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Abstract
During the course of polymicrobial sepsis, a range of pro- and antiinflammatory cytokines are produced by the host immune system. Successful recovery from sepsis involves striking a balance between these counteracting cytokines. We herein investigated the circulating cytokine profiles in preprotachykinin-A knockout (PPTA(-/-)) mice, which have been found to be protected significantly against microbial sepsis, by employing multiplexed bead-based suspension arrays for the measurement of 18 plasma cytokines. Four sets of PPTA(-/-) and wild-type mice, each with six mice, were subjected to cecal ligation and puncture-induced sepsis or a sham procedure and were killed at 1, 5, 8 and 24 h post surgery. The cytokine profiles revealed, rather interestingly, that both pro- and antiinflammatory cytokines were elevated in the knockout group in response to a septic challenge. The higher systemic levels of both pro- and antiinflammatory cytokines in PPTA(-/-) septic mice was similar to the increase that we observed earlier in lung tissue of PPTA(-/-) mice after induction of sepsis. Thus, elevated levels of both pro- and antiinflammatory mediators may act simultaneously and help to resolve the infectious assault at the early stages of sepsis without excessively damaging the host tissue in PPTA(-/-) mice. In addition, our results underline the importance of comprehensive clinical analysis of multiple biomarkers to provide a better prognostic tool.
Highlights
Sepsis is a state of systemic inflammatory response syndrome (SIRS) resulting from bacteria, viruses, fungi or parasites [1]
The initial proinflammatory response to eliminate pathogens is followed by a counteracting production of antiinflammatory mediators that contributes to the pathophysiology of sepsis [5,6,7]
Among all the cytokines tested, levels of both pro- (Figure 1A–M) and antiinflammatory (Figure 2A, B) cytokines were elevated significantly in the PPTA–/– septic mice compared with the wild-type mice
Summary
Sepsis is a state of systemic inflammatory response syndrome (SIRS) resulting from bacteria, viruses, fungi or parasites [1]. Injury and inflammation trigger the release of cytokines that act as immune mediators [3,4]. These inflammatory proteins are elevated in various disease states such as autoimmune diseases, inflammatory bowel disease and sepsis. Large numbers of cytokines are produced mainly within tissues and released into systemic circulation to mediate the inflammatory responses in sepsis. The initial proinflammatory response to eliminate pathogens is followed by a counteracting production of antiinflammatory mediators that contributes to the pathophysiology of sepsis [5,6,7]. Multiple mediators have been reported to be involved in the development of sepsis [8,9]
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