{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T13:19:18Z","timestamp":1790860758153,"version":"4.1.0"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2011,1,1]],"date-time":"2011-01-01T00:00:00Z","timestamp":1293840000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2011,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Coxiella burnetii<\/jats:italic>, the etiological agent of Q fever, is a small, Gram-negative, obligate intracellular bacterium. Replication of<jats:italic>C. burnetii<\/jats:italic>during infection has been shown to be increased by decreasing oxidative stress using p47<jats:sup>phox \u2212\/\u2212<\/jats:sup>and iNOS<jats:sup>\u2212\/\u2212<\/jats:sup>mice<jats:italic>in vivo<\/jats:italic>and by pharmacologic inhibitors<jats:italic>in vitro<\/jats:italic>. Building upon this model, we investigated the role polymorphonuclear leukocytes (PMN) play in the control of infection, since NADPH oxidase-mediated release of reactive oxygen intermediates (ROI) is a primary bactericidal mechanism for these cells that is critical for early innate clearance. Earlier studies suggested that<jats:italic>C. burnetii<\/jats:italic>actively inhibited release of ROI from PMN through expression of an unidentified acid phosphatase (ACP). Recent genomic annotations identified one open reading frame (CBU0335) which may encode a Sec- and type II-dependent secreted ACP. To test this model, viable<jats:italic>C. burnetii<\/jats:italic>propagated in tissue culture host cells or axenic media,<jats:italic>C. burnetii<\/jats:italic>extracts, or purified recombinant ACP (rACP) was combined with human PMN induced with 4-phorbol 12-myristate 13-acetate (PMA). The release of ROI was inhibited when PMN were challenged with viable<jats:italic>C. burnetii<\/jats:italic>,<jats:italic>C. burnetii<\/jats:italic>extracts, or rACP but not when PMN were challenged with electron beam-inactivated<jats:italic>C. burnetii. C. burnetii<\/jats:italic>extracts and rACP were also able to inhibit PMA-induced formation of NADPH oxidase complex on PMN membranes, suggesting a molecular mechanism responsible for this inhibition. These data support a model in which<jats:italic>C. burnetii<\/jats:italic>eludes the primary ROI killing mechanism of activated PMN by secreting at least one acid phosphatase.<\/jats:p>","DOI":"10.1128\/iai.01011-10","type":"journal-article","created":{"date-parts":[[2010,11,16]],"date-time":"2010-11-16T05:57:00Z","timestamp":1289887020000},"page":"414-420","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":41,"title":["<i>Coxiella burnetii<\/i>Acid Phosphatase Inhibits the Release of Reactive Oxygen Intermediates in Polymorphonuclear Leukocytes"],"prefix":"10.1128","volume":"79","author":[{"given":"J.","family":"Hill","sequence":"first","affiliation":[{"name":"Department of Microbial and Molecular Pathogenesis, Texas A&amp;M Health Science Center, College Station, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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