Premium
The Inflammatory Reflex Controls Inflammation in Response to Viral Challenges
Author(s) -
Martelli Davide,
Farmer David G. S.,
Komegae Evilin N.,
McKinley Michael Joseph,
McAllen Robin Michael
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.885.2
Subject(s) - inflammation , reflex , splanchnic , viral meningitis , medicine , immunology , tumor necrosis factor alpha , cytokine , lipopolysaccharide , immune system , efferent , meningitis , bacterial meningitis , hemodynamics , surgery , afferent
The nervous and immune systems talk to and influence each other. In particular, the nervous system helps maintain inflammation within appropriate limits. It is known that a neural reflex, termed the inflammatory reflex, is engaged and inhibits inflammation in response to lipopolysaccharide, a component of the wall of gram negative bacteria. This reflex has its efferent motor arm in the splanchnic nerves. Viral infections are different from bacterial infections and the innate immune system detects and responds differently to them. The aim of this study was to test the hypothesis that the inflammatory reflex is involved in the control of inflammation triggered by viruses as well as bacteria. For this purpose, we investigated whether the injection of polyinosinic:polycytidylic acid (Poly I:C; 1mg/kg i.v.), which mimics viral challenge, is able to activate splanchnic sympathetic nerve activity (SSNA) in urethane anesthetized rats. We also studied the effect of bilateral section of the greater splanchnic nerves on the systemic inflammatory response 90 minutes after the injection of the same dose of Poly I:C. Our results showed that poly I:C induces an activation of the SSNA that lasted for at least 7 hours. Furthermore, splanchnic nerve section resulted respectively in 3‐fold higher and 4‐fold lower levels of the pro‐inflammatory cytokine plasma tumor necrosis factor α (TNF) and the anti‐inflammatory cytokine interleukin 10. These results show that a viral challenge activates the inflammatory reflex in the same way as a bacterial challenge. Viral infections can lead to secondary bacterial infections. Because viral stimulation of the inflammatory reflex would suppress innate immune function, this may be why the host's ability to fight off a secondary attack by bacteria is compromised. Support or Funding Information This work was supported by project grant number 1098887 from the National Health and Medical Research Council (NHMRC) of Australia and from the Victorian Government Operational Infrastructure Support Program. E. N. Komegae was the recipient of a postdoctoral fellowship from Fundação de Amparo a Pesquisa do Estado de São Paulo (FAPESP 2016/1555‐6). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .