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			PubMed Journals: PLoS One

  Source:		PMID: 20090954
  Download:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806919/pdf/pone.0008729.pdf

    		PLoS One. 2010 Jan 15;5(1):e8729. doi:
     		10.1371/journal.pone.0008729.

			Dynamic innate immune responses of human
			bronchial epithelial cells to 
			severe acute respiratory syndrome-associated
			coronavirus infection.

			Yoshikawa T(1), Hill TE, Yoshikawa N, Popov
			VL, Galindo CL, Garner HR, Peters CJ, Tseng
			CT.

			Author Information
			(1) Department of Microbiology and Immunology,
			University of Texas Medical Branch, Galveston,
			Texas, United States of America.

			Human lung epithelial cells are likely among
			the first targets to encounter invading
			severe acute respiratory syndrome-associated
			coronavirus (SARS-CoV). Not only can these cells
			support the growth of SARS-CoV infection,
			but they are also capable of secreting inflammatory
			cytokines to initiate and, eventually, aggravate
			host innate inflammatory responses, causing
			detrimental immune-mediated pathology within
			the lungs. Thus, a comprehensive evaluation
			of the complex epithelial signaling to SARS-CoV
			is crucial for paving the way to better
			understand SARS pathogenesis. Based on
			microarray-based functional genomics, we
			report here the global gene response of
			2B4 cells, a cloned bronchial epithelial
			cell line derived from Calu-3 cells. Specifically,
			we found a temporal and spatial activation
			of nuclear factor (NF)kappaB, activator protein (AP)-1,
			and interferon regulatory factor (IRF)-3/7 in infected
			2B4 cells at 12-, 24-, and 48-hrs post infection (p.i.),
			resulting in the activation of many antiviral
			genes, including interferon (IFN)-beta,
			-lambdas, inflammatory mediators, and many
			IFN-stimulated genes (ISGs). We also showed,
			for the first time, that IFN-beta and IFN-lambdas
			were capable of exerting previously unrecognized,
			non-redundant, and complementary abilities
			to limit SARS-CoV replication, even though
			their expression could not be detected in
			infected 2B4 bronchial epithelial cells
			until 48 hrs p.i. Collectively, our results
			highlight the mechanics of the sequential
			events of antiviral signaling pathway/s
			triggered by SARS-CoV in bronchial epithelial
			cells and identify novel cellular targets
			for future studies, aiming at advancing
			strategies against SARS.

			DOI: 10.1371/journal.pone.0008729
			PMCID: PMC2806919 PMID: 20090954 [Indexed
			for MEDLINE]

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