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Here, we report that progressive Mtb infection is associated with upregulation of guanylate\u2010binding protein\u20101 (GBP1), hypoxia\u2010inducible factor\u20101 alpha (HIF\u20101\u03b1), and elevated NLR family pyrin domain\u2010containing (NLRP3) inflammasome activation pathways. Using rabbit lungs and primary rabbit and human macrophages, as well as human monocytic THP\u20101\u2010derived macrophages for infection with Mtb strains (H\n                    <jats:sub>37<\/jats:sub>\n                    Rv, HN878, or CDC1551) that differ in virulence, we show that NLRP3 inflammasome activation by HIF\u20101\u03b1 and GBP1 leads to elevated mitochondrial stress, apoptosis, and necrosis during progressive infection by HN878. These biological functions and pathways are dampened during nonprogressive TB in rabbit lungs, and in primary rabbit and human macrophages infected by CDC1551. These findings are consistent with and confirmed by Mtb infection studies of macrophages knocked down for HIF\u20101\u03b1 or GBP1 expression. Our study indicates that differences in HIF\u20101\u03b1\u2010 and GBP1\u2010mediated NLRP3 inflammasome activation influence the outcome of Mtb infection in the host.\n                  <\/jats:p>","DOI":"10.1002\/mco2.70486","type":"journal-article","created":{"date-parts":[[2025,11,23]],"date-time":"2025-11-23T15:47:27Z","timestamp":1763912847000},"source":"Crossref","is-referenced-by-count":1,"title":["Inflammasome Activation Differences Underpin Different\n                    <i>Mycobacterium tuberculosis<\/i>\n                    Infection Outcomes"],"prefix":"10.1002","volume":"6","author":[{"given":"Ranjeet","family":"Kumar","sequence":"first","affiliation":[{"name":"The Public Health Research Institute at New Jersey Medical School Rutgers University  Newark New Jersey USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Afsal","family":"Kolloli","sequence":"additional","affiliation":[{"name":"The Public Health Research Institute at New Jersey Medical School 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