Inflammatory cytokine response in patients with septic shock secondary to generalized peritonitis

Abstract

The systemic release of TNF-alpha and IL-6 during septic shock caused by generalized peritonitis was maximal on day 1 and decreased rapidly during the next days. No systemic release of IL-1 was observed. IL-6 serum concentrations remained higher in patients who subsequently died. Among the different features of peritonitis studied, only bacteremia influenced the systemic cytokine response (higher TNF-alpha).

Acute Reversible Myocardial Depression Associated with Sepsis.

“…These findings suggest that one cannot ascertain whether IL-ip plays a role in the pathogenesis of septic myocardial depression in the clinical setting on the basis of serum IL-lp concentration alone. On the other hand, the concentrations of the other cytokines TNF-a and IL-6 have been shown to be related to the severity of sepsis and prognosis of the patients with sepsis and/or septic shock (14,15). This may reflect the pathophysiologic relation between these cytokines and "septic myocardial depression" previously shown in many experimental studies (6-10, ll).…”

“…TNF-a and IL-ip have similar biological properties and often act synergistically (10) , but clinical studies which have examined the serum levels of these proinflammatory cytokines during septic shock have constantly shown a lack of elevation of serum IL-i p concentration despite a concomitant increased level of 15). These findings suggest that one cannot ascertain whether IL-ip plays a role in the pathogenesis of septic myocardial depression in the clinical setting on the basis of serum IL-lp concentration alone.…”

Management of Peritonitis in the Critically Ill Patient

“…The combined effect of these mediators contributes to observed inflammatory response during peritonitis. As there is destruction of the bacteria, the lipo-polysacharids of gram-negative Enterobacteria constitute a powerful stimulus for further generation of inflammatory cytokines [18,19].…”

Reactive Oxygen Species and p38 Mitogen-activated Protein Kinase Mediate Tumor Necrosis Factor α-Converting Enzyme (TACE/ADAM-17) Activation in Primary Human Monocytes

“…TACE has also been shown to be involved in the cleavage of other immunologically relevant substrates, including both TNF receptors and L-selectin (6,7). Consequently, TACE is in a position to regulate the pleiotropic biology of TNF, a cytokine known to play a major role in both acute (8) and chronic (9) inflammation. An understanding of the regulation of TACE activity therefore provides insight into the pathophysiology of inflammatory disease and may aid the development of TACE-directed therapeutics.…”