Document Detail


Innate immune response of human alveolar type II cells infected with severe acute respiratory syndrome-coronavirus.
MedLine Citation:
PMID:  23418343     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Severe acute respiratory syndrome (SARS)-coronavirus (CoV) produces a devastating primary viral pneumonia with diffuse alveolar damage and a marked increase in circulating cytokines. One of the major cell types to be infected is the alveolar type II cell. However, the innate immune response of primary human alveolar epithelial cells infected with SARS-CoV has not been defined. Our objectives included developing a culture system permissive for SARS-CoV infection in primary human type II cells and defining their innate immune response. Culturing primary human alveolar type II cells at an air-liquid interface (A/L) improved their differentiation and greatly increased their susceptibility to infection, allowing us to define their primary interferon and chemokine responses. Viral antigens were detected in the cytoplasm of infected type II cells, electron micrographs demonstrated secretory vesicles filled with virions, virus RNA concentrations increased with time, and infectious virions were released by exocytosis from the apical surface of polarized type II cells. A marked increase was evident in the mRNA concentrations of interferon-β and interferon-λ (IL-29) and in a large number of proinflammatory cytokines and chemokines. A surprising finding involved the variability of expression of angiotensin-converting enzyme-2, the SARS-CoV receptor, in type II cells from different donors. In conclusion, the cultivation of alveolar type II cells at an air-liquid interface provides primary cultures in which to study the pulmonary innate immune responses to infection with SARS-CoV, and to explore possible therapeutic approaches to modulating these innate immune responses.
Authors:
Zhaohui Qian; Emily A Travanty; Lauren Oko; Karen Edeen; Andrew Berglund; Jieru Wang; Yoko Ito; Kathryn V Holmes; Robert J Mason
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of respiratory cell and molecular biology     Volume:  48     ISSN:  1535-4989     ISO Abbreviation:  Am. J. Respir. Cell Mol. Biol.     Publication Date:  2013 Jun 
Date Detail:
Created Date:  2013-06-04     Completed Date:  2013-08-05     Revised Date:  2014-06-03    
Medline Journal Info:
Nlm Unique ID:  8917225     Medline TA:  Am J Respir Cell Mol Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  742-8     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Antigens, Viral / immunology,  metabolism
Cell Differentiation
Cytoplasm / immunology,  ultrastructure,  virology
Epithelial Cells / immunology*,  virology
Humans
Immunity, Innate*
Interferon-beta / immunology,  metabolism
Interleukins / immunology,  metabolism
Peptidyl-Dipeptidase A / immunology,  metabolism
Primary Cell Culture
Pulmonary Alveoli / cytology,  immunology,  virology
RNA, Messenger / metabolism
Receptors, Virus / metabolism
Respiratory Mucosa / cytology,  immunology,  virology
SARS Virus / immunology*
Severe Acute Respiratory Syndrome / immunology*
Time Factors
Virus Release
Grant Support
ID/Acronym/Agency:
AI05976/AI/NIAID NIH HHS; R01-HL-29891/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, Viral; 0/IL29 protein, human; 0/Interleukins; 0/RNA, Messenger; 0/Receptors, Virus; 77238-31-4/Interferon-beta; EC 3.4.15.1/Peptidyl-Dipeptidase A; EC 3.4.17.-/angiotensin converting enzyme 2
Comments/Corrections

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