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In this study, we have used a larval zebrafish model for tuberculosis, based on<jats:italic>Mycobacterium marinum<\/jats:italic>(<jats:italic>Mm<\/jats:italic>) infection, to study the effect of glucocorticoids. Our results show that the synthetic glucocorticoid beclomethasone increases the bacterial burden and the dissemination of a systemic<jats:italic>Mm<\/jats:italic>infection. The exacerbated<jats:italic>Mm<\/jats:italic>infection was associated with a decreased phagocytic activity of macrophages, higher percentages of extracellular bacteria, and a reduced rate of infected cell death, whereas the bactericidal capacity of the macrophages was not affected. The inhibited phagocytic capacity of macrophages was associated with suppression of the transcription of genes involved in phagocytosis in these cells. The decreased bacterial phagocytosis by macrophages was not specific for<jats:italic>Mm<\/jats:italic>, since it was also observed upon infection with<jats:italic>Salmonella<\/jats:italic>Typhimurium. In conclusion, our results show that glucocorticoids inhibit the phagocytic activity of macrophages, which may increase the severity of bacterial infections like tuberculosis.<\/jats:p>","DOI":"10.3389\/fimmu.2021.618569","type":"journal-article","created":{"date-parts":[[2021,5,11]],"date-time":"2021-05-11T05:16:42Z","timestamp":1620710202000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":26,"title":["Glucocorticoid-Induced Exacerbation of Mycobacterial Infection Is Associated With a Reduced Phagocytic Capacity of Macrophages"],"prefix":"10.3389","volume":"12","author":[{"given":"Yufei","family":"Xie","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiajun","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annemarie H.","family":"Meijer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcel J. 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