Potential mechanisms and therapeutic strategies for LPS-associated female fertility decline.

As a major component of the outer membrane of Gram-negative bacteria, lipopolysaccharide (LPS) can be recognized by toll-like receptors (TLRs) and induce inflammation through MyD88 or the TIR domain-containing adapter-inducing interferon-β (TRIF) pathway. Previous studies have found that LPS-associated inflammatory/immune challenges were associated with ovarian dysfunction and reduced female fertility. However, the etiology and pathogenesis of female fertility decline associated with LPS are currently complex and multifaceted. In this review, PubMed was used to search for references on LPS and fertility decline so as to elucidate the potential mechanisms of LPS-associated female fertility decline and summarize therapeutic strategies that may improve LPS-associated fertility decline.