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Study points to essential role of IL-22 in lung repair after the flu
Date:3/10/2013

at sites of influenza-associated injury.

The investigators also reported that 10 days after influenza infection, IL-22deficient mice showed significantly more severe damage and greater lung edema than WT control mice, as indicated by higher lactate dehydrogenase levels and more total protein content in bronchoalveolar lavage. No differences were found in viral load. Another indication of more severe lung injury was an increase in the number of lymphocytes in the IL-22deficient animals.

IL-22deficient mice also showed functional impairments. For instance, those infected with influenza showed significantly decreased compliance (referring to lung distensibility) and increased hysteresis (referring to compliance differences during inspiration and expiration), indicating lung stiffness. Histological examination 21 days after influenza infection showed that IL-22deficient mice displayed regions of diffuse inflammation and alveolar injury, few areas of metaplasia, higher intimal thickening, proteinaceous accumulation, and increased collagen deposition compared to WT mice. Gene expression analysis revealed aberrant expression of epithelial genes involved in repair processes in the mice lacking IL-22.

"The role of IL-22 in promoting epithelial repair is emerging. We demonstrate that IL-22 plays a critical role in regulating pulmonary epithelial repair responses during influenza infection and resolution," says Dr. Alcorn. IL-22 is currently under development as a potential therapeutic in human clinical trials.


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Contact: David Sampson
ajpmedia@elsevier.com
215-239-3171
Elsevier Health Sciences
Source:Eurekalert

Page: 1 2

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