Helicobacter species and liver diseases: association or causation?

Pellicano, Rinaldo; Ménard, Armelle; Rizzetto, M.; Mégraud, Françis

doi:10.1016/s1473-3099(08)70066-5

Cited by 124 publications

(100 citation statements)

References 76 publications

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“…to the hepatobiliary tree including either the ascending duodenum infection or the portal system circulation pathway. 23 In conclusion, the results of the present study revealed an important association between gallstones and the presence of Helicobacter DNA in the bile. Further studies are needed to determine whether Helicobacter spp.…”

Section: Discussionsupporting

confidence: 60%

Molecular detection of Helicobacter species in the bile and histopathological evaluation of gall bladders of patients with calculus cholycystitis in Duhok province, Kurdistan region of Iraq

Raziq

Arif

2017

ZJMS

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Section: Discussionsupporting

confidence: 60%

Molecular detection of Helicobacter species in the bile and histopathological evaluation of gall bladders of patients with calculus cholycystitis in Duhok province, Kurdistan region of Iraq

Raziq

Arif

2017

ZJMS

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“…Only H. pylori strains were grown, and H. pylori DNA was detected in the hepatic tissue of the population studied, although the methods employed allow the growth and/or detection of other Helicobacter species, including those already described in human and animal livers (Pellicano et al 2008). Positive liver culture and histology in only 1.8% of the all included individuals indicate that, in most cases, the bacterial load in the liver may be too low to be detected by these methods and/or that the presence of viable H. pylori in the liver is not common.…”

Section: Discussionmentioning

confidence: 99%

“…106(6): 748-754, September 2011 The hypothesis that Helicobacter spp might be a risk factor for human liver diseases has arisen after the discovery of Helicobacter hepaticus and its association with murine hepatitis and hepatocellular carcinoma (HCC). Subsequent studies in humans have shown the presence of Helicobacter DNA in hepatic tissue of patients with hepatobiliary diseases, mainly cirrhosis and/ or HCC secondary to hepatitis B virus (HBV) and hepatitis C virus (HCV) (Avenaud et al 2000, Dore et al 2002, Fan et al 2002, Verhoef et al 2003, Rocha et al 2005, Pellicano et al 2008. Although these studies have contributed to the debate on the participation of Helicobacter species in the severe human liver disease outcomes, no explanation that justifies the presence of the bacterium in the human liver has yet been proposed.…”

mentioning

confidence: 99%

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

Silva

Rocha

et al. 2011

Mem. Inst. Oswaldo Cruz

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The hypothesis that Helicobactermight be a risk factor for human liver diseases has arisen after the detection of Helicobacter DNA in hepatic tissue of patients with hepatobiliary diseases. Nevertheless, no explanation that justifies the presence of the bacterium in the human liver has been proposed. We evaluated the presence of Helicobacterin the liver of patients with hepatic diseases of different aetiologies. We prospectively evaluated 147 patients (106 with primary hepatic diseases and 41 with hepatic metastatic tumours) and 20 liver donors as controls. Helicobacter species were investigated in the liver by culture and specific 16S rDNA nested-polymerase chain reaction followed by sequencing. Serum and hepatic levels of representative cytokines of T regulatory cell, T helper (Th)1 and Th17 cell lineages were determined using enzyme linked immunosorbent assay. The data were evaluated using logistic models. Detection of Helicobacter pylori DNA in the liver was independently associated with hepatitis B virus/hepatitis C virus, pancreatic carcinoma and a cytokine pattern characterised by high interleukin (IL)-10, low/absent interferon-γ and decreased IL-17A concentrations (p < 10-3). The bacterial DNA was never detected in the liver of patients with alcoholic cirrhosis and autoimmune hepatitis that are associated with Th1/Th17 polarisation. H. pylori may be observed in the liver of patients with certain hepatic and pancreatic diseases, but this might depend on the patient cytokine profile

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“…However, there has been controversy on whether or not H. pylori could have a role in the development of cirrhosis and HCC. 21 For this reason, the possible role of H. pylori in the progression of liver diseases remains to be determined. Meanwhile, our recent study supports a possible implication of H. pylori in the pathogenesis of hepatic fibrosis and cirrhosis by showing that H. pylori significantly accelerated the CCl 4 -induced hepatic fibrosis in both rats and mice models.…”

mentioning

confidence: 99%

Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

Goo

Park

et al. 2010

Laboratory Investigation

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Our earlier report has shown that Helicobacter pylori promoted hepatic fibrosis in a murine model. Herein, in order to elucidate the mechanism by which H. pylori accelerate liver fibrosis, the authors investigated the changes in expression levels of mitogen-activated protein kinases (MAPKs), p53-related proteins, antioxidants, and proinflammatory cytokines in liver samples. H. pylori infection enhanced CCl 4 -induced MAP kinase activation and p53 signaling pathway as well as Bax-and proliferating-cell nuclear antigen expressions, whereas H. pylori alone induced neither of these expressions nor hepatic fibrosis. Moreover, mRNA expressions of inflammatory cytokines, glutathione peroxidase expression, and the proliferative index were strongly augmented in livers of the H. pylori with CCl 4 treatment group compared with those of the CCl 4 -alone treatment group, whereas there was no difference in apoptotic index between the two groups. Interestingly, H. pylori treatment increased the number of a-fetoprotein-expressing hepatocytes independently of CCl 4 intoxication. In vitro analyses, using an immortalized rat hepatic stellate cell (HSC) line, revealed that H. pylori lysates increased the proliferation of HSCs, which was boosted by the addition of transforming growth factor-beta1 (TGF-b1). Furthermore, the treatment of H. pylori lysates promoted the translocation of nuclear factor kappa-light-chain enhancer of activated B cells (NF-kB) into the nucleus based on an increase in the degradation of NF-kB inhibitor alpha, in the presence of TGF-b1, as did H 2 O 2 treatment. In conclusion, H. pylori infection along with an elevated TGF-b1 may accelerate hepatic fibrosis through increased TGF-b1-induced pro-inflammatory signaling pathways in HSCs. Moreover, H. pylori infection might increase the risk of TGF-b1-mediated tumorigenesis by disturbing the balance between apoptosis and proliferation of hepatocytes.

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Helicobacter species and liver diseases: association or causation?

Cited by 124 publications

References 76 publications

Molecular detection of Helicobacter species in the bile and histopathological evaluation of gall bladders of patients with calculus cholycystitis in Duhok province, Kurdistan region of Iraq

Molecular detection of Helicobacter species in the bile and histopathological evaluation of gall bladders of patients with calculus cholycystitis in Duhok province, Kurdistan region of Iraq

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

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