Contribution of the gut association lymphoid tissue inflammatory response under bacterial translocation and sepsis challenge is the relevant factor for the onset of multiple organ dysfunction syndrome
© Menchaca-Diaz et al; licensee BioMed Central Ltd. 2008
Published: 18 November 2008
The gastrointestinal tract has been implicated in sepsis and organ failure by bacterial translocation (BT) and gut-immune system crosstalk with the systemic immunity, but is not yet clearly demonstrated in clinics. Herein we examined the role of gut-associated lymphoid tissue on host inflammatory response by BT as a contributing feature for multiorgan dysfunction in sepsis.
Wistar rats were challenged to BT (10 ml Escherichia coli R6, 1010 colony-forming units (CFU)/ml), sepsis (2 ml Enterobacter cloacae 89, 107 CFU/ml), and sepsis plus BT, with/without mesenteric lymph flow interruption (MLFI) by canulation and lymph deviation or by mesenteric lymphadenectomy plus lymph duct ligation 5 days before in the following groups (n = 20/group): BT (BT-G); BT with MLFI (BTL-G); sepsis (S-G); sepsis with MLFI (SL-G); combination of BT to sepsis (C-G); combination with MLFI (CL-G); sham-BT (SBT-G); sham-sepsis (SS-G); and sham-combination (SC-G). Samples (mesenteric lymph node, blood, spleen and liver) were collected 2 hours after and were cultured for bacterial recovery of both sepsis and BT origin. Tissue perfusion (jejunum, ileum, liver, kidneys) and mesenteric microcirculation were monitored at 0 and 2 hours. Systemic blood and intestinal lymph were collected for cell count and phenotyping. The groups' mortality was followed.
The gut-associated lymphoid tissue response following bacterial challenge and its crosstalk with the systemic immunity via the lymphatic system is the key factor related to the aggravation of systemic inflammation and death in sepsis.
This article is published under license to BioMed Central Ltd.