Systemic inflammatory response syndrome (SIRS) is a generalized, dysregulated inflammatory state defined by a constellation of clinical signs reflecting widespread activation of the innate immune system. It is conventionally identified by the presence of abnormalities across temperature, heart rate, respiratory rate…
Systemic inflammatory response syndrome (SIRS) is a generalized, dysregulated inflammatory state defined by a constellation of clinical signs reflecting widespread activation of the innate immune system. It is conventionally identified by the presence of abnormalities across temperature, heart rate, respiratory rate and white blood cell count, and may be triggered by infectious causes such as bacterial endotoxin (lipopolysaccharide) and live pathogens, or by noninfectious insults including trauma, burns, pancreatitis and ischemia-reperfusion. When SIRS results from confirmed or suspected infection it constitutes sepsis, and its progression can drive tissue injury, coagulopathy and multiple organ dysfunction. Mechanistically, the syndrome reflects an exaggerated release of pro-inflammatory cytokines and other mediators, oxidative stress and endothelial activation, often followed by a compensatory anti-inflammatory phase, with the balance between these responses shaping outcome. Experimental models, such as cecal slurry, lipopolysaccharide and Escherichia coli challenge in rodents, are used to reproduce the syndrome and to evaluate interventions by measuring serum cytokine profiles and antioxidant and anti-inflammatory activity in target tissues including the brain. From the perspective of Tissue Repair and Regeneration, the magnitude and resolution of the systemic inflammatory response are critical determinants of whether injured organs recover or sustain lasting damage, making the control of cytokine signaling and oxidative injury central to both understanding pathophysiology and assessing candidate therapies.
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