Hypothesis: Helicobacter Toxins and Liver (original) (raw)
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Helicobacter, 2018
Helicobacter pylori is a gram negative, spiral shaped, and microaerophilic bacteria. H. pylori colonizes the stomach of more than half of the world population. Previously, it was believed that because of the uncongenial acidic environment bacteria cannot grow in the stomach. However, after the confirmation of the presence of H. pylori in the human stomach was reported, various colonization strategies through virulence factors were studied. H. pylori is classified as a Class-1 carcinogen. H. pylori colonization in the gastric environment causes chronic inflammation through invading the inner lining of stomach which leads to the development of gastric ulcer. Despite the acidic environment of gastric mucosa of the host cell, bacteria come across the barrier of the epithelial cells. The presence of H. pylori is mostly associated with the development of various gastric diseases including peptic ulcers, gastric ulcers, adenocarcinoma, MALT lymphoma, and gastric cancer. H. pylori finds multiple ways for its survival in the human host which is performed by various virulence factors. Over the period of time, these virulence factors are collectively responsible for persistence and colonization. One of the major virulence factors produced by H. pylori is Vacuolating cytotoxin A (VacA). VacA is one of the most studied toxins of H pylori. As
Helicobacter pylori: pathological mechanism involved in gastric colonization
Romanian journal of internal medicine = Revue roumaine de médecine interne, 2009
Since 1982, when Marshall and Warren highlighted the presence of H. pylori at the apical pole of the epithelial gastric cells, the medical literature has registered a cascade of subsequent researches concerning this amazing bacterium, its action on the human body and the body response. The apogee of these studies and conclusions about the pathogenic role of HP was touched with its certain recognition as class one carcinogenic agent (Peura 1997, WHO), becoming the first bacteria with such an action. The data gathered in the last period identify different virulence factors of HP, but fail to fully explain the relatively low incidence of gastric cancer in HP carriers; therefore, it is now considered that the carcinogenic potential related to HP infection in humans is due to the synergic and complementary association of the bacterial genetic equipment with diet and host response.
Helicobacter pylori promotes hepatic fibrosis in the animal model
Laboratory Investigation, 2009
Helicobacter pylori infection has been reported to be very common in patients with chronic liver diseases, including cirrhosis. To elucidate the pathological effect of H. pylori infection on the progression of hepatic fibrosis, C57BL/6 mice and Sprague-Dawley rats were orally inoculated with H. pylori, and hepatic fibrosis was induced with carbon tetrachloride (CCl 4 ) administration. We observed the histopathological changes and the presence of H. pylori genes by PCR in the liver. Significant increase in the fibrotic score as well as in serum alanine aminotransferase and aspartate aminotransferase levels was shown in the CCl 4 þ H. pylori group compared with that in the CCl 4 -treated group. Compared with the CCl 4treated group, a-smooth muscle actin and transforming growth factor-b1 were enhanced; however, senescence marker protein-30, a multifunctional protein protecting hepatocytes against oxidative stress and apoptosis, was suppressed in the CCl 4 þ H. pylori group. The 16S rRNA (400 bp) was demonstrated by PCR for H. pylori genes from genomic DNA extracted from the liver, and H. pylori-infected mice showed 93.8% (15 of 16) seropositivity by contrast with seronegativity in all H. pylori-noninfected mice. In addition, immunohistochemical study against H. pylori showed positive antigen fragments in the liver of the infected groups. Consequently, our data suggest that H. pylori infection could be an important contributing infectious factor to the development of liver cirrhosis.
Helicobacter and hepatobiliary diseases: update 2023
Arquivos de Gastroenterologia, 2023
Helicobacter Pylori (H. pylori) is one of the main infectious causes of gastroduodenal diseases, however, its role in developing different extragastric diseases has been proven. The possible involvement of H. pylori in the pathogenesis of cardiovascular, metabolic, neurodegenerative, skin, and hepatobiliary diseases is suggested. The bacterium has been found in tissue samples from the liver, biliary tract, and gallstones of animals and humans. However, the role of H. pylori infection in the pathogenesis of liver and biliary diseases has not been finally established. The histopathological confirmation of the positive effect of H. pylori eradication is needed. In addition, there are discussions on the clinical significance of other Helicobacter species. The review presents the data available for and against the involvement of H. pylori in hepatobiliary disease development and progression.
Momina Sajjad et al, The Pathology Of The Pylori Induced Helicobacter Duodenal Gastro., Indo Am
The key drivers of peptic ulceration, distal gastric adenocarcinoma and gastric lymphoma are Helicobacter pyloris. Just 15% of colonized individuals trigger diseases, and pathogenesis depends on the degradation of strains, genetic susceptibility and ecopoeia. Destructive factors include a proinflammatory, proliferative cell-flagging factor for the cag-pathogenicity island, the VacA cytoxin which causes epithelial harm and BabA. It hosts genetic polymorphisms that raise malignancies in the growth risk in view of contamination leading to considerable levels favorable for prevocational cytokine production. Our current research was conducted at Jinnah Hospital, Lahore from May 2019 to April 2020. Irritating, a Th-1 obtained excruciating reaction and hormonal modifications such as hypergastrinaemia are essential for pathogenesis. Antral-domination aggravation contributes to accelerated corrosion from the uninflamed corpus and inclinations to twin ulceration; body-dominant gastritis induces hypochlorohydration and tends to adenocarcinoma and gastric ulceration. The dominant decline of H. In produced countries, pylori have caused associated diseases to decline in prevalence. However, irrespective of whether a H is harmful. The threat to thosephageal adenocarcinoma, for example, extended, remains indistinct without pylori stomach.
Frontiers in Microbiology, 2021
Pathogenic potentials of the gastric pathogen, Helicobacter pylori, have been proposed, evaluated, and confirmed by many laboratories for nearly 4 decades since its serendipitous discovery in 1983 by Barry James Marshall and John Robin Warren. Helicobacter pylori is the first bacterium to be categorized as a definite carcinogen by the International Agency for Research on Cancer (IARC) of the World Health Organization (WHO). Half of the world’s population carries H. pylori, which may be responsible for severe gastric diseases like peptic ulcer and gastric cancer. These two gastric diseases take more than a million lives every year. However, the role of H. pylori as sole pathogen in gastric diseases is heavily debated and remained controversial. It is still not convincingly understood, why most (80–90%) H. pylori infected individuals remain asymptomatic, while some (10–20%) develop such severe gastric diseases. Moreover, several reports indicated that colonization of H. pylori has pos...