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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,4,14]]},"abstract":"<jats:p>\n                    Bacterial sepsis remains a devastating clinical problem. Here, we describe a protective role for the recently discovered acid-sensitive, proton-activated chloride channel, PACC1 (PAC\/ASOR\/TMEM206), during sepsis. Initially, we found PACC1 was enriched in healthy human and mouse mononuclear phagocytes, particularly macrophages, and differentially regulated by inflammatory stimuli, suggesting PACC1 involvement in innate immunity. To further investigate, we generated\n                    <jats:italic toggle=\"yes\">de novo Pacc1<\/jats:italic>\n                    knockout (\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) mice, which presented without major immunologic abnormalities at baseline. Compared to wild-type (WT),\n                    <jats:italic toggle=\"yes\">\n                      Pacc1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    myeloid cells showed normal phagocytic uptake of acid-insensitive\n                    <jats:italic toggle=\"yes\">\n                      <jats:italic toggle=\"yes\">Escherichia coli<\/jats:italic>\n                      BioParticles\n                    <\/jats:italic>\n                    , but impaired development of the acidifying phagolysosome using acid-sensitive\n                    <jats:italic toggle=\"yes\">\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                    <\/jats:italic>\n                    BioParticles. Transcriptomic profiling of\n                    <jats:italic toggle=\"yes\">Pacc1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    macrophages revealed dysregulated phagolysosomal and cytokine networks (e.g., interferons). Because phagolysosomal bacterial clearance is essential to resolve infection, we challenged\n                    <jats:italic toggle=\"yes\">\n                      Pacc1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice with intraperitoneal gram-negative\n                    <jats:italic toggle=\"yes\">\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                    <\/jats:italic>\n                    sepsis.\n                    <jats:italic toggle=\"yes\">\n                      Pacc1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice displayed increased bacterial burden, immune cell infiltration, inflammation, and lethality. In contrast, phagocytosis-independent\n                    <jats:italic toggle=\"yes\">\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                    <\/jats:italic>\n                    lipopolysaccharide (LPS)-induced endotoxemia yielded comparable WT and\n                    <jats:italic toggle=\"yes\">\n                      Pacc1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    survival, as well as similar inflammatory responses. Finally, we engineered\n                    <jats:italic toggle=\"yes\">Pacc1<\/jats:italic>\n                    -floxed (\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    ) mice crossed with a myeloid lineage Cre-deleter strain to interrogate myeloid cell\u2013intrinsic PACC1 in vivo. Consistent with a predominate role for PACC1 during phagocytosis and bacterial clearance in these cells,\n                    <jats:italic toggle=\"yes\">\n                      LysM-Cre\/Pacc1\n                      <jats:sup>fl\/fl<\/jats:sup>\n                    <\/jats:italic>\n                    mice exhibited impaired\n                    <jats:italic toggle=\"yes\">\n                      <jats:italic toggle=\"yes\">E. coli<\/jats:italic>\n                    <\/jats:italic>\n                    sepsis survival but indifferent endotoxemia phenotypes. In conclusion, PACC1 links sterilizing phagolysosomal activity with immune networks in sepsis pathobiology.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2515768123","type":"journal-article","created":{"date-parts":[[2026,4,6]],"date-time":"2026-04-06T19:12:12Z","timestamp":1775502732000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":0,"title":["Proton-activated chloride channel 1 is essential for innate host defense against bacterial sepsis"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5369-1958","authenticated-orcid":false,"given":"Lucien P.","family":"Garo","sequence":"first","affiliation":[{"name":"Pulmonary Center, Department of Medicine, Boston University Chobanian and Avedisian School of Medicine","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin","family":"Brueck","sequence":"additional","affiliation":[{"name":"Pulmonary Center, Department of Medicine, Boston University Chobanian and Avedisian School of Medicine","place":["Boston"]},{"name":"Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz","place":["Mainz, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5702-3404","authenticated-orcid":false,"given":"Sarah","family":"Walachowski","sequence":"additional","affiliation":[{"name":"Pulmonary Center, Department of Medicine, Boston University Chobanian and Avedisian School of Medicine","place":["Boston"]},{"name":"Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz","place":["Mainz, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0871-6305","authenticated-orcid":false,"given":"Archana","family":"Jayaraman","sequence":"additional","affiliation":[{"name":"Pulmonary Center, Department of Medicine, Boston University Chobanian and Avedisian School of Medicine","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0296-4343","authenticated-orcid":false,"given":"Marcel","family":"Strueve","sequence":"additional","affiliation":[{"name":"Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz","place":["Mainz, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-7731-5585","authenticated-orcid":false,"given":"Shuang","family":"Xu","sequence":"additional","affiliation":[{"name":"Pulmonary Center, Department of Medicine, Boston University Chobanian and Avedisian School of Medicine","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-4371-4790","authenticated-orcid":false,"given":"Hulbert","family":"Yang","sequence":"additional","affiliation":[{"name":"Pulmonary Center, Department of Medicine, Boston University Chobanian and Avedisian School of Medicine","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-7657-3301","authenticated-orcid":false,"given":"Matthew","family":"Helmkamp","sequence":"additional","affiliation":[{"name":"Pulmonary Center, Department of Medicine, Boston University Chobanian and Avedisian School of Medicine","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seung Hoan","family":"Choi","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Boston University School of Public 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Zhang, S. Y. Liu, X. Yang, Y. Q. Wang, Y. X. Cheng, TMEM206 is a potential prognostic marker of hepatocellular carcinoma. Oncol. Lett. 20, 174 (2020).","journal-title":"Oncol. Lett."},{"key":"e_1_3_4_73_2","doi-asserted-by":"publisher","DOI":"10.18240\/ijo.2024.11.01"},{"key":"e_1_3_4_74_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-022724-105357"},{"key":"e_1_3_4_75_2","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2020.00096"},{"key":"e_1_3_4_76_2","first-page":"11.21.11","article-title":"Three decades of chloride intracellular channel proteins: From organelle to organ physiology","volume":"80","author":"Gururaja Rao S.","year":"2018","unstructured":"S. Gururaja Rao, D. Ponnalagu, N. J. Patel, H. Singh, Three decades of chloride intracellular channel proteins: From organelle to organ physiology. Curr. Protoc. Pharmacol. 80, 11.21.11\u201311.21.17 (2018).","journal-title":"Curr. Protoc. 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