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Unlike\n                    <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                    and\n                    <jats:italic>Mycobacterium marinum<\/jats:italic>\n                    ,\n                    <jats:italic>M. avium<\/jats:italic>\n                    lacks ESX-1, a subtype of Type VII secretion system (T7SS) and a key virulence determinant. The absence of ESX-1 in\n                    <jats:italic>M. avium<\/jats:italic>\n                    raises questions about its alternative intracellular survival strategies. To investigate\n                    <jats:italic>M. avium<\/jats:italic>\n                    pathogenesis, we exploited our recently established infection model in zebrafish larvae, enabling live imaging of early host-pathogen interactions. Macrophage depletion significantly increased\n                    <jats:italic>M. avium<\/jats:italic>\n                    burden and larval mortality, while neutrophil depletion had no major effect, emphasizing macrophages as key defenders against\n                    <jats:italic>M. avium<\/jats:italic>\n                    . In support, imaging of\n                    <jats:italic>tnfa<\/jats:italic>\n                    activation showed that macrophages polarized to a proinflammatory phenotype. However, like\n                    <jats:italic>M. marinum<\/jats:italic>\n                    ,\n                    <jats:italic>M. avium<\/jats:italic>\n                    exploits chemokine receptor\n                    <jats:italic>Cxcr3.2<\/jats:italic>\n                    signaling in macrophages for its expansion in granuloma-like clusters. Both\n                    <jats:italic>M. avium and M. marinum<\/jats:italic>\n                    preferentially infected macrophages, but\n                    <jats:italic>M. avium<\/jats:italic>\n                    -induced granuloma-like clusters were more compact and exhibited less cell death. Supporting this, lytic cell death pathways were enriched in\n                    <jats:italic>M. marinum<\/jats:italic>\n                    but not\n                    <jats:italic>M. avium<\/jats:italic>\n                    transcriptome signatures. Consequently, we investigated pyroptosis, an important form of inflammation-induced lytic cell death. We found that knockdown of critical mediators of pyroptosis, namely inflammatory caspase a (\n                    <jats:italic>caspa<\/jats:italic>\n                    ) and gasdermin Eb (\n                    <jats:italic>gsdmeb<\/jats:italic>\n                    ), produced opposing effects on the two mycobacterial pathogens, indicating a host-protective role during\n                    <jats:italic>M. avium<\/jats:italic>\n                    infection, while exacerbating\n                    <jats:italic>M. marinum<\/jats:italic>\n                    growth. These findings highlight the interaction with host cell death signaling as a determining factor for the pathogenic potential of mycobacterial species.\n                  <\/jats:p>","DOI":"10.1038\/s41419-026-08810-1","type":"journal-article","created":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T14:48:30Z","timestamp":1777560510000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Protective versus deleterious roles of pyroptosis in Mycobacterium avium and Mycobacterium marinum infections"],"prefix":"10.1038","volume":"17","author":[{"given":"Wanbin","family":"Hu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Federico","family":"Pagliaro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4128-9501","authenticated-orcid":false,"given":"Herman P.","family":"Spaink","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1325-0725","authenticated-orcid":false,"given":"Annemarie H.","family":"Meijer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,30]]},"reference":[{"key":"8810_CR1","doi-asserted-by":"publisher","first-page":"87","DOI":"10.1055\/s-0033-1333567","volume":"34","author":"BA Kendall","year":"2013","unstructured":"Kendall BA, Winthrop KL. 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