MYD88 and infection: Thus, it may bethe case that our study provides potentially compelling evidence of a moleculardistinction between normal, term parturition and infection-induced preterm labor.Signaling through the TLR4 receptor, which is responsive to Gram-negativelipopolysaccharide, may proceed through the MyD88-dependent pathway (like the IL-1receptor), or via additional adapter proteins, such as TIR-domain-containingadapter-inducing interferon-β (TRIF) [38].