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| Bacterial translocation (BT) can be defined as the passage of bacterial flora from the intestinal lumen to mesenteric lymph nodes (MLNs) or other extra-intestinal sites (Manuela Merli, 2015). Several studies have demonstrated the importance of BT in cirrhosis and it’s role in the pathogenesis of spontaneous bacterial peritonitis (SBP) (Runyon BA, 1994). Although the mechanisms driving the translocation of the gut flora in cirrhosis are not fully understood, recent evidence suggests that translocation of bacteria and bacterial products, such as endotoxin from the intestinal lumen into the systemic circulation, is a key factor in the pathogenesis of chronic liver diseases and the development of complications in cirrhosis (Kirsten E. Pijls et al 2013). In addition to changes in the intestinal flora and the immune system, dysfunction of the intestinal epithelial barrier may also contribute to BT (Kirsten E. Pijls ''et al'', 2013). This review discusses the multiple mechanisms involved in the process of BT, with an emphasis on alterations in intestinal flora and mucosal barrier function (Reiner Wiest et al, 2014). | Bacterial translocation (BT) can be defined as the passage of bacterial flora from the intestinal lumen to mesenteric lymph nodes (MLNs) or other extra-intestinal sites (Manuela Merli ''et al'', 2015). Several studies have demonstrated the importance of BT in cirrhosis and it’s role in the pathogenesis of spontaneous bacterial peritonitis (SBP) (Runyon BA ''et al'', 1994). Although the mechanisms driving the translocation of the gut flora in cirrhosis are not fully understood, recent evidence suggests that translocation of bacteria and bacterial products, such as endotoxin from the intestinal lumen into the systemic circulation, is a key factor in the pathogenesis of chronic liver diseases and the development of complications in cirrhosis (Kirsten E. Pijls ''et al'' 2013). In addition to changes in the intestinal flora and the immune system, dysfunction of the intestinal epithelial barrier may also contribute to BT (Kirsten E. Pijls ''et al'', 2013). This review discusses the multiple mechanisms involved in the process of BT, with an emphasis on alterations in intestinal flora and mucosal barrier function (Reiner Wiest ''et al'', 2014). |
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| Gut associated lymphatic tissue (GALT) is a defence organ against bacteria. The bacteria microbial-associated molecular patterns (MAMPs) are recognised by pattern- recognition receptors (PRR). In response to bacterial translocation, gut epithelial cells release chemokines. This will attract dendrite cells (DCs) to the mucosa. DCs induce production and maturation of B and T cells which are then released into the blood. In cirrhotic patients, a reduction of B cells can be seen. The degree to which this contributes to BT is unknown. Reduction of T cells causes an accumulation of bacteria in the MLN and to the spreading of bacteria to extra-intestinal sites (Reiner Wiest et al, 2014). | Gut associated lymphatic tissue (GALT) is a defence organ against bacteria. The bacteria microbial-associated molecular patterns (MAMPs) are recognised by pattern- recognition receptors (PRR). In response to bacterial translocation, gut epithelial cells release chemokines. This will attract dendrite cells (DCs) to the mucosa. DCs induce production and maturation of B and T cells which are then released into the blood. In cirrhotic patients, a reduction of B cells can be seen. The degree to which this contributes to BT is unknown. Reduction of T cells causes an accumulation of bacteria in the MLN and to the spreading of bacteria to extra-intestinal sites (Reiner Wiest ''et al'', 2014). |
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| Part of the GALT and play a role in the adaptive and the innate immune response (Bellot et al., 2013). Normally bacteria transported to MLN by DCs are killed without inducing systemic immunity. Immune-suppression permits the translocation of bacteria from intestines, which can cause sepsis and death (Reiner Wiest et al, 2014). Patients with cirrhosis have systemic immune alterations which may promote development of infections and BT. Examples of these alterations include: decreased activity of reticuloendothelial system (RES) which are a defence against bacteraemia and other haematogenous infections. This will have an effect on bacterial products such as endotoxin or bacterial DNA (Bellot et al, 2013). Advanced cirrhosis is associated with a decrease in both cellular and humoral components of the immune response (Bellot et al, 2013). | Part of the GALT and play a role in the adaptive and the innate immune response (Bellot ''et al'', 2013). Normally bacteria transported to MLN by DCs are killed without inducing systemic immunity. Immune-suppression permits the translocation of bacteria from intestines, which can cause sepsis and death (Reiner Wiest ''et al'', 2014). Patients with cirrhosis have systemic immune alterations which may promote development of infections and BT. Examples of these alterations include: decreased activity of reticuloendothelial system (RES) which are a defence against bacteraemia and other haematogenous infections. This will have an effect on bacterial products such as endotoxin or bacterial DNA (Bellot ''et al'', 2013). Advanced cirrhosis is associated with a decrease in both cellular and humoral components of the immune response (Bellot ''et al'', 2013). |
Bacterial Translocation in Liver Cirrhosis
Lorraine Cunningham, Alan O’Sullivan-Weekes & Sarah Ward
Contents
Introduction
Bacterial translocation (BT) can be defined as the passage of bacterial flora from the intestinal lumen to mesenteric lymph nodes (MLNs) or other extra-intestinal sites (Manuela Merli et al, 2015). Several studies have demonstrated the importance of BT in cirrhosis and it’s role in the pathogenesis of spontaneous bacterial peritonitis (SBP) (Runyon BA et al, 1994). Although the mechanisms driving the translocation of the gut flora in cirrhosis are not fully understood, recent evidence suggests that translocation of bacteria and bacterial products, such as endotoxin from the intestinal lumen into the systemic circulation, is a key factor in the pathogenesis of chronic liver diseases and the development of complications in cirrhosis (Kirsten E. Pijls et al 2013). In addition to changes in the intestinal flora and the immune system, dysfunction of the intestinal epithelial barrier may also contribute to BT (Kirsten E. Pijls et al, 2013). This review discusses the multiple mechanisms involved in the process of BT, with an emphasis on alterations in intestinal flora and mucosal barrier function (Reiner Wiest et al, 2014).
Compartments involved in pathological bacterial translocation
GALT
Gut associated lymphatic tissue (GALT) is a defence organ against bacteria. The bacteria microbial-associated molecular patterns (MAMPs) are recognised by pattern- recognition receptors (PRR). In response to bacterial translocation, gut epithelial cells release chemokines. This will attract dendrite cells (DCs) to the mucosa. DCs induce production and maturation of B and T cells which are then released into the blood. In cirrhotic patients, a reduction of B cells can be seen. The degree to which this contributes to BT is unknown. Reduction of T cells causes an accumulation of bacteria in the MLN and to the spreading of bacteria to extra-intestinal sites (Reiner Wiest et al, 2014).
MLN
Part of the GALT and play a role in the adaptive and the innate immune response (Bellot et al, 2013). Normally bacteria transported to MLN by DCs are killed without inducing systemic immunity. Immune-suppression permits the translocation of bacteria from intestines, which can cause sepsis and death (Reiner Wiest et al, 2014). Patients with cirrhosis have systemic immune alterations which may promote development of infections and BT. Examples of these alterations include: decreased activity of reticuloendothelial system (RES) which are a defence against bacteraemia and other haematogenous infections. This will have an effect on bacterial products such as endotoxin or bacterial DNA (Bellot et al, 2013). Advanced cirrhosis is associated with a decrease in both cellular and humoral components of the immune response (Bellot et al, 2013).
MECHANICAL COMPONENTS
SECRETARY COMPONENTS
MUCUS
IGA ANTIBODIES