What is the role of counter-inflammatory response syndrome (CARS) in the pathogenesis of systemic inflammatory response syndrome (SIRS)?

Updated: May 07, 2018
  • Author: Lewis J Kaplan, MD, FACS, FCCM, FCCP; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM  more...
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The cumulative effect of this inflammatory cascade is an unbalanced state with inflammation and coagulation dominating. To counteract the acute inflammatory response, the body is equipped to reverse this process via the counter-inflammatory response syndrome (CARS). IL-4 and IL-10 are cytokines responsible for decreasing the production of TNF-α, IL-1, IL-6, and IL-8. In fact, this proinflammatory and anti-inflammatory activation mirrors other homeostatic processes, like coagulation, anticoagulation, complement activation, and complement suppression.

Clearly, the normal homeostatic processes attempt to keep these very toxic inflammatory processes in check. Inflammation is an essential component of host defense and serves a very strongly positive survival function in suppressing and then eliminating local infection and tissue injury. It is only when this localized aggressive injury process gains access to the whole body through the blood stream and lymphatics that a SIRS develops.

The acute phase response also produces antagonists to TNF-α and IL-1 receptors. These antagonists either bind the cytokine, and thereby inactivate it, or block the receptors. Comorbidities and other factors can influence a patient's ability to respond appropriately.

The balance of SIRS and CARS helps determine a patient's outcome after an insult. Some researchers believe that, because of CARS, many of the new medications meant to inhibit the proinflammatory mediators may lead to deleterious immunosuppression.

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