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Stress and influenza viral infection: modulation of proinflammatory cytokine responses in the lung.

Authors: Konstantinos, AP  Sheridan, JF 
Citation: Konstantinos AP and Sheridan JF, Respir Physiol. 2001 Oct;128(1):71-7.
Pubmed: (View Article at PubMed) PMID:11535264

Viral infection of the respiratory tract induces a complex series of cellular and molecular events leading to immunological responses designed to terminate viral replication. Anti-viral immunity involves natural resistance mechanisms that overlap and modulate the development of the subsequent adaptive immune responses. An experimental murine infection with influenza A/PR8 virus was used to examine the effects of stress-induced activation of the nervous and endocrine systems on components of innate immunity. Proinflammatory cytokine responses (IL-1alpha, IL-6 and TNFalpha) were measured in the lungs during an influenza A/PR8 viral infection. For activation of the nervous and endocrine systems, restraint stress (RST) was applied prior to and during infection. Following infection, IL-1alpha increased transiently, while elevated IL-6 persisted; TNFalpha was not detected. RST suppressed virally-induced IL-1alpha, while IL-6 was unaffected. These data demonstrate differential regulation of proinflammatory cytokines by stress. The mechanism underlying suppression of the lung IL-1alpha in stressed mice is currently unknown; its downregulation may contribute to increased viral pathogenesis in stressed individuals.


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RGD Object Information
RGD ID: 4142860
Created: 2010-09-14
Species: All species
Last Modified: 2010-09-14
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.