BACKGROUND: Cholangitis, an infection of the biliary tract, is most commonly caused by Gram negative bacteria, particularly Escherichia coli. Factors governing the severity of cholangitis, including the role of biliary IgA, are poorly understood. AIMS: The aim of this work was to find out if biliary IgA directed against E coli protects rats against hepatobiliary infection with E coli. SUBJECTS: Male Sprague-Dawley rats weighing 270-350 grams were used in all of the experiments. METHODS: At laparotomy, rats were immunised by injecting killed E coli or normal saline (controls) into Peyer's patches. With or without subsequent antigenic boosting (by oral administration of killed E coli), bile was collected at a second laparotomy, and rats were infected by introducing viable E coli into the bile duct. Production of IgA anti-E coli antibody was measured by enzyme linked immunosorbent assay of bile, and the presence of hepatobiliary infection was determined by quantitative culture of liver homogenates. RESULTS: Systemic infection was present in six of 12 control rats and in one of 24 immunised rats (p = 0.005) after death. There was an inverse correlation between immunisation and E coli colony counts in cultured liver homogenates (p = 0.024). CONCLUSION: The findings suggest that biliary IgA directed against E coli protected rats against hepatobiliary E coli infection and systemic sepsis.
BACKGROUND:Cholangitis, an infection of the biliary tract, is most commonly caused by Gram negative bacteria, particularly Escherichia coli. Factors governing the severity of cholangitis, including the role of biliary IgA, are poorly understood. AIMS: The aim of this work was to find out if biliary IgA directed against E coli protects rats against hepatobiliary infection with E coli. SUBJECTS: Male Sprague-Dawley rats weighing 270-350 grams were used in all of the experiments. METHODS: At laparotomy, rats were immunised by injecting killed E coli or normal saline (controls) into Peyer's patches. With or without subsequent antigenic boosting (by oral administration of killed E coli), bile was collected at a second laparotomy, and rats were infected by introducing viable E coli into the bile duct. Production of IgA anti-E coli antibody was measured by enzyme linked immunosorbent assay of bile, and the presence of hepatobiliary infection was determined by quantitative culture of liver homogenates. RESULTS: Systemic infection was present in six of 12 control rats and in one of 24 immunised rats (p = 0.005) after death. There was an inverse correlation between immunisation and E coli colony counts in cultured liver homogenates (p = 0.024). CONCLUSION: The findings suggest that biliary IgA directed against E coli protected rats against hepatobiliary E coli infection and systemic sepsis.