Cutting edge: Sympathetic nervous system increases proinflammatory cytokines and exacerbates influenza A virus pathogenesis.
Although the sympathetic nervous system innervates the lung, little is known about its participation in host immunity to pulmonary pathogens. In this study, we show that peripheral sympathectomy reduces mouse morbidity and mortality from influenza A virus-induced pneumonia due to reduced inflammatory influx of monocytes, neutrophils, and NK cells. Mortality was also delayed by treating mice with an alpha-adrenergic antagonist. Sympathectomy diminished the immediate innate cytokine responses, particularly IL-1, which was profoundly reduced. These findings demonstrate an unexpected role for the sympathetic nervous system in innate antiviral immunity and in exacerbating the pathology of a virus of great significance to human and animal health.
Grebe
Kristie M
KM
Laboratories of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Takeda
Kazuyo
K
Hickman
Heather D
HD
Bailey
Adam L
AL
Bailey
Adam M
AM
Embry
Alan C
AC
Bennink
Jack R
JR
Yewdell
Jonathan W
JW
D000818:Animals; D002465:Cell Movement / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis*; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology*; D009980:Influenza A virus / Q000472:pathogenicity*; D007375:Interleukin-1 / Q000096:biosynthesis; D051379:Mice; D009976:Orthomyxoviridae Infections / Q000276:immunology; D011014:Pneumonia / Q000821:virology; D015996:Survival Rate; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000276:immunology*
D016207:Cytokines; D007375:Interleukin-1