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  • Title: Rhinovirus-induced macrophage cytokine expression does not require endocytosis or replication.
    Author: Saba TG, Chung Y, Hong JY, Sajjan US, Bentley JK, Hershenson MB.
    Journal: Am J Respir Cell Mol Biol; 2014 May; 50(5):974-84. PubMed ID: 24783958.
    Abstract:
    Rhinovirus (RV) is responsible for the majority of virus-induced asthma exacerbations. We showed previously that RV infection of ovalbumin-sensitized and -challenged BALB/c mice induces production of type 2 cytokines from M2-polarized macrophages. In the present study, we sought to determine the mechanism of RV-induced cytokine expression. We infected bone marrow-derived macrophages (BMMs) from BALB/c mice with RV serotype 1B, a minor group virus that infects mouse cells. Selected cultures were pretreated with IL-4, a type 2 cytokine increased in allergic asthma. RV infection of untreated cells increased messenger RNA and protein expression of the M1 cytokines TNF-α, CXCL1, and IL-6 but failed to induce expression of the M2 cytokines CCL22 and CCL24. Cells pretreated with IL-4 showed decreased expression of M1 cytokines but increased expression of Ym-1, Arg-1 (M2 markers), CCL22, and CCL24. Infection with ultraviolet (UV)-irradiated, replication-deficient RV elicited similar cytokine responses, suggesting that the outcome is replication independent. Consistent with this, viral RNA copy number did not increase in RV-treated BMMs or bronchoalveolar macrophages. RV-induced cytokine expression was not affected when cells were pretreated with cytochalasin D, suggesting that viral endocytosis is not required for the response. Finally, RV-induced cytokine expression and viral attachment were abolished in BMMs from myeloid differentiation factor 88 and Toll-like receptor (TLR)2 KO mice, suggesting a specific requirement of TLR2. We conclude that RV elicits a proinflammatory cytokine response in BMMs through a cell-surface-mediated, TLR2-dependent mechanism that does not require viral endocytosis or replication.
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