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Infection and Immunity, March 2006, p. 1924-1932, Vol. 74, No. 3
0019-9567/06/$08.00+0 doi:10.1128/IAI.74.3.1924-1932.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Division of Cell and Molecular Biology, Biochemistry Building, Imperial College London, London SW7 2AZ, United Kingdom,1 Kennedy Institute of Rheumatology, Imperial College London, London W6 8LM, United Kingdom2
Received 23 September 2005/ Returned for modification 2 November 2005/ Accepted 28 December 2005
Illness due to respiratory virus infection is often induced by excessive infiltration of cells into pulmonary tissues, leading to airway occlusion. We show here that infection with Trichinella spiralis results in lower levels of tumor necrosis factor in bronchoalveolar lavage fluid and inhibits cellular recruitment into the airways of mice coinfected with influenza A virus. Infiltration of neutrophils and CD4+ and CD8+ lymphocytes was reduced, resulting in animals gaining weight more rapidly following the initial phase of infection. Influenza resulted in a generalized increase in vascular permeability in pulmonary tissues, and this was suppressed by parasite infection, although the effects were restricted to the early phase of trichinosis. Moreover, the number of cells producing interleukin-10 (IL-10), and the local levels of this cytokine, were reduced, suggesting that amelioration of pulmonary pathology by parasite infection occurs independently of IL-10 production.
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