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Investigators at University of Georgia, Medical Department target asthma
2009 JUN 2 - (NewsRx.com) -- "Infections with respiratory pathogens such as respiratory syncytial virus and rhinovirus have been associated with the development of long-term chronic airway disease. To better understand the events responsible for this clinical outcome, a rodent model of virus-induced chronic airway disease has been characterized," scientists in the United States report. "Upon infection with Sendai virus (parainfluenza virus type-1), Brown Norway (BN) rats develop an asthma-like clinical syndrome, while Fischer 344 (F344) rats fully recover. Our previous studies demonstrated that after infection, tumor necrosis factor-alpha (TNF-alpha) expression is substantially higher in BN rats compared to F344 rats, and this may at least partially mediate the virus-induced airway abnormalities. To investigate the underlying mechanism(s) for the increased TNF-alpha expression, the role of nuclear factor-kappa B (NF-kappa B), an important regulator of TNF-alpha gene transcription, was examined. Supershift electrophoretic mobility shift assays (EMSAs) indicate that normal F344 rats predominantly express the p65 subunit of NF-kappa B in the lungs, and virus infection temporarily increases expression of the p50 subunit. In contrast, normal BN rats have higher expression of the p50 subunit in the pulmonary tract. Upon infection, p50-subunit expression in BN rats increases to levels higher than those observed in virus-infected F344 rats. Interestingly, treatment of infected BN rats with dexamethasone at doses known to prevent virus-induced airway abnormalities increases pulmonary expression of the p65 subunit, and decreases TNF-alpha mRNA levels in the lungs. Furthermore, direct inhibition of TNF-alpha also increases pulmonary expression of p65 in virus-infected BN, but not F344, rats," wrote E.W. Uhl and colleagues, University of Georgia, Medical Department. The researchers concluded: "Taken together, these results suggest that differential expression of NF-kappa B subunits may play an important role in the development of post-viral chronic airway abnormalities." Uhl and colleagues published their study in Viral Immunology (Differential Expression of Nuclear Factor-kappa B Mediates Increased Pulmonary Expression of Tumor Necrosis Factor-alpha and Virus-Induced Asthma. Viral Immunology, 2009;22(2):79-89). For more information, contact E.W. Uhl, University of Georgia, College Vet. Medical, Dept. of Pathology, Athens, GA 30602, USA. Publisher contact information for the journal Viral Immunology is: Mary Ann Liebert Inc., 140 Huguenot Street, 3RD FL, New Rochelle, NY 10801, USA. Keywords: United States, Athens, Allergies, Allergy Medicine, Asthma, Clinical Syndrome, Common Cold, Immunology, Infectious Disease, Necrosis, Parainfluenza Virus, Paramyxoviridae, Paramyxovirus, Pulmonology, Respiratory Syncytial Virus, Rhinovirus, Sendai Virus, Viral Research, Virology, University of Georgia, Medical Department. This article was prepared by Life Science Weekly editors from staff and other reports. Copyright 2009, Life Science Weekly via NewsRx.com.
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