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Prevention of bone marrow cell apoptosis and regulation of hematopoiesis by type I IFNs during systemic responses to pneumocystis (PC) lung infection


ABSTRACT: IFrag-/- but not RAG-/- mice develop rapidly progressing bone marrow failure in response to PC lung infection. Changes contributing to accelerated bone marrow cell apoptosis in IFrag-/- mice appear to be initiated around day 7 post infection. To gain further insight into the mechanism underlying the induction of bone marrow failure in IFRag-/- but not RAG-/- mice in response to PC lung infection, IFRag and RAG mice were PC infected via intra-tracheal inocculation of 10e7 nuclei and bone marrow responses were assessed at day 0, and 7 post infection. One group of IFRag-/- mice also received anti-oxidants treatment with N-Acetyl cysteine in drinking water (100mg/ml) throughout the course of infection (IFRag-/- +NAC) as oxidative stress appeared to be a contributing factor. RT2 profiler PCR array, 5 conditions, 3 biological replicates

ORGANISM(S): Mus musculus

SUBMITTER: Kate McInnerney 

PROVIDER: E-GEOD-27835 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Prevention of bone marrow cell apoptosis and regulation of hematopoiesis by type I IFNs during systemic responses to pneumocystis lung infection.

Taylor David D   Wilkison Michelle M   Voyich Jovanka J   Meissner Nicole N  

Journal of immunology (Baltimore, Md. : 1950) 20110406 10


We recently demonstrated that lack of type I IFN signaling (IFNAR knockout) in lymphocyte-deficient mice (IFrag(-/-)) results in bone marrow (BM) failure after Pneumocystis lung infection, whereas lymphocyte-deficient mice with intact IFNAR (RAG(-/-)) had normal hematopoiesis. In the current work, we performed studies to define further the mechanisms involved in the induction of BM failure in this system. BM chimera experiments revealed that IFNAR expression was required on BM-derived but not st  ...[more]

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