Menstrual blood‑derived stromal cells modulate functional properties of mouse and human macrophages
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AuthorMartínez Aguilar, Rocío; Romero Pinedo, Salvador; Ruiz Magaña, María José; García Olivares, Enrique Fernando; Ruiz Ruiz, María Carmen; Abadía Molina, Ana Clara
Martínez-Aguilar, R., Romero-Pinedo, S., Ruiz-Magaña, M. J., Olivares, E. G., Ruiz-Ruiz, C., & Abadía-Molina, A. C. (2020). Menstrual blood-derived stromal cells modulate functional properties of mouse and human macrophages. Scientific reports, 10(1), 1-14. [| https://doi.org/10.1038/s41598-020-78423-x]
SponsorshipPlan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016, ISCIII-Subdirección General de Evaluación y Fomento de la Investigación, Ministerio de Economía y Competitividad, Spain PI16/01642 PI10/01096; European Union (EU); Catedra de Investigación Antonio Chamorro-Alejandro Otero, Universidad de Granada CACH2017-1
Menstrual blood-derived stromal cells (MenSCs) are emerging as a strong candidate for cell-based therapies due to their immunomodulatory properties. However, their direct impact on innate immune populations remains elusive. Since macrophages play a key role in the onset and development of inflammation, understanding MenSCs implication in the functional properties of these cells is required to refine their clinical effects during the treatment of inflammatory disorders. In this study, we assessed the effects that MenSCs had on the recruitment of macrophages and other innate immune cells in two mouse models of acute inflammation, a thioglycollate (TGC)-elicited peritonitis model and a monobacterial sepsis model. We found that, in the TGC model, MenSCs injection reduced the percentage of macrophages recruited to the peritoneum and promoted the generation of peritoneal immune cell aggregates. In the sepsis model, MenSCs exacerbated infection by diminishing the recruitment of macrophages and neutrophils to the site of infection and inducing defective bacterial clearance. Additional in vitro studies confirmed that co-culture with MenSCs impaired macrophage bactericidal properties, affecting bacterial killing and the production of reactive oxygen intermediates. Our findings suggest that MenSCs modulate the macrophage population and that this modulation must be taken into consideration when it comes to future clinical applications.