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  • Title: Cytokine levels during symptomatic viral upper respiratory tract infection.
    Author: Gentile DA, Villalobos E, Angelini B, Skoner D.
    Journal: Ann Allergy Asthma Immunol; 2003 Oct; 91(4):362-7. PubMed ID: 14582815.
    Abstract:
    BACKGROUND: Previous studies suggest a role for locally produced proinflammatory cytokines in the development and expression of illness during experimental infection with a variety of respiratory viruses. However, most of these studies fail to make comparisons between symptomatic and asymptomatic infected subjects. OBJECTIVE: To compare the pattern of nasal cytokine elaboration in asymptomatic and symptomatic subjects experimentally infected with rhinovirus-39 (RV-39). METHODS: Healthy adults underwent experimental intranasal inoculation with a safety-tested clinical isolate of RV-39. Nasal lavages were collected, nasal symptoms were recorded, and expelled nasal secretions were weighed before and then daily for 6 days after challenge. Nasal lavages were submitted for viral culture and assayed for cytokine protein levels by enzyme-linked immunosorbent assay. RESULTS: Twenty-nine subjects were enrolled in the study. All subjects were infected as evidenced by viral shedding and/or seroconversion. Sixteen subjects were symptomatic and 13 were asymptomatic as evaluated by subject self-report. During infection, significant increases in mean levels of nasal interleukin 6 (IL-6) (P = .01) and IL-1 (P = .02) were observed in symptomatic but not asymptomatic subjects. In symptomatic subjects, these increases were temporally related to the development of nasal symptoms and production of secretions. Mean levels of IL-8, IL-10, and tumor necrosis factor a were not increased in either group during infection. CONCLUSIONS: The results of this study demonstrate elevations in certain locally produced cytokines during symptomatic but not asymptomatic respiratory infection with RV-39. Future studies using selected anticytokine therapies may help elucidate the precise role of cytokines in mediating disease expression.
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