Prevention of bacterial translocation using beta-(1-3)-D-glucan in small bowel ischemia and reperfusion in rats<A NAME="volta1"></A>

Abstract

PURPOSE: To investigate the role of beta-(1-3)-D-glucan on 99mTc labelled Escherichia coli translocation and cytokines secretion in rats submitted to small bowel ischemia/reperfusion injury. METHODS: Five groups (n=10 each) of Wistar rats were subjected to control(C), sham(S), group IR subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R), and group I/R+glucan subjected to 45 min of bowel ischemia/60 min of reperfusion(I/R) and injected with 2mg/Kg intramuscular. Translocation of labelled bacteria to mesenteric lymph nodes, liver, spleen, lung and serum was determined using radioactivity/count and colony forming units/g(CFU/g). Serum TNFalpha, IL-1beta, IL-6, IL-10 were measured by ELISA. RESULTS: CFU/g and radioactivity/count were higher in I/R than in I/R+glucan rats. In C, S and S+glucan groups, bacteria and radioactivity/count were rarely detected. The I/R+glucan rats had enhancement of IL-10 and suppressed production of serum TNFalpha, IL-1beta and, IL-6, compared to I/R untreated animals. CONCLUSION: The beta-(1-3)-D-glucan modulated the production of pro-inflammatory and anti-inflammatory cytokines during bowel ischemia/reperfusion, and attenuated translocation of labelled bacteria.

Protective effect of β-glucan and glutamine on intestinal and immunological damage in mice induced by cytarabine (Ara-C)

“…An in vitro study (Poutsiaka et al 1993) investigating the stimulation of human macrophages with β-glucan did not show changes in IL-1β concentrations, as shown in our study and another study (Araújo-filho et al 2006), suggesting that the β-glucan does not promote increase in this cytokine in vivo.…”

“…This provides evidence for a role of β-glucan as an immunomodulator. After its recognition as a classical pathogen-associated molecular pattern, β-glucan causes a decrease in the secretion of anti-inflammatory cytokines and enhances the immune response done by inflammation (Araújo-filho et al 2006, Sato et al 2006, Novak & Vetvicka, 2009, Arena et al 2016. INF-γ is responsible for increasing the permeability of the mucosa and is considered an important factor in villous atrophy (Feng et al 2012).…”

Human adrenomedullin combined with human adrenomedullin binding protein-1 is protective in gut ischemia and reperfusion injury in the rat

“…Curiously, reperfusion injury can produce even greater local damage as well as amplify the effects of the ischemia by making a focal injury a global insult [5]. Multiple explanations for this amplification have included translocation of bacteria and bacterial products [6,7], production of cytokines [8], and activation of circulation neutrophils and macrophages [3]. As a result, numerous agents and interventions have been studied to reduce gut ischemia and reperfusion (I/R)-induced organ injury and its mortality, but none has so far been entirely successful [9].…”

Pré-condicionamento isquêmico em diferentes tempos e seu efeito na translocação bacteriana induzida por isquemia e reperfusão intestinal em ratos

“…A study of Araujo-Filho et al S\showed that â-D-glucan was able to control the release of inflammatory cytokines in injury produced by ischemia and reperfusion, reducing translocation of Escherichia coli 17 . Aksoyek et al performed intestinal preconditioning for ten minutes and observed a reduction of BT for bloodstream, liver, spleen and mesenteric lymph nodes, corroborating our results 10 .…”