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Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE67721 | GEO | 2015/10/10

SECONDARY ACCESSION(S): PRJNA280747

REPOSITORIES: GEO

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Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice.

Project description: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.

| S-EPMC4554965 | biostudies-literature

Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice (part 2)

Project description:In wild-type mice, expression of chemokines that are ligands for Ccr2, Cxcr3, and Cxcr2 increased at days 32 to 41 post-infection, with a return to baseline by day 75. Concomitant increases were seen in Ccr2 and Cxcr3 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 and Cxcr3 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.

2015-10-10 | GSE67720 | GEO

Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice (part 3)

2015-10-10 | GSE67718 | GEO

Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice (part 4)

Project description:For both CD4 and micropajfe cell types, upregulated genes were primarily related to immune activation and proliferation, while down-regulated genes represented more diverse processes, including cell membranes, vasculature development, cell adhesion, and lipid-related metabolic processes.

2015-10-10 | GSE67717 | GEO

Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice (part 1)

2015-10-10 | GSE67716 | GEO

Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice

Project description:Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice

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Borrelia burgdorferi population dynamics and prototype gene expression during infection of immunocompetent and immunodeficient mice.

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Suppression of innate immune pathology by regulatory T cells during Influenza A virus infection of immunodeficient mice.

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