Infection of human alveolar macrophages by human coronavirus strain 229E
| Autor: | Jieru Wang, Emily A. Travanty, Dennis R. Voelker, C. Joel Funk, Robert J. Mason, Yoko Ito, Kathryn V. Holmes |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
medicine.medical_treatment
Gene Expression Enzyme-Linked Immunosorbent Assay Viral Plaque Assay Biology CCL5 Interferon Coronavirus 229E Human Virology Macrophages Alveolar medicine Humans Macrophage inflammatory protein Cells Cultured Lung Innate immune system Respiratory tract infections Animal Gene Expression Profiling virus diseases Epithelial Cells Surfactant protein A medicine.anatomical_structure Cytokine Fluorescent Antibody Technique Direct Immunology Cytokines medicine.drug |
| Zdroj: | Journal of General Virology |
| ISSN: | 1465-2099 |
| Popis: | Human coronavirus strain 229E (HCoV-229E) commonly causes upper respiratory tract infections. However, lower respiratory tract infections can occur in some individuals, indicating that cells in the distal lung are susceptible to HCoV-229E. This study determined the virus susceptibility of primary cultures of human alveolar epithelial cells and alveolar macrophages (AMs). Fluorescent antibody staining indicated that HCoV-229E could readily infect AMs, but no evidence was found for infection in differentiated alveolar epithelial type II cells and only a very low level of infection in type II cells transitioning to the type I-like cell phenotype. However, a human bronchial epithelial cell line (16HBE) was readily infected. The innate immune response of AMs to HCoV-229E infection was evaluated for cytokine production and interferon (IFN) gene expression. AMs secreted significant amounts of tumour necrosis factor alpha (TNF-α), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and macrophage inflammatory protein 1β (MIP-1β/CCL4) in response to HCoV-229E infection, but these cells exhibited no detectable increase in IFN-β or interleukin-29 in mRNA levels. AMs from smokers had reduced secretion of TNF-α compared with non-smokers in response to HCoV-229E infection. Surfactant protein A (SP-A) and SP-D are part of the innate immune system in the distal lung. Both surfactant proteins bound to HCoV-229E, and pre-treatment of HCoV-229E with SP-A or SP-D inhibited infection of 16HBE cells. In contrast, there was a modest reduction in infection in AMs by SP-A, but not by SP-D. In summary, AMs are an important target for HCoV-229E, and they can mount a pro-inflammatory innate immune response to infection. |
| Databáze: | OpenAIRE |
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