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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Immunol
2013 ; 190
(9
): 4676-84
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gab.com Text
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English Wikipedia
Inflammatory response of mast cells during influenza A virus infection is
mediated by active infection and RIG-I signaling
#MMPMID23526820
Graham AC
; Hilmer KM
; Zickovich JM
; Obar JJ
J Immunol
2013[May]; 190
(9
): 4676-84
PMID23526820
show ga
Influenza A virus (IAV) is a major respiratory pathogen of both humans and
animals. The lung is protected from pathogens by alveolar epithelial cells,
tissue-resident alveolar macrophages, dendritic cells, and mast cells. The role
of alveolar epithelial cells, endothelial cells, and alveolar macrophages during
IAV infection has been studied previously. In this study, we address the role of
mast cells during IAV infection. Respiratory infection with A/WSN/33 causes
significant disease and immunopathology in C57BL/6 mice but not in
B6.Cg-Kit(W-sh) mice, which lack mast cells. During in vitro coculture, A/WSN/33
caused mast cells to release histamine, secrete cytokines and chemokines, and
produce leukotrienes. Moreover, when mast cells were infected with IAV, the virus
did not replicate within mast cells. Importantly, human H1N1, H3N2, and influenza
B virus isolates also could activate mast cells in vitro. Mast cell production of
cytokines and chemokines occurs in a RIG-I/MAVS-dependent mechanism; in contrast,
histamine production occurred through a RIG-I/MAVS-independent mechanism. Our
data highlight that, following IAV infection, the response of mast cells is
controlled by multiple receptors. In conclusion, we identified a unique
inflammatory cascade activated during IAV infection that could potentially be
targeted to limit morbidity following IAV infection.