PMID: 9423872Jan 10, 1998Paper

Activated pulmonary macrophages are insufficient for resistance against Pneumocystis carinii

Infection and Immunity
R HananoS H Kaufmann

Abstract

CD4+ T cells are pivotal for elimination of Pneumocystis carinii from infected lungs, and alveolar macrophages are considered the main effector cells clearing the infected host of P. carinii organisms. To investigate this issue, several mutant mouse strains were used in a previously established experimental setup which facilitates natural acquisition of disease through inhalation of airborne fungal organisms. Mutant mice deficient in major histocompatibility complex class II molecules (A beta(-/-)), T-cell receptor alphabeta cells (TCR beta(-/-)), or all mature T and B lymphocytes (RAG-1(-/-)) were naturally susceptible to P. carinii, whereas mouse mutants lacking the gamma interferon (IFN-gamma) receptor (IFN-gamma-R(-/-)) or tumor necrosis factor alpha (TNF-alpha) type I receptor (p55) (TNF-alpha-RI(-/-)) resisted disease acquisition. Analysis of pulmonary cytokine patterns and free radical expression revealed the presence of superoxide, nitric oxide, and interleukin-1 (IL-1) mRNA and elevated levels of IFN-gamma, TNF-alpha, and IL-12 in diseased TCR beta(-/-) and RAG-1(-/-) mice. Pulmonary macrophages of all diseased mouse mutants expressed scavenger and mannose receptors. Morbid A beta(-/-) mutants displayed significant NO ...Continue Reading

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Citations

Feb 17, 2005·Medical Mycology·Chad SteeleJay K Kolls
Apr 4, 2007·Infection and Immunity·Xiaowen L RudnerJudd E Shellito
Jul 23, 2003·The Journal of Immunology : Official Journal of the American Association of Immunologists·Frances E LundBeth A Garvy
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Mar 6, 1999·Clinical and Diagnostic Laboratory Immunology·P D Walzer

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