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Seasonal and pandemic influenza H1N1 viruses induce differential expression of
SOCS-1 and RIG-I genes and cytokine/chemokine production in macrophages
#MMPMID23434273
Ramírez-Martínez G
; Cruz-Lagunas A
; Jiménez-Alvarez L
; Espinosa E
; Ortíz-Quintero B
; Santos-Mendoza T
; Herrera MT
; Canché-Pool E
; Mendoza C
; Bañales JL
; García-Moreno SA
; Morán J
; Cabello C
; Orozco L
; Aguilar-Delfín I
; Hidalgo-Miranda A
; Romero S
; Suratt BT
; Selman M
; Zúñiga J
Cytokine
2013[Apr]; 62
(1
): 151-9
PMID23434273
show ga
BACKGROUND: Infection with pandemic (pdm) A/H1N1 virus induces high levels of
pro-inflammatory mediators in blood and lungs of experimental animals and humans.
METHODS: To compare the involvement of seasonal A/PR/8/34 and pdm A/H1N1 virus
strains in the regulation of inflammatory responses, we analyzed the changes in
the whole-genome expression induced by these strains in macrophages and A549
epithelial cells. We also focused on the functional implications (cytokine
production) of the differential induction of suppressors of cytokine signaling
(SOCS)-1, SOCS-3, retinoid-inducible gene (RIG)-I and interferon receptor 1
(IFNAR1) genes by these viral strains in early stages of the infection. RESULTS:
We identified 130 genes differentially expressed by pdm A/H1N1 and A/PR/8/34
infections in macrophages. mRNA levels of SOCS-1 and RIG-I were up-regulated in
macrophages infected with the A/PR/8/34 but not with pdm A/H1N1 virus. mRNA
levels of SOCS-3 and IFNAR1 induced by A/PR/8/34 and pdm A/H1N1 strains in
macrophages, as well as in A549 cells were similar. We found higher levels of
IL-6, TNF-?, IL-10, CCL3, CCL5, CCL4 and CXCL8 (p < 0.05) in supernatants from
cultures of macrophages infected with the pdm A/H1N1 virus compared to those
infected with the A/PR/8/34 strain, coincident with the lack of SOCS-1 and RIG-I
expression. In contrast, levels of INF-? were higher in cultures of macrophages
48h after infection with the A/PR/8/34 strain than with the pdm A/H1N1 virus.
CONCLUSIONS: These findings suggest that factors inherent to the pdm A/H1N1 viral
strain may increase the production of inflammatory mediators by inhibiting SOCS-1
and modifying the expression of antiviral immunity-related genes, including
RIG-I, in human macrophages.
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