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Immunol."],"published-print":{"date-parts":[[2026,4,24]]},"abstract":"<jats:p>\n                    Animals engage pleiotropic immune defense mechanisms to survive infections. Here, we present a function for mitochondrial fission in host defense. Challenge of macrophages with\n                    <jats:italic toggle=\"yes\">Escherichia coli<\/jats:italic>\n                    increased mitochondrial fission, with this response promoting bacterial clearance in mammalian macrophages and\n                    <jats:italic toggle=\"yes\">Caenorhabditis elegans<\/jats:italic>\n                    .\n                    <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                    \u2013induced mitochondrial fission engaged dual antibacterial responses via the mitochondrial unfolded protein response (UPR\n                    <jats:sup>mt<\/jats:sup>\n                    ) and inducible lipid droplet production. Mitochondrial fission\u2013triggered UPR\n                    <jats:sup>mt<\/jats:sup>\n                    , characterized by activation of activating transcription factor 5 (ATF5) in mouse macrophages and the paralog ATFS-1 in\n                    <jats:italic toggle=\"yes\">C. elegans<\/jats:italic>\n                    , curtailed inducible lipid droplets to cross-regulate these pathways. The intramacrophage pathogen\n                    <jats:italic toggle=\"yes\">Salmonella enterica<\/jats:italic>\n                    suppressed antibacterial mitochondrial fission, but restoring this response by inhibiting mitochondrial fusion\u2013promoting histone deacetylase 6 (HDAC6) reactivated lipid droplet production and bacterial clearance. Therefore, we propose that mitochondrial fission is an ancient host defense pathway that can be exploited for anti-infective design.\n                  <\/jats:p>","DOI":"10.1126\/sciimmunol.aed2623","type":"journal-article","created":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T17:58:11Z","timestamp":1777053491000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":1,"title":["Mitochondrial fission mediates an evolutionarily conserved antibacterial defense response"],"prefix":"10.1126","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2908-1014","authenticated-orcid":true,"given":"Ronan","family":"Kapetanovic","sequence":"first","affiliation":[{"name":"Institute for Molecular Bioscience (IMB), University of Queensland, Brisbane, QLD, Australia."},{"name":"Australian Infectious Diseases Research Centre, University of Queensland, Brisbane, QLD, Australia."},{"name":"Friedrich Miescher Institute for Biomedical Research, Basel, BS, Switzerland."},{"name":"Infectiologie et Sant\u00e9 Publique (ISP), INRAE, Universit\u00e9 de Tours, Nouzilly, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6066-3445","authenticated-orcid":true,"given":"Syeda Farhana","family":"Afroz","sequence":"additional","affiliation":[{"name":"Institute for Molecular Bioscience (IMB), University of Queensland, Brisbane, QLD, Australia."},{"name":"Australian Infectious Diseases Research Centre, University of Queensland, Brisbane, QLD, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4672-3357","authenticated-orcid":true,"given":"James E. 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