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This Article Full Text Full Text (PDF) All Versions of this Article: 290/3/L442    most recent 00112.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Vuk-Pavlovic, Z. Articles by Limper, A. H. Search for Related Content PubMed PubMed Citation Articles by Vuk-Pavlovic, Z. Articles by Limper, A. H.

Surfactant protein D enhances Pneumocystis infection in immune-suppressed mice

Zvezdana Vuk-Pavlovi,¹ Eun K. Mo,¹ Crystal R. Icenhour,¹ Joseph E. Standing,¹ James H. Fisher, and Andrew H. Limper^1,2

¹Thoracic Diseases Research Unit, Division of Pulmonary, Critical Care and Internal Medicine, Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota; and ²Division of Pulmonary and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, Colorado

Submitted 11 March 2005 ; accepted in final form 26 September 2005

To further determine the role of surfactant protein (SP)-D in the pathogenesis of Pneumocystis pneumonia, a mouse model of transgenic overexpression (OE) of SP-D was studied. These animals produce roughly 30- to 50-fold greater SP-D than their wild-type (WT) counterparts but show no other differences in lung morphology and function. Animals in both the SP-D OE and WT groups were depleted of CD4 lymphocytes with weekly injections of GK1.5 antibody, before Pneumocystis inoculation, and throughout the subsequent infection period. At various time points, mice were killed and analyzed for inflammatory parameters and organism burden. Proinflammatory cytokines in bronchoalveolar lavage fluid were elevated throughout the period of infection, with OE animals exhibiting significantly higher levels of TNF- and macrophage inflammatory protein-2 compared with WT controls. The total number of cells in the lavage fluid was also increased significantly only in the OE group, whereas the cell differential composition demonstrated lymphocyte and eosinophil infiltration in both groups of animals. Significantly, the organism burden was markedly higher in the SP-D OE animals, whereas the WT mice demonstrated little alteration in organism number over the course of infection. These results further indicate that SP-D facilitates the development of Pneumocystis infection and related lung inflammation in an immunosuppressed mouse model.

inflammation; cytokine; chemokine

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