Abstract:
:Alveolar macrophages are the effector cells largely responsible for clearance of Pneumocystis carinii from the lungs. Binding of organisms to beta-glucan and mannose receptors has been shown to stimulate phagocytosis of the organisms. To further define the mechanisms used by alveolar macrophages for clearance of P. carinii, mice deficient in the expression of scavenger receptor A (SRA) were infected with P. carinii, and clearance of organisms was monitored over time. SRA-deficient (SRAKO) mice consistently cleared P. carinii faster than did wild-type control mice. Expedited clearance corresponded to elevated numbers of activated CD4(+) T cells in the alveolar spaces of SRAKO mice compared to wild-type mice. Alveolar macrophages from SRAKO mice had increased expression of CD11b on their surfaces, consistent with an activated phenotype. However, they were not more phagocytic than macrophages expressing SRA, as measured by an in vivo phagocytosis assay. SRAKO alveolar macrophages produced significantly more tumor necrosis factor alpha (TNF-alpha) than wild-type macrophages when stimulated with lipopolysaccharide in vitro but less TNF-alpha in response to P. carinii in vitro. However, upon in vivo stimulation, SRAKO mice produced significantly more TNF-alpha, interleukin 12 (IL-12), and IL-18 in response to P. carinii infection than did wild-type mice. Together, these data indicate that SRA controls inflammatory cytokines produced by alveolar macrophages in the context of P. carinii infection.
journal_name
Infect Immunjournal_title
Infection and immunityauthors
Hollifield M,Bou Ghanem E,de Villiers WJ,Garvy BAdoi
10.1128/IAI.00393-07subject
Has Abstractpub_date
2007-08-01 00:00:00pages
3999-4005issue
8eissn
0019-9567issn
1098-5522pii
IAI.00393-07journal_volume
75pub_type
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journal_title:Infection and immunity
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doi:
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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doi:10.1128/IAI.4.5.660-661.1971
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journal_title:Infection and immunity
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journal_title:Infection and immunity
pub_type: 杂志文章
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