Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Oct;41(10):2739-2758.
doi: 10.1007/s10815-024-03226-2. Epub 2024 Aug 21.

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

Xue Qin  1 , Junhong Du  1 , Ruifen He  1 , Yaxi Li  1 , Hongli Li  2 , Xiaolei Liang  3
Affiliations
Review

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

Xue Qin et al. J Assist Reprod Genet. 2024 Oct.

Abstract

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.

Keywords: Female fertility decline; Lipopolysaccharide (LPS); Potential mechanisms; Therapeutic strategies.

PubMed Disclaimer

Conflict of interest statement

The authors declare no competing interests.

Similar articles

See all similar articles

References

    1. Wang YT, Sansone A, Smirnov A, Stallings CL, Orvedahl A. myeloid autophagy genes protect mice against fatal TNF- and LPS-induced cytokine storm syndromes. Autophagy. 2023;19(4):1114–27. 10.1080/15548627.2022.2116675. - PMC - PubMed
    1. Yamaguchi T, Yamamoto Y, Egashira K, Sato A, Kondo Y, Saiki S, et al. Oxidative stress inhibits endotoxin tolerance and may affect periodontitis. J Dent Res. 2023;102(3):331–9. 10.1177/00220345221138523. - PubMed
    1. McKenna S, Eckman M, Parker A, Bok R, Hurt KJ, Wright CJ. Perinatal endotoxemia induces sustained hepatic COX-2 expression through an Nfκb-dependent mechanism. J Innate Immun. 2016;8(4):386–99. 10.1159/000445541. - PMC - PubMed
    1. Mohammad S, Thiemermann C. Role of Metabolic endotoxemia in systemic inflammation and potential interventions. Front Immunol. 2020;11:594150. 10.3389/fimmu.2020.594150. - PMC - PubMed
    1. Tremellen K, Syedi N, Tan S, Pearce K. Metabolic endotoxaemia–a potential novel link between ovarian inflammation and impaired progesterone production. Gynecol Endocrinol. 2015;31(4):309–12. 10.3109/09513590.2014.994602. - PubMed

MeSH terms

Substances

LinkOut - more resources