Abstract
Bacterial translocation (BT) is thought to play an important role in the development of liver cirrhosis, but the mechanisms have not been fully explored. This study aims to investigate the distribution of Treg (CD3+CD4+CD25+Foxp3+), Th17 (CD3+CD4+IL-17+), and Th1 (CD3+CD4+IFN-γ+) cells in the intestinal lamina propria, liver and blood and to explore their relationships with BT. Cirrhotic rats with ascites were induced by CCl4. We found that there were lower levels of total protein and albumin, lower albumin/globulin ratio, lower body weight and higher spleen weight and ascites volume in cirrhotic rats with than without BT. We found that BT may cause increase of Treg cells in the proximal small intestine and decrease of Th17 cells in the whole intestine and blood in cirrhotic rats. It may also aggravate the CCl4-induced decrease in Th1 cells in the whole intestine, liver, caecum, and blood and the CCl4-induced increase in Th17 cells in the liver and Tregs in the distal small intestine, colon, and liver. Our data suggest that BT may aggravate liver injury and decrease liver function via an interaction with CD4+ T Cells. The results of this study may be helpful for the development of new treatments for liver cirrhosis.
Highlights
Bacterial translocation (BT) is a phenomenon in which intestinal bacteria or their products cross the intestinal barriers and enter the mesenteric lymph nodes (MLNs) and/or other extraintestinal organs[1,2]
To determine whether cirrhosis affects BT, MLNs were isolated using sterile procedures for bacterial cultures according to the BT diagnostic criteria[8]
In addition to the number of bacteria obtained from MLN tissue cultures, we used LBP, a soluble acute-phase protein that binds to bacterial lipopolysaccharide and elicits immune responses by presenting lipopolysaccharide to cell surface pattern recognition receptors, as an indicator of BT severity[15,16,17]
Summary
Bacterial translocation (BT) is a phenomenon in which intestinal bacteria or their products cross the intestinal barriers and enter the mesenteric lymph nodes (MLNs) and/or other extraintestinal organs[1,2]. Bacterial overgrowth into the small intestine, intestinal mucosal barrier damage, and increased intestinal permeability have been observed in patients with liver cirrhosis with BT, the mechanism of interaction between BT and liver cirrhosis had not previously been fully explained[2,7]. Some gut disorders have been associated with BT and CD4+ T cells; these include overgrown bacteria in the small intestine, a damaged gastrointestinal barrier, increased intestinal permeability[4,9], and an altered gut microbiome[10,11,12]. We aimed to investigate differences in the enrichment of CD4+ T cells in the liver, blood and intestines between CCl4-induced cirrhotic rats with and without BT and to explore the relationship and the mechanism of interaction between BT and alterations in CD4+ T cells in liver cirrhosis
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