The Delicate Balance between the Good and the Bad IL-1 Proinflammatory Effects in Endometriosis

Justyna Sikora, Simone Ferrero, Aleksandra Mielczarek-Palacz, Aleksandra Mielczarek‐Palacz, Zdzislawa Kondera-Anasz, Zdzisława Kondera‐Anasz
Current medicinal chemistry · 2018 · vol. 25(18) , pp. 2105–2121 · doi:10.2174/0929867325666180111093547 · PMID:29332562 · W2782596501
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Imbalances in IL-1 family cytokines within the peritoneal cavity contribute to endometriosis by altering immune activation and promoting ectopic endometrial cell implantation and proliferation.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-13 · read from full text ⓘ

This paper reviews published evidence (via an electronic PubMed/MEDLINE search from 1950 to July 2017) on how cytokines in the IL-1 family influence endometriosis pathogenesis and development. It reports that dysregulation of the IL-1 cytokine network may alter immune activation in the peritoneal cavity and that changes in ectopic endometrial cell adhesion, implantation, and proliferation may be driven by reduced IL-1–mediated suppression. The review emphasizes an imbalance among IL-1α, pro-IL-1β, mature IL-1β, and soluble IL-1 receptor/IL-1 signaling components (sIL-1R2, sIL-1RAcP) in peritoneal fluid and serum, which is proposed to help convert acute inflammation into chronic inflammation; it notes that peritoneal macrophages in affected women secrete more anti-inflammatory IL-1Ra and less pro-inflammatory IL-1, yet inflammation still develops. This paper is centrally about endometriosis—focusing on IL-1 family pro- and anti-inflammatory regulation in the peritoneal cavity.

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Abstract

BACKGROUND: Endometriosis is an inflammatory gynaecological disease with an associated chronic inflammation. Interleukin(IL)-1 is one of the most important immune and proinflammatory factors, produced mainly by monocytes and macrophages. Studies indicate the role of the cytokine from IL-1 family in endometrium-related disorders, particularly in endometriosis. METHODS: The information about the impact of cytokine from IL-1 cytokine family on the pathogenesis and development of endometriosis was obtained with an electronic literature search based on the PubMed and Medline databases, spanning the period of January 1950 to July 2017 and includes associated references in the published studies. RESULTS: The impairment of the IL-1 family cytokine-network may lead to changes in the activation of immune system in the peritoneal cavity of women with endometriosis. The aberrant ectopic endometrial cell properties of adhesion, implantation and proliferation may be the result of a reduced suppressive capacity controlling the IL-1. The imbalance between IL-1α, pro-IL-1β, mature IL-1β and sIL-1R2 and sIL-1RAcP in the peritoneal fluid and serum of women with endometriosis may be linked to the ability of transforming an acute inflammation into a chronic one. Despite the fact that peritoneal macrophages secrete more antiinflammatory IL-1Ra and less proinflammatory IL-1 in the peritoneal cavity in affected women, the inflammation still develops. CONCLUSIONS: This observation clearly suggested a significant inadequacy in the specific regulatory mechanisms of IL-1 activity at the peritoneal cavity level. The imbalance between all studied cytokines in endometriosis may escalate peritoneal inflammation and, in consequence, develop endometriosis.
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Abstract

Methods: The information about the impact of cytokine from IL-1 cytokine family on the pathogenesis and development of endometriosis was obtained with an electronic literature search based on the PubMed and Medline databases, spanning the period of January 1950 to July 2017 and includes associated references in the published studies.

Results

The impairment of the IL-1 family cytokine-network may lead to changes in the activation of immune system in the peritoneal cavity of women with endometriosis. The aberrant ectopic endometrial cell properties of adhesion, implantation and proliferation may be the result of a reduced suppressive capacity controlling the IL-1. The imbalance between IL-1α, pro-IL-1β, mature IL-1β and sIL-1R2 and sIL-1RAcP in the peritoneal fluid and serum of women with endometriosis may be linked to the ability of transforming an acute inflammation into a chronic one. Despite the fact that peritoneal macrophages secrete more antiinflammatory IL-1Ra and less proinflammatory IL-1 in the peritoneal cavity in affected women, the inflammation still develops.

Conclusions

This observation clearly suggested a significant inadequacy in the specific regulatory mechanisms of IL-1 activity at the peritoneal cavity level. The imbalance between all studied cytokines in endometriosis may escalate peritoneal inflammation and, in consequence, develop endometriosis.

Keywords

Endometriosis, inflammation, interleukin-1, interleukin-1 receptors, peritoneal fluid, serum.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Inflammation Interleukin-1 Endometriosis Female Humans Inflammation Interleukin-1 Interleukin 1 Receptor Antagonist Protein Interleukin 1 Receptor Antagonist Protein Receptors, Interleukin-1 Type I Receptors, Interleukin-1 Type I Receptors, Interleukin-1 Type II Receptors, Interleukin-1 Type II

Citation neighborhood

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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