| pubmed-article:17593964 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17593964 | lifeskim:mentions | umls-concept:C0016192 | lld:lifeskim |
| pubmed-article:17593964 | lifeskim:mentions | umls-concept:C0033809 | lld:lifeskim |
| pubmed-article:17593964 | lifeskim:mentions | umls-concept:C0143146 | lld:lifeskim |
| pubmed-article:17593964 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:17593964 | lifeskim:mentions | umls-concept:C0449297 | lld:lifeskim |
| pubmed-article:17593964 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:17593964 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:17593964 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:17593964 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:17593964 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:17593964 | pubmed:dateCreated | 2007-6-27 | lld:pubmed |
| pubmed-article:17593964 | pubmed:abstractText | Surfactant protein A (SP-A) is an important lung innate immune protein that kills microbial pathogens by opsonization and membrane permeabilization. We investigated the basis of SP-A-mediated pulmonary clearance of Pseudomonas aeruginosa using genetically-engineered SP-A mice and a library of signature-tagged P. aeruginosa mutants. A mutant with an insertion into flgE, the gene that encodes flagellar hook protein, was preferentially cleared by the SP-A(+/+) mice, but survived in the SP-A(-/-) mice. Opsonization by SP-A did not play a role in flgE clearance. However, exposure to SP-A directly permeabilized and killed the flgE mutant, but not the wild-type parental strain. P. aeruginosa strains with mutation in other flagellar genes, as well as mucoid, nonmotile isolates from cystic fibrosis patients, were also permeabilized by SP-A. Provision of the wild-type fliC gene restored the resistance to SP-A-mediated membrane permeabilization in the fliC-deficient bacteria. In addition, non-mucoid, motile revertants of CF isolates reacquired resistance to SP-A-mediated membrane permeability. Resistance to SP-A was dependent on the presence of an intact flagellar structure, and independent of flagellar-dependent motility. We provide evidence that flagellar-deficient mutants harbor inadequate amounts of LPS required to resist membrane permeabilization by SP-A and cellular lysis by detergent targeting bacterial outer membranes. Thus, the flagellum of P. aeruginosa plays an indirect but important role resisting SP-A-mediated clearance and membrane permeabilization. | lld:pubmed |
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| pubmed-article:17593964 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17593964 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17593964 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17593964 | pubmed:issn | 1932-6203 | lld:pubmed |
| pubmed-article:17593964 | pubmed:author | pubmed-author:LevesqueRoger... | lld:pubmed |
| pubmed-article:17593964 | pubmed:author | pubmed-author:McCormackFran... | lld:pubmed |
| pubmed-article:17593964 | pubmed:author | pubmed-author:ZhangShipingS | lld:pubmed |
| pubmed-article:17593964 | pubmed:author | pubmed-author:O'TooleGeorge... | lld:pubmed |
| pubmed-article:17593964 | pubmed:author | pubmed-author:LauGee WGW | lld:pubmed |
| pubmed-article:17593964 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:17593964 | pubmed:volume | 2 | lld:pubmed |
| pubmed-article:17593964 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17593964 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17593964 | pubmed:pagination | e564 | lld:pubmed |
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