Dataset Information

Low potassium disrupt intestinal barrier and result in bacterial translocation.

ABSTRACT:

Background

Bacterial translocation was observed in critical illness and patients with chronic diseases such as liver cirrhosis and chronic kidney disease (CKD). Hypokalemia is a common complication in these diseases. Whether low potassium diet may increase intestinal permeability and result in bacterial translocation lack of evidence. The present study was aimed to investigate the potential effects of LK on intestinal permeability.

Methods

Grade 8-week-old male Bal B/C mice were randomly placed either on a normal potassium (NK) mouse chow or a low potassium (LK) diet for 28 days. Intestinal permeability and expression of tight junction proteins were compared between the two groups.

Results

Compared with the NK group, the mice in LK group had significantly lower serum potassium level, increased levels of plasmas endotoxin and plasma D-lactate. The bacterial translocation was higher and in occurred mainly in mesenteric lymph nodes (MLN), liver and spleen. The pathologic change of small intestine was obvious with thinner villus lamina propria, shorter crypt depth and thinner intestinal wall. Slight increases in the expression of proteins and mRNA levels of both claudin-1 and claudin-2 were observed in LK group.

Conclusions

Low potassium diet could increase intestinal permeability and thereby lead to bacterial translocation, which was suspected to result from impaired intestinal epithelial barrier and biological barrier.

SUBMITTER: Wu H

PROVIDER: S-EPMC9258207 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BACKGROUND: Although clinical and experimental studies have demonstrated a correlation between obstructive jaundice and the development of sepsis, the mechanism has not been fully elucidated. PURPOSE: The aim of this study was to investigate the influence of biliary obstruction on bacterial translocation as a possible source of infection in cases of obstructive jaundice. MATERIAL AND METHODS: Two groups of 12 Wistar rats were examined: rats subjected to common bile duct (CBD) ligation (group A) and rats subjected to a sham operation (group B). After 7 days, blood samples were taken and liver, spleen, and mesenteric lymph nodes (MLNs) from the ileocecal area were removed, divided into small pieces, and cultured. Quantitative culture results were determined by the number of colony-forming units (CFU) per milliliter of homogenate. Bacterial translocation was defined as the presence of a positive culture of MLNs, blood, liver, and/or spleen. Samples for histopathological examination were taken from the mucosa of the ileum and the colon and evaluated for inflammatory and destructive changes. RESULTS: There was no evidence of bacterial translocation to MLNs, blood, spleen, or liver detected in any of the 12 sham-operated control rats. In contrast, bacterial translocation was demonstrated in 8 of the 12 CBD-ligated rats (P < 0.01). In all eight cases in which translocation occurred, Escherichia coli were cultured from the MLNs. There were no histological changes in the mucosal samples of the control animals. In the CBD-ligated rats, hyperemia, vacuolization, reduction of goblet cells, decreased mitotic activity, and infiltration by lymphocytes and polymorphonuclear leukocytes (PMNLs) were detected. Cases in which translocation occurred were significantly associated with decreased mitotic activity in the colon (r = -0.5, P < 0.01) and higher infiltration by PMNLs in the ileum (r = -0.62, P < 0.05). CONCLUSION: Obstructive jaundice in a rat model predisposes to bacterial translocation. This suggests a mechanism whereby jaundiced patients are susceptible to septic complication.