Premium
Human macrophage exposure to major or minor group rhinovirus elicits differential inflammatory cytokine responses, depending on donor asthmatic status
Author(s) -
Hall David J,
Wilson Megan L,
Raugi Da
Publication year - 2007
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.21.5.a248-a
Subject(s) - rhinovirus , immunology , cytokine , asthma , medicine , immune system , pathogenesis , common cold , macrophage , biology , in vitro , virus , biochemistry
Rhinoviruses are small, positive‐strand RNA viruses that cause 50% of common colds and are a major cause of asthma exacerbations. Rhinovirus only productively infects bronchial epithelial cells, however previous studies have implicated monocytic cells in the cytokine dysregulation observed in rhinovirus infection. Although monocytic cells are not productively infected, they are prominent in the lung and participate in the immune response. Thus, the hypothesis of this study is that macrophages participate in the exacerbation of asthma symptoms through the secretion of a variety of inflammatory cytokines. Both MCP‐1 and IP‐10 have important inflammatory functions that have been linked to the pathogenesis of many disease conditions, including asthma. This study examines the effect of hyperresponsive airway conditions such as asthma and allergic rhinitis on rhinovirus‐induced secretion of MCP‐1 and IP‐10 by monocyte‐derived macrophages (MDMs). MDMs are stimulated in vitro with major‐ and minor‐ group rhinovirus, which use different binding receptors. In addition, the study uses inhibitors to the ERK, PKB and PKC signaling pathways to determine if MCP‐1 and IP‐10 production varies between viruses and donor airway conditions. MCP‐1 and IP‐10 responses differ between major‐ and minor group rhinovirus, between respiratory conditions and appear to involve the ERK, PKB and PKC signaling pathways.