Infection of human alveolar macrophages by human coronavirus strain 229E

C. Joel Funk, Jieru Wang, Yoko Ito, Emily A. Travanty, Dennis R. Voelker, Kathryn V. Holmes, Robert J. Mason

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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-a), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and macrophage inflammatory protein 1b (MIP-1b/CCL4) in response to HCoV-229E infection, but these cells exhibited no detectable increase in IFN-b or interleukin-29 in mRNA levels. AMs from smokers had reduced secretion of TNF-a 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.

Original languageEnglish
Pages (from-to)494-503
Number of pages10
JournalJournal of General Virology
Volume93
Issue number3
DOIs
Publication statusPublished - 2012 Mar

Fingerprint

Human Coronavirus 229E
Alveolar Macrophages
Infection
Pulmonary Surfactant-Associated Protein D
Pulmonary Surfactant-Associated Protein A
Alveolar Epithelial Cells
Innate Immunity
Respiratory Tract Infections
Interferons
Tumor Necrosis Factor-alpha
Macrophage Inflammatory Proteins
Chemokine CCL5
Lung
Interleukins
Surface-Active Agents
Immune System
Epithelial Cells

ASJC Scopus subject areas

  • Virology

Cite this

Joel Funk, C., Wang, J., Ito, Y., Travanty, E. A., Voelker, D. R., Holmes, K. V., & Mason, R. J. (2012). Infection of human alveolar macrophages by human coronavirus strain 229E. Journal of General Virology, 93(3), 494-503. https://doi.org/10.1099/vir.0.038414-0

Infection of human alveolar macrophages by human coronavirus strain 229E. / Joel Funk, C.; Wang, Jieru; Ito, Yoko; Travanty, Emily A.; Voelker, Dennis R.; Holmes, Kathryn V.; Mason, Robert J.

In: Journal of General Virology, Vol. 93, No. 3, 03.2012, p. 494-503.

Research output: Contribution to journalArticle

Joel Funk, C, Wang, J, Ito, Y, Travanty, EA, Voelker, DR, Holmes, KV & Mason, RJ 2012, 'Infection of human alveolar macrophages by human coronavirus strain 229E', Journal of General Virology, vol. 93, no. 3, pp. 494-503. https://doi.org/10.1099/vir.0.038414-0
Joel Funk C, Wang J, Ito Y, Travanty EA, Voelker DR, Holmes KV et al. Infection of human alveolar macrophages by human coronavirus strain 229E. Journal of General Virology. 2012 Mar;93(3):494-503. https://doi.org/10.1099/vir.0.038414-0
Joel Funk, C. ; Wang, Jieru ; Ito, Yoko ; Travanty, Emily A. ; Voelker, Dennis R. ; Holmes, Kathryn V. ; Mason, Robert J. / Infection of human alveolar macrophages by human coronavirus strain 229E. In: Journal of General Virology. 2012 ; Vol. 93, No. 3. pp. 494-503.
@article{ec7219ae8b9d40d2ba2930b630eb0222,
title = "Infection of human alveolar macrophages by human coronavirus strain 229E",
abstract = "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-a), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and macrophage inflammatory protein 1b (MIP-1b/CCL4) in response to HCoV-229E infection, but these cells exhibited no detectable increase in IFN-b or interleukin-29 in mRNA levels. AMs from smokers had reduced secretion of TNF-a 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.",
author = "{Joel Funk}, C. and Jieru Wang and Yoko Ito and Travanty, {Emily A.} and Voelker, {Dennis R.} and Holmes, {Kathryn V.} and Mason, {Robert J.}",
year = "2012",
month = "3",
doi = "10.1099/vir.0.038414-0",
language = "English",
volume = "93",
pages = "494--503",
journal = "Journal of General Virology",
issn = "0022-1317",
publisher = "Society for General Microbiology",
number = "3",

}

TY - JOUR

T1 - Infection of human alveolar macrophages by human coronavirus strain 229E

AU - Joel Funk, C.

AU - Wang, Jieru

AU - Ito, Yoko

AU - Travanty, Emily A.

AU - Voelker, Dennis R.

AU - Holmes, Kathryn V.

AU - Mason, Robert J.

PY - 2012/3

Y1 - 2012/3

N2 - 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-a), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and macrophage inflammatory protein 1b (MIP-1b/CCL4) in response to HCoV-229E infection, but these cells exhibited no detectable increase in IFN-b or interleukin-29 in mRNA levels. AMs from smokers had reduced secretion of TNF-a 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.

AB - 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-a), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and macrophage inflammatory protein 1b (MIP-1b/CCL4) in response to HCoV-229E infection, but these cells exhibited no detectable increase in IFN-b or interleukin-29 in mRNA levels. AMs from smokers had reduced secretion of TNF-a 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.

UR - http://www.scopus.com/inward/record.url?scp=84863180709&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84863180709&partnerID=8YFLogxK

U2 - 10.1099/vir.0.038414-0

DO - 10.1099/vir.0.038414-0

M3 - Article

C2 - 22090214

AN - SCOPUS:84863180709

VL - 93

SP - 494

EP - 503

JO - Journal of General Virology

JF - Journal of General Virology

SN - 0022-1317

IS - 3

ER -