{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T17:15:57Z","timestamp":1772817357792,"version":"3.50.1"},"reference-count":43,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2006,8,1]],"date-time":"2006-08-01T00:00:00Z","timestamp":1154390400000},"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":[[2006,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Alveolar surfactant modulates the antimicrobial function of bronchoalveolar macrophages (BAM). Little is known about the effect of surfactant-associated proteins in bronchoalveolar lavage fluid (BALF) on the interaction of BAM and<jats:italic>Blastomyces dermatitidis<\/jats:italic>. We investigated BALF enhancement or inhibition of TNF-\u03b1 production by BAM stimulated by<jats:italic>B. dermatitidis<\/jats:italic>. BAM from CD-1 mice were stimulated with<jats:italic>B. dermatitidis<\/jats:italic>without or with normal BALF, surfactant protein A-deficient (SP-A<jats:sup>\u2212\/\u2212<\/jats:sup>) or surfactant protein D-deficient (SP-D<jats:sup>\u2212\/\u2212<\/jats:sup>) BALF, or a mixture of SP-A<jats:sup>\u2212\/\u2212<\/jats:sup>and SP-D<jats:sup>\u2212\/\u2212<\/jats:sup>BALF. An enzyme-linked immunosorbent assay was used to measure tumor necrosis factor alpha (TNF-\u03b1) in culture supernatants. BALFs were standardized in protein concentration. BAM plus<jats:italic>B. dermatitidis<\/jats:italic>(BAM-<jats:italic>B. dermatitidis<\/jats:italic>) TNF-\u03b1 production was inhibited \u226547% by BALF or SP-A<jats:sup>\u2212\/\u2212<\/jats:sup>BALF (at 290 or 580 \u03bcg of protein\/ml,<jats:italic>P<\/jats:italic>&lt; 0.05 to 0.01); in contrast, SP-D<jats:sup>\u2212\/\u2212<\/jats:sup>BALF did not significantly inhibit TNF-\u03b1 production. If SP-A<jats:sup>\u2212\/\u2212<\/jats:sup>BALF was mixed in equal amounts with SP-D<jats:sup>\u2212\/\u2212<\/jats:sup>BALF, TNF-\u03b1 production by BAM-<jats:italic>B. dermatitidis<\/jats:italic>was inhibited (<jats:italic>P<\/jats:italic>&lt; 0.01). Finally, pure SP-D added to SP-D<jats:sup>\u2212\/\u2212<\/jats:sup>BALF inhibited TNF-\u03b1 production by BAM-<jats:italic>B. dermatitidis<\/jats:italic>(<jats:italic>P<\/jats:italic>&lt; 0.01).<jats:italic>B. dermatitidis<\/jats:italic>incubated with BALF and washed, plus BAM, stimulated 63% less production of TNF-\u03b1 than did unwashed<jats:italic>B. dermatitidis<\/jats:italic>(<jats:italic>P<\/jats:italic>&lt; 0.05). SP-D was detected by anti-SP-D antibody on BALF-treated unwashed<jats:italic>B. dermatitidis<\/jats:italic>in an immunofluorescence assay (IFA). The BALF depleted by a coating of<jats:italic>B. dermatitidis<\/jats:italic>lost the ability to inhibit TNF-\u03b1 production (<jats:italic>P<\/jats:italic>\u2009&lt; 0.05). 1,3-\u03b2-Glucan was a good stimulator of BAM for TNF-\u03b1 production and was detected on<jats:italic>B. dermatitidis<\/jats:italic>by IFA. \u03b2-Glucan incubated with BALF inhibited the binding of SP-D in BALF to<jats:italic>B. dermatitidis<\/jats:italic>as demonstrated by IFA. Our data suggest that SP-D in BALF binds \u03b2-glucan on<jats:italic>B. dermatitidis<\/jats:italic>, blocking BAM access to \u03b2-glucan, thereby inhibiting TNF-\u03b1 production. Thus, whereas BALF constituents commonly mediate antimicrobial activity,<jats:italic>B. dermatitidis<\/jats:italic>may utilize BALF constituents, such as SP-D, to blunt the host defensive reaction; this effect could reduce inflammation and tissue destruction but could also promote disease.<\/jats:p>","DOI":"10.1128\/iai.00243-06","type":"journal-article","created":{"date-parts":[[2006,7,22]],"date-time":"2006-07-22T00:24:50Z","timestamp":1153527890000},"page":"4549-4556","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Effect of Lung Surfactant Collectins on Bronchoalveolar Macrophage Interaction with<i>Blastomyces dermatitidis<\/i>: Inhibition of Tumor Necrosis Factor Alpha Production by Surfactant Protein D"],"prefix":"10.1128","volume":"74","author":[{"given":"Madhavi","family":"Lekkala","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Santa Clara Valley Medical Center, and California Institute for Medical Research, San Jose, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ann Marie","family":"LeVine","sequence":"additional","affiliation":[{"name":"Division of Pulmonary Biology and Critical Care Medicine, Children's Hospital Medical Center, Cincinnati, Ohio"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael J.","family":"Linke","sequence":"additional","affiliation":[{"name":"Veterans Affairs Medical Center, Cincinnati, Ohio"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Erika C.","family":"Crouch","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bruce","family":"Linders","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elmer","family":"Brummer","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Santa Clara Valley Medical Center, and California Institute for Medical Research, San Jose, California"},{"name":"Department of Medicine, Stanford University School of Medicine, Stanford, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David A.","family":"Stevens","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Santa Clara Valley Medical Center, and California Institute for Medical Research, San Jose, California"},{"name":"Department of Medicine, Stanford University School of Medicine, Stanford, California"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.72.7.4159-4171.2004"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/155.3.568"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1086\/383130"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1042\/bj1140557"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.28.2.594-600.1980"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/35092620"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20020470"},{"key":"e_1_3_2_9_2","doi-asserted-by":"crossref","first-page":"2786","DOI":"10.4049\/jimmunol.140.8.2786","volume":"140","year":"1988","unstructured":"Brummer, E., L. 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