RESUMO
The key pathogenic mechanism initiating spontaneous bacterial peritonitis (SBP) is bacterial translocation (BT), a process through which enteric bacteria cross the intestinal barrier and infect the mesenteric lymph nodes, thus entering the blood circulation and ascitic fluid. The high rate of bacterial translocation in cirrhosis is due to injury to the three pilars composing the intestinal mucosal barrier (the balance of intraluminal bacterial flora, the integrity of the intestinal epithelial barrier, and the local immune system). Blood dissemination and microbial growth in ascitic fluid resulting from SBP are a consequence of damage to the immune system in cirrhosis. Hyperproduction of proinflammatory cytokines and other vasoactive substances contributes to the arterial vasodilation and renal failure that frequently complicate the course of SBP. Even in the absence of SBP, translocation of bacteria and bacterial products from the intestinal lumen contribute to systemic inactivation of immune cells in cirrhosis.
Assuntos
Translocação Bacteriana/fisiologia , Cirrose Hepática/complicações , Peritonite/etiologia , Animais , Humanos , Cirrose Hepática/fisiopatologia , Linfadenite Mesentérica/etiologia , Peritonite/microbiologiaRESUMO
El mecanismo patogénico clave que inicia la peritonitis bacteriana espontánea (PBE) es la translocación bacteriana (TB), proceso por el cual las bacterias entéricas cruzan la barrera mucosa intestinal e infectan los ganglios linfáticos mesentéricos, y desde donde alcanzan la circulación sanguínea y, posteriormente, el líquido ascítico. La alta tasa de TB en la cirrosis se debe al daño en los 3 pilares que constituyen la barrera mucosa del intestino: equilibrio de la flora bacteriana intraluminal, integridad de la barrera epitelial intestinal y sistema inmunitario local. La diseminación sanguínea y el crecimiento de los gérmenes en el líquido ascítico que se produce en la PBE es consecuencia del daño en el sistema inmunitario que conlleva la cirrosis. La hiperproducción en el líquido ascítico de citocinas proinflamatorias y otras sustancias con propiedades vasoactivas contribuye a la vasodilatación arterial y a la insuficiencia renal que, con frecuencia, complica el curso de la PBE. Aun en ausencia de PBE, la translocación de bacterias y productos bacterianos desde la luz intestinal contribuye a la activación sistémica de las células inmunitarias en la cirrosis
The key pathogenic mechanism initiating spontaneous bacterial peritonitis (SBP) is bacterial translocation (BT), a process through which enteric bacteria cross the intestinal barrier and infect the mesenteric lymph nodes, thus entering the blood circulation and ascitic fluid. The high rate of bacterial translocation in cirrhosis is due to injury to the three pilars composing the intestinal mucosal barrier (the balance of intraluminal bacterial flora, the integrity of the intestinal epithelial barrier, and the local immune system). Blood dissemination and microbial growth in ascitic fluid resulting from SBP are a consequence of damage to the immune system in cirrhosis. Hyperproduction of proinflammatory cytokines and other vasoactive substances contributes to the arterial vasodilation and renal failure that frequently complicate the course of SBP. Even in the absence of SBP, translocation of bacteria and bacterial products from the intestinal lumen contribute to systemic inactivation of immune cells in cirrhosis
