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MAPK Response to X31 Influenza A Virus Infection in Murine Macrophage Cell Lines
Author(s) -
Can Georgetta,
Gronemus Jenny Q.,
Williams Margaret S.,
Callahan Michelle A.,
Lowy R. Joel
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.948.2
Subject(s) - mapk/erk pathway , kinase , p38 mitogen activated protein kinases , microbiology and biotechnology , biology , phosphorylation , cell culture , genetics
RAW 264.7 and J774.1 murine macrophage cells are widely used to model responses to infectious diseases; therefore they were selected to explore early molecular responses to FLUA. NF‐kappa B is reported to be central to FLUA host‐response in other cell types. Previous data show that FLUA (X31/H3N2) does not activate the classical NF‐kappa B dependent pathway in these macrophages. Regulator proteins, I kappa B ‐alpha and ‐beta, are not degraded in response to FLUA infection, and p65 does not translocate from the cytoplasm to the nucleus. However, the cells display the expected increase in TNF‐alpha and other inflammatory cytokine and chemokine secretions. Mitogen Activated Phosphokinase (MAPK) signaling pathways are also reported to control production of inflammatory cytokines in response to FLUA. The activation of the MAPK pathway intermediates p38, Janus Kinases 1 and 2 (JNK 1/2), and Extracellular Regulated Kinases 1 and 2 (ERK 1/2) were investigated in both cell lines between 0.25 and 3 hours post‐infection. Each of these kinases showed increased phosphorylation post FLUA infection. JNK phosphorylation occurred early while p38 phosphorylation appeared late. Phosphorylation of ERK 1/2 occurred earlier in J774.1 cells as compared to RAW 264.7 cells. The results suggest that in these monocytic cells the MAPK pathways are important in the early pathogen activated molecular pattern (PAMP) response to FLUA.