Local and systemic innate immune response to secondary human peritonitis

Abstract

IntroductionOur aim was to describe inflammatory cytokines response in the peritoneum and plasma of patients with peritonitis. We also tested the hypothesis that scenarios associated with worse outcome would result in different cytokine release patterns. Therefore, we compared cytokine responses according to the occurrence of septic shock, mortality, type of peritonitis and peritoneal microbiology.MethodsPeritoneal and plasma cytokines (interleukin (IL) 1, tumor necrosis factor α (TNFα), IL-6, IL-10, and interferon γ (IFNγ)) were measured in 66 patients with secondary peritonitis.ResultsThe concentration ratio between peritoneal fluid and plasma cytokines varied from 5 (2 to 21) (IFNγ) to 1310 (145 to 3888) (IL-1). There was no correlation between plasma and peritoneal fluid concentration of any cytokine. In the plasma, TNFα, IL-6, IFNγ and IL-10 were higher in patients with shock versus no shock and in nonsurvivors versus survivors (P ≤0.03). There was no differential plasma release for any cytokine between community-acquired and postoperative peritonitis. The presence of anaerobes or Enterococcus species in peritoneal fluid was associated with higher plasma TNFα: 50 (37 to 106) versus 38 (29 to 66) and 45 (36 to 87) versus 39 (27 to 67) pg/ml, respectively (P = 0.02). In the peritoneal compartment, occurrence of shock did not result in any difference in peritoneal cytokines. Peritoneal IL-10 was higher in patients who survived (1505 (450 to 3130) versus 102 (9 to 710) pg/ml; P = 0.04). The presence of anaerobes and Enterococcus species was associated with higher peritoneal IFNγ: 2 (1 to 6) versus 10 (5 to 28) and 7 (2 to 39) versus 2 (1 to 6), P = 0.01 and 0.05, respectively).ConclusionsPeritonitis triggers an acute systemic and peritoneal innate immune response with a simultaneous release of pro and anti-inflammatory cytokines. Higher levels of all cytokines were observed in the plasma of patients with the most severe conditions (shock, non-survivors), but this difference was not reflected in their peritoneal fluid. There was always a large gradient in cytokine concentration between peritoneal and plasma compartments highlighting the importance of compartmentalization of innate immune response in peritonitis.

Chronic Lupus Peritonitis Is Characterized by the Ascites with a Large Content of Interleukin-6

“…IL-6 is also involved in endothelial cell permeability (Desai et al 2002;Wei et al 2013;Goldman et al 2014). Riche et al (2013) reported that ascitic TNF-α, IL-1, and IL-6 levels were all increased in bacterial peritonitis caused by gastrointestinal disorders and that the ranges of ascitic cytokines were 90-882 pg/mL (TNF-α), 1,180-22,670 pg/mL (IL-1), and 22,859-328,410 pg/mL (IL-6). Yamamoto et al (2011) also reported that ascitic TNF-α, IL-1β, and IL-6 significantly increased in patients who developed peritonitis compared with patients who did not after colorectal surgery.…”

Interleukin Expression in the Area damaged by the Development of Abdominal Cavity Adhesions

“…(4) However, Florence Riché and colleagues did not find such a correlation in their study. (5) F. Fredriksson and colleagues established that the levels of IL-6, IL-1β, TNF-α in the peritoneal fluid increased 6 hours post-injury, whereas only the level of IL-6 increased in the plasma at this time point. According to various researchers, the peak concentrations of proinflammatory cytokines were observed during the first 24 hours after peritoneal damage; these levels stabilized on the third day and decreased by the seventh day post-injury.…”

Insulin modulates energy and substrate sensing and protein catabolism induced by chronic peritonitis in skeletal muscle of neonatal pigs

“…Since we performed small cecal punctions to allow a 5-d survival, the insult may not have been severe enough to maintain elevated TNF-α plasma levels throughout the study. Similarly, low TNF-α concentrations have been also observed in surviving or non-bacteremic patients and in long-term murine survivors of CLP (20,21). In addition, in newborns, IL-8, rather than TNF-α, has been shown to be a more important mediator in the pathogenesis of neonatal sepsis (22).…”