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Bacterial Translocation and Host Immune Activation in Chronic Hepatitis C Infection.

ABSTRACT: Hepatitis C virus (HCV) infects 71 million individuals, and barriers to treatment remain. Bacterial translocation is a complication of chronic HCV infection, and this study evaluated circulating microbial components including lipopolysaccharide, peptidoglycan, and ?-D-glucan in addition to their pattern recognition receptors and degree of hepatic macrophage uptake. The findings suggest that regulation of serum peptidoglycan and ?-D-glucan differs from that of lipopolysaccharide. Additionally, macrophage activation in the liver may be better reflected by the degree of macrophage uptake than by circulating levels of microbial markers. These findings allow for a greater understanding of bacterial translocation and host immune activation during HCV infection.

SUBMITTER: Moon MS

PROVIDER: S-EPMC6667717 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Bacterial Translocation and Host Immune Activation in Chronic Hepatitis C Infection.

Moon Mi Sun MS Quinn Gabriella G Townsend Elizabeth C EC Ali Rabab O RO Zhang Grace Y GY Bradshaw Alyson A Hill Kareen K Guan Hannah H Hamilton Destanee D Kleiner David E DE Koh Christopher C Heller Theo T

Open forum infectious diseases 20190701 7

Hepatitis C virus (HCV) infects 71 million individuals, and barriers to treatment remain. Bacterial translocation is a complication of chronic HCV infection, and this study evaluated circulating microbial components including lipopolysaccharide, peptidoglycan, and β-D-glucan in addition to their pattern recognition receptors and degree of hepatic macrophage uptake. The findings suggest that regulation of serum peptidoglycan and β-D-glucan differs from that of lipopolysaccharide. Additionally, ma ...[more]

PMID: 31363763

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Project description:BackgroundPlasmodium vivax and Hepatitis B virus (HBV) are globally outspread in similar geographic regions. The concurrence of both infections and its association with some degree of protection against symptomatic and/or severe vivax malaria has been already described. Nevertheless, data on how host response to both pathogens undermines the natural progression of the malarial infection are scarce. Here, a large cohort of vivax malaria and HBV patients is retrospectively analyzed in an attempt to depict how inflammatory characteristics could be potentially related to the protection to severe malaria in coinfection.MethodsA retrospective analysis of a databank containing 601 individuals from the Brazilian Amazon, including 179 symptomatic P. vivax monoinfected patients, 145 individuals with asymptomatic P. vivax monoinfection, 28 P. vivax-HBV coinfected patients, 29 HBV monoinfected subjects and 165 healthy controls, was performed. Data on plasma levels of multiple chemokines, cytokines, acute phase proteins, hepatic enzymes, bilirubin and creatinine were analyzed to describe and compare biochemical profiles associated to each type of infection.ResultsCoinfected individuals predominantly presented asymptomatic malaria, referred increased number of previous malaria episodes than symptomatic vivax-monoinfected patients, and were predominantly younger than asymptomatic vivax-monoinfected individuals. Coinfection was hallmarked by substantially elevated concentrations of interleukin (IL)-10 and heightened levels of C-C motif chemokine ligand (CCL)2. Correlation matrices showed that coinfected individuals presented a distinct biomarker profile when compared to asymptomatic or symptomatic P. vivax patients, or HBV-monoinfected individuals. Parasitemia could distinguish coinfected from symptomatic or asymptomatic P. vivax-monoinfected patients. HBV viremia was associated to distinct inflammatory profiles in HBV-monoinfected and coinfected patients.ConclusionThe findings demonstrate a distinct inflammatory profile in coinfected patients, with characteristics associated with immune responses to both pathogens. These host responses to P. vivax and HBV, in conjunction, could be potentially associated, if not mainly responsible, for the protection against symptomatic vivax malaria.

Project description:AIM:To investigate the early diagnostic methods of bacterial and fungal infection in patients with chronic cholestatic hepatitis B. METHODS:One hundred and one adult in-patients with chronic hepatitis B were studied and divided into 3 groups: direct bilirubin (DBil)/total bilirubin (TBil) > or = 0.5, without bacterial and fungal infection (group A, n=38); DBil/TBil <0.5, without bacterial and fungal infection (group B, n=23); DBil/TBil> or = 0.5, with bacterial or fungal infection (group C, n=40). The serum biochemical index and pulse rate were analyzed. RESULTS:Level of TBil, DBil, alkaline phosphatase (ALP) and DBil/ALP in group A increased compared with that in group B. The level of ALP in group C decreased compared with that in group A, whereas the level of TBil, DBil and DBil/ALP increased (ALP: 156+/-43, 199+/-68, respectively, P<0.05; TBil: 370+/-227, 220+/-206, respectively, P<0.01; DBil: 214+/-143, 146+/-136, respectively, P<0.01; DBil/ALP: 1.65+/-1.05, 0.78+/-0.70, respectively, P<0.001). The level of DBil and infection affected DBil/ALP. Independent of the effect of DBil, infection caused DBil/ALP to rise (P<0.05). The pulse rate in group A decreased compared with that in group B (63.7+/-6.4, 77.7+/-11.4, respectively, P<0.001), and the pulse rate in group C increased compared with that in group A (81.2+/-12.2, 63.7+/-6.4, respectively, P<0.001). The equation (infection=0.218 pusle rate +1.064 DBil/ALP -16.361), with total accuracy of 85.5%, was obtained from stepwise logistic regression. Pulse rate (> or =80/min) and DBil/ALP (> or =1.0) were used to screen infection. The sensitivity was 62.5% and 64.7% respectively, and the specificity was 100% and 82.8% respectively. CONCLUSION:Bacterial and fungal infection deteriorate jaundice and increase pulse rate, decrease serum ALP and increase DBil/ALP. Pulse rate, DBil/ALP and the equation (infection=0.218 pusle rate+1.064 DBil/ALP-16.361) are helpful to early diagnosis of bacterial and fungal infection in patients with chronic cholestatic hepatitis B.

Dataset Information

Bacterial Translocation and Host Immune Activation in Chronic Hepatitis C Infection.

Publications

Bacterial Translocation and Host Immune Activation in Chronic Hepatitis C Infection.

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