Surfactant protein D enhances Pneumocystis infection in immune-suppressed mice

Zvezdana Vuk-Pavlović, Eun K. Mo, Crystal R. Icenhour, Joseph E. Standing, James H. Fisher, Andrew Harold Limper

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

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-α 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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume290
Issue number3
DOIs
StatePublished - Mar 2006

Fingerprint

Pulmonary Surfactant-Associated Protein D
Pneumocystis Infections
Infection
Pneumocystis
Lymphocytes
Chemokine CXCL2
Pneumocystis Pneumonia
Wild Animals
Therapeutic Irrigation
Bronchoalveolar Lavage Fluid
Eosinophils
Transgenic Mice
Pneumonia
Cell Count
Cytokines
Lung
Injections

Keywords

  • Chemokine
  • Cytokine
  • Inflammation

ASJC Scopus subject areas

  • Cell Biology
  • Physiology
  • Pulmonary and Respiratory Medicine

Cite this

Surfactant protein D enhances Pneumocystis infection in immune-suppressed mice. / Vuk-Pavlović, Zvezdana; Mo, Eun K.; Icenhour, Crystal R.; Standing, Joseph E.; Fisher, James H.; Limper, Andrew Harold.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 290, No. 3, 03.2006.

Research output: Contribution to journalArticle

Vuk-Pavlović, Zvezdana ; Mo, Eun K. ; Icenhour, Crystal R. ; Standing, Joseph E. ; Fisher, James H. ; Limper, Andrew Harold. / Surfactant protein D enhances Pneumocystis infection in immune-suppressed mice. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 2006 ; Vol. 290, No. 3.
@article{d5c63f92b32645c7b40ab1c70856ead9,
title = "Surfactant protein D enhances Pneumocystis infection in immune-suppressed mice",
abstract = "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-α 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.",
keywords = "Chemokine, Cytokine, Inflammation",
author = "Zvezdana Vuk-Pavlović and Mo, {Eun K.} and Icenhour, {Crystal R.} and Standing, {Joseph E.} and Fisher, {James H.} and Limper, {Andrew Harold}",
year = "2006",
month = "3",
doi = "10.1152/ajplung.00112.2005",
language = "English (US)",
volume = "290",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "3",

}

TY - JOUR

T1 - Surfactant protein D enhances Pneumocystis infection in immune-suppressed mice

AU - Vuk-Pavlović, Zvezdana

AU - Mo, Eun K.

AU - Icenhour, Crystal R.

AU - Standing, Joseph E.

AU - Fisher, James H.

AU - Limper, Andrew Harold

PY - 2006/3

Y1 - 2006/3

N2 - 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-α 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.

AB - 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-α 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.

KW - Chemokine

KW - Cytokine

KW - Inflammation

UR - http://www.scopus.com/inward/record.url?scp=33644965079&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33644965079&partnerID=8YFLogxK

U2 - 10.1152/ajplung.00112.2005

DO - 10.1152/ajplung.00112.2005

M3 - Article

C2 - 16199436

AN - SCOPUS:33644965079

VL - 290

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 3

ER -