Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice |
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| Institution: | 1. Critical Care Medicine Department, NIH Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA;2. Fungal Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA;3. Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA;4. Laboratory of Immunopathogenesis and Bioinformatics, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA;1. Department of Physics, Eski?ehir Osmangazi University, Me?elik Campus, 26480, Turkey;2. Primary Science Education Department, Bayburt University, 69000, Turkey;1. Senior Director, Computer Vision, Solar Field Calibration and Network, BrightSource Industries (Israel). 11 Kiryat Mada St, Har Hotzvim, PO Box 45220, Jerusalem 91450 Israel;2. BrightSource Industries (Israel), 11 Kiryat Mada St, Har Hotzvim, PO Box 45220, Jerusalem 91450 Israel;1. Department of Biomolecular Sciences, Section of Biochemistry and Molecular Biology, Università degli Studi “Carlo Bo”, via A. Saffi 2, 61029, Urbino, Italy;2. Istituto Auxologico Italiano, Neurobiology Laboratory, Strada Cadorna 90, 28824, Piancavallo di Oggebbio, Italy;3. Department of Life and Environmental Sciences, Università Politecnica delle Marche, via Brecce Bianche, 60131, Ancona, Italy;4. Institute of Ecosystem Study (ISE), Microbial Ecology Group (MEG), Consiglio Nazionale delle ricerche (CNR), largo V. Tonolli 50, 28922, Verbania, Italy;5. Section of Toxicological, Hygienistic and Environmental Sciences, Università degli Studi “Carlo Bo”, via A. Saffi 2, 61029, Urbino, Italy |
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| Abstract: | We examined gene expression levels of multiple chemokines and chemokine receptors during Pneumocystis murina infection in wild-type and immunosuppressed mice, using microarrays and qPCR. In wild-type mice, expression of chemokines that are ligands for Ccr2, Cxcr3, Cxcr6, and Cxcr2 increased at days 32–41 post-infection, with a return to baseline by day 75–150. Concomitant increases were seen in Ccr2, Cxcr3, and Cxcr6, but not in Cxcr2 expression. Induction of these same factors also occurred in CD40-ligand and CD40 knockout mice but only at a much later time-point, during uncontrolled Pneumocystis pneumonia (PCP). Expression of CD4 Th1 markers was increased in wild-type mice during clearance of infection. Ccr2 and Cx3cr1 knockout mice cleared Pneumocystis infection with kinetics similar to wild-type mice, and all animals developed anti-Pneumocystis antibodies. Upregulation of Ccr2, Cxcr3, and Cxcr6 and their ligands supports an important role for T helper cells and mononuclear phagocytes in the clearance of Pneumocystis infection. However, based on the current and prior studies, no single chemokine receptor appears to be critical to the clearance of Pneumocystis. |
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| Keywords: | PCP Chemokines Chemokine receptor Knock-out mice |
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