Stress and influenza viral infection: modulation of proinflammatory cytokine responses in the lung.
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.
Konstantinos
A P
AP
Department of Oral Biology, The Ohio State University Health Sciences Center, 305 W. 12th Avenue, PO Box 182357, Columbus, OH 43218-2357, USA.
Sheridan
J F
JF
D000818:Animals; D016207:Cytokines / Q000096:biosynthesis*; D006727:Hormone Antagonists / Q000494:pharmacology; D018836:Inflammation Mediators / Q000378:metabolism*; D007375:Interleukin-1 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008168:Lung / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015735:Mifepristone / Q000494:pharmacology; D009490:Neurosecretory Systems / Q000276:immunology; D009976:Orthomyxoviridae Infections / Q000150:complications / Q000276:immunology*; D012149:Restraint, Physical / Q000009:adverse effects; D013312:Stress, Physiological / Q000150:complications / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D016207:Cytokines; D006727:Hormone Antagonists; D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D015735:Mifepristone