Unknown,Transcriptomics,Genomics,Proteomics

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Lipopolysaccharide modulates rhinovirus-induced chemokine secretion in monocytes and macrophages.

ABSTRACT: Rhinovirus (RV) infection has been shown to exacerbate asthma. Understanding of the underlying mechanisms by which RV infections provoke airway inflammation and remodeling in asthma may offer significant insight into asthma pathogenesis and exacerbations as well as offer opportunities for improved disease management. Expression analysis of RV A16-treated primary peripheral blood monocytes from human donors was performed to determine what pattern of gene expression is associated with RV infection of monocytes in vitro. Peripheral blood monocytes were isolated from 5 adults. Following overnight incubation in RPMI supplemented with 10% FBS, the monocytes were stimulated with purified major group RV A16 at multiplicity of infection of 10 plaque forming units (pfu) per cell or with growth media alone (mock). Cells were lysed 4 hours after treatment and isolated total RNAs were pooled per treatment and analyzed using the Affymetrix GeneChip HuGeneFL Array (Hu6800, Affymetrix, Santa Clara, CA).

ORGANISM(S): Homo sapiens

SUBMITTER: Maya Karta

PROVIDER: E-GEOD-54558 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Rhinoviruses (RVs) are major instigators of acute exacerbations of asthma, COPD and other respiratory diseases. RVs are categorized into three species (RV-A, RV-B, and RV-C), which comprise more than 160 serotypes, making it difficult to develop an effective vaccine. Currently no effective treatment for RV infection is available. Pulmonary surfactant is an extracellular complex of lipids and proteins that plays a central role in regulating innate immunity in the lung. The minor pulmonary surfactant lipids, palmitoyl-oleoyl-phosphatidylglycerol (POPG) and phosphatidylinositol (PI), are potent regulators of inflammatory processes, and exert antiviral activity against respiratory syncytial virus (RSV) and influenza A viruses (IAV). In the current study, we examined the potencies of POPG and PI against rhinovirus A16 (RV-A16) in primary human airway epithelial cells (AECs) differentiated at an air-liquid interface (ALI). After AECs were infected with RV-A16, PI reduced viral RNA copy number by 80% and downregulated (55-65%) expression of antiviral genes (MDA5, IRF7 and IFN-lambda). In contrast, POPG only slightly decreased MDA5 (24%) and IRF7 (11%) gene expression but did not inhibit IFN-lambda gene expression or RV-A16 replication in AECs. However, both POPG and PI inhibited (50-80%) IL6 and CXCL11 gene expression and protein secretion. PI treatment dramatically attenuated global gene expression changes induced by RV-A16 infection in AECs. Cell type enrichment analysis of viral regulated genes opposed by PI treatment revealed that PI inhibited viral induction of goblet cell metaplasia and virus-induced downregulation of ciliated, club, and ionocyte cell types. Notably, PI treament altered the ability of RV-A16 to regulate expression of some phosphatidylinositol 4-kinase (PI4K), acyl-CoA binding domain containing (ACBD) and low density lipoprotein receptor (LDLR) genes that play critical roles in the formation and functioning of replication organelles (ROs) required for RV replication in host cells. These data suggest PI can be used as a potent, non-toxic antiviral agent for RV infection prophylaxis and treatment.

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Lipopolysaccharide modulates rhinovirus-induced chemokine secretion in monocytes and macrophages.

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