{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T19:38:44Z","timestamp":1793129924165,"version":"4.5.0"},"reference-count":55,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T00:00:00Z","timestamp":1791936000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T00:00:00Z","timestamp":1791936000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2013\/08216-2"],"award-info":[{"award-number":["2013\/08216-2"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2017\/04347-6"],"award-info":[{"award-number":["2017\/04347-6"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2019\/12991-8"],"award-info":[{"award-number":["2019\/12991-8"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2019\/14643-7"],"award-info":[{"award-number":["2019\/14643-7"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","award":["407805\/2021-4"],"award-info":[{"award-number":["407805\/2021-4"]}],"id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]},{"name":"All of Us Research Program","award":["RO1-AI 143790"],"award-info":[{"award-number":["RO1-AI 143790"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2026,10,14]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Interleukin-1 (IL-1) is a pleiotropic cytokine important in inflammatory and infectious diseases, but its roles in visceral leishmaniasis (VL) remain poorly understood. Here, we evaluated the role of IL-1 cytokines during experimental visceral leishmaniasis. We showed that IL-1 receptor 1 (IL-1R1) deficiency enhanced the gamma interferon (IFN\u03b3)-mediated response and restricted parasites in an IL-1\u03b1-dependent manner, whereas IL-1\u03b2 deficiency had no effect. The absence of IL-1R1 and IL-1\u03b1 led to intestinal microbiota dysbiosis. The infection induced IL-1\u03b1 expression in the gut. The absence of IL-1\u03b1 led to reduced expression of tight-junction molecules, increased intestinal permeability, and bacterial translocation. These alterations amplified non-\n                      <jats:italic toggle=\"yes\">Leishmania<\/jats:italic>\n                      -specific IFN-\u03b3 production, which was reversed by broad-spectrum antibiotic treatment. Bone marrow chimeric transplantation showed that hematopoietic cells are the source of IL-1\u03b1 during VL. Together, our findings reveal that IL-1\u03b1 acts as a key regulator of gut barrier integrity in VL and indirectly restrains systemic IFN\u03b3-driven inflammation. This work highlights IL-1\u03b1-dependent intestinal protection as an overlooked component of VL pathogenesis.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Visceral leishmaniasis (VL) is a systemic and chronic disease caused by\n                        <jats:italic toggle=\"yes\">Leishmania<\/jats:italic>\n                        parasites. Most infected individuals remain asymptomatic due to an appropriate IFN\u03b3-mediated response. By contrast, the disease progression is characterized by excessive inflammation, with high levels of cytokines, among them IFN\u03b3. IL-1 cytokines play a role in modulating immune responses and epithelial barriers. We report that IL-1\u03b1 protects the intestinal environment and indirectly regulates the IFN\u03b3-mediated response during experimental VL. The infection induces IL-1\u03b1 expression in the intestine, and its absence leads to dysbiosis, gut permeability, and bacterial translocation. Overall, this study reveals the role of IL-1\u03b1 in intestinal integrity during VL and in regulating the IFN\u03b3-mediated response. Expanding the knowledge of IL-1\u03b1 in intestinal protection may support therapeutic approaches to improve the outcomes of infection.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.00657-26","type":"journal-article","created":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T13:00:50Z","timestamp":1789390850000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["IL-1\u03b1 protects intestinal barrier in murine visceral leishmaniasis"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1987-8369","authenticated-orcid":true,"given":"La\u00eds A.","family":"Sacramento","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036rp1748","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biochemistry and Immunology, Ribeir\u00e3o Preto Medical School, University of S\u00e3o 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