) or pro-inflammatory mediators (PGF2α or Nitric Oxide, NO), compromising early embryo development (Soto et al, 2003, Schwarz et al, 2008, Gilbert, 2011. After contact with endotoxin LPS, endometrial immune receptors (toll-like receptors, TLR), recognize the pathogen and trigger the expression of proinflammatory cytokines (TNFα, IL1β, IL6) and chemokines (IL8) which in turn attract and activate neutrophils and macrophages to the site of inflammation (Ahmadi et al, 2005, Galvao et al, 2011, Gilbert, 2011. Hill and Gilbert (2008) demonstrated that embryos exposed to pro-inflammatory cytokines in the culture media had a reduced number of trophectoderm cells thereby impairing their ability to produce IFNτ required for successful MRP.…”