Pathogenesis of endometriosis: The role of initial infection and subsequent sterile inflammation (Review)

Hiroshi Kobayashi, Yumi Higashiura, Hiroshi Shigetomi, Hirotaka Kajihara
Molecular medicine reports · 2013 · vol. 9(1) , pp. 9–15 · doi:10.3892/mmr.2013.1755 · PMID:24173432 · W2071905880
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review explores how initial microbial infections trigger innate immune responses and subsequent sterile inflammation via danger-associated molecular patterns and oxidative stress, contributing to endometriosis pathogenesis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This review examines published English-language evidence on how infection-driven inflammation and subsequent sterile inflammation contribute to endometriosis pathogenesis, using information drawn from human studies, animal models, and basic gene/protein expression research. It argues that intrauterine microbes may initiate disease via microbial activation of Toll-like receptors (TLRs), leading to innate proinflammatory signaling and later nuclear factor-κB–dependent sterile inflammation fueled by DAMPs, alongside progression linked to iron influx and oxidative stress during retrograde menstruation; it proposes two phases of development (initial TLR activation followed by a second wave of sterile inflammation) in a bidirectional “danger signal spiral.” The authors’ caveat is that abstracts were excluded and the review focuses on the contemporary literature available in English. This paper is centrally about endometriosis — specifically reviewing infection-related TLR activation and sterile inflammation mechanisms in endometriosis development and progression.

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Abstract

Endometriosis is a common type of chronic inflammatory disease with an immunological background. In this review, we aimed to explore the contemporary literature on the infection and sterile inflammation that support the pathogenesis of endometriosis. This article reviews the English‑language literature on inflammatory, environmental, immunological and oxidative factors associated with endometriosis in an effort to identify factors that cause a predisposition to endometriosis. Intrauterine microbes may be critical for the initiation of endometriosis; the initial activation of pathogen recognition receptors by microbial stimuli results in the activation of proinflammatory pathways and innate immunity. In addition to their response to various exogenous pathogen‑associated molecular patterns, Toll‑like receptors (TLRs) also recognize a wide range of endogenous danger‑associated molecular patterns (DAMPs). The increased expression levels of DAMPs may be involved in the subsequent process of nuclear transcription factor‑κB‑dependent sterile inflammation. Oxidative stress, secondary to the influx of iron during retrograde menstruation, is involved in the progression of endometriosis. DAMP‑mediated danger signals and oxidative stress are bidirectional during sterile inflammation (danger signal spiral). This review supports the hypothesis that there are at least two distinct phases of endometriosis development: The initial wave of TLR activation in modulating innate immune responses would be followed by the second big wave of sterile inflammation.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Inflammation Cytokines Cytokines Endometriosis Endometriosis Endometriosis Female Humans Immunity, Innate NF-kappa B NF-kappa B Oxidative Stress Signal Transduction Toll-Like Receptor 4 Toll-Like Receptor 4

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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