Total lung gene expression data of Pneumocystis-infected wildtype and IFN-gamma knockout mice.

ABSTRACT: Pulmonary hypertension (PH) is a disease of diverse etiology. While primary PH can develop in the absence of prior disease, PH more commonly develops in conjunction with other pulmonary pathologies. We previously reported a mouse model in which PH occurs as a sequelae of Pneumocystis infection in the context of transient CD4 depletion. Here, we demonstrate that instead of the expected Th2 pathways, the Th1 cytokine IFN-M-NM-3 was essential for the development of PH, as wild type mice developed PH, but not IFN-M-NM-3 knockout mice. Because gene expression analysis showed few strain differences that were not immune function related, we focused on those responses as potential pathologic mechanisms. While there were several differences in cellular and cytokine response that warrant further exa

ORGANISM(S): Mus musculus

SUBMITTER: Steve Swain 

PROVIDER: E-GEOD-51750 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress