Contribution of CD4+ cells in the emotional alterations induced by endometriosis in mice

Alejandra Escudero-Lara, David Cabañero, Rafael Maldonado, Rafaël Maldonado
Frontiers in behavioral neuroscience · 2022 · vol. 16 , pp. 946975 · doi:10.3389/fnbeh.2022.946975 · PMID:36311856 · PMC9596757 · W4304813506
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

Endometriosis in mice induced hypersensitivity, cognitive deficits, anxiety, and depressive-like behaviors, with CD4+ cell depletion reducing anxiety while other symptoms persisted.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

This study used a non-surgical mouse model of endometriosis in immunocompetent female C57BL/6J mice to evaluate nociceptive, affective, and cognitive outcomes, comparing endometriosis injections of donor endometrium versus vehicle controls, with behavioral testing across multiple time points. Endometriosis mice developed persistent abdomino-pelvic mechanical hypersensitivity and showed increased anxiety-like and depressive-like behaviors, alongside cognitive deficits, which the authors report correlated with inflammatory marker expression in brain regions including immune-cell marker CD4. To test immune-cell causality, CD4+ cell depletion with anti-CD4 antibody reduced anxiety-like behavior but did not alter mechanical hypersensitivity, depressive-like behavior, or cognitive deficits, and CD4 depletion efficiency was assessed by splenic flow cytometry at study end. This paper is centrally about endometriosis — specifically, it examines how CD4+ immune cells contribute to anxiety-like behavioral alterations in a non-surgical endometriosis mouse model.

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Abstract

Endometriosis is a disease defined by the presence of endometrial tissue in extrauterine locations. This chronic condition is frequently associated with pain and emotional disorders and has been related with altered immune function. However, the specific involvement of immune cells in pain and behavioral symptoms of endometriosis has not been yet elucidated. Here, we implement a mouse model of non-surgical endometriosis in which immunocompetent mice develop abdomino-pelvic hypersensitivity, cognitive deficits, anxiety and depressive-like behaviors. This behavioral phenotype correlates with expression of inflammatory markers in the brain, including the immune cell marker CD4. Depletion of CD4 + cells decreases the anxiety-like behavior of mice subjected to the endometriosis model, whereas abdomino-pelvic hypersensitivity, depressive-like behavior and cognitive deficits remain unaltered. The present data reveal the involvement of the immune response characterized by CD4 + white blood cells in the anxiety-like behavior induced by endometriosis in mice. This model, which recapitulates the symptoms of human endometriosis, may be a useful tool to study the immune mechanisms involved in pain and behavioral alterations associated to endometriosis.

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endometriosis

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