scholarly journals Helicobacter pylori and Immune-mediated Disorders

Author(s):  
Jae Yong Park

Recently, many studies have reported the potential association of <i>Helicobacter pylori</i> (<i>H. pylori</i>) with various extragastric diseases. <i>H. pylori</i>, a major component of the gastric microbiota, is in symbiosis with humans. It is, therefore, assumed to potentially influence immune homeostasis in humans to some extent. There are several reports highlighting the possible association of <i>H. pylori</i> with allergic diseases. However, these were mainly based on cross-sectional or epidemiological studies. With a greater emphasis on the effects of human microbiota on host immunity and disease development, studies have attempted to explain the association between <i>H. pylori</i> infection and allergic diseases. Nevertheless, no concrete evidence for a causal relationship has been clearly demonstrated yet. The association of <i>H. pylori</i> infection with autoimmune disorders has also been reported in the literature. It has been hypothesized that environmental triggers act on genetically vulnerable hosts, leading to autoimmune disorders. The role of <i>H. pylori</i> infection as one of the triggers in autoimmune diseases has been explored previously. However, the results were conflicting and indistinct with respect to most autoimmune diseases. Similar findings were also detected in skin disorders where <i>H. pylori</i> infection was deemed to be a causative factor. The role of <i>H. pylori</i> in majority of the immune-mediated disorders or skin disorders remains controversial. In this review, the association of <i>H. pylori</i> with various immune-mediated disorders and skin disorders is discussed. The epidemiological, serological, and experimental evidences relevant to the aforementioned association are also addressed.

2020 ◽  
Vol 182 (1) ◽  
pp. 53-64
Author(s):  
Zhi Tong Zuo ◽  
Ya Ma ◽  
Yan Sun ◽  
Cui Qing Bai ◽  
Chun Hua Ling ◽  
...  

As an ancient Gram-negative bacterium, <i>Helicobacter pylori</i> has settled in human stomach. Eradicating <i>H. pylori</i> increases the morbidities of asthma and other allergic diseases. Therefore, <i>H. pylori</i> might play a protective role against asthma. The “disappearing microbiota” hypothesis suggests that the absence of certain types of the ancestral microbiota could change the development of immunology, metabolism, and cognitive ability in our early life, contributing to the development of some diseases. And the Hygiene Hypothesis links early environmental and microbial exposure to the prevalence of atopic allergies and asthma. Exposure to the environment and microbes can influence the growing immune system and protect subsequent immune-mediated diseases. <i>H. pylori</i> can inhibit allergic asthma by regulating the ratio of helper T cells 1/2 (Th1/Th2), Th17/regulatory T cells (Tregs), etc. <i>H. pylori</i> can also target dendritic cells to promote immune tolerance and enhance the protective effect on allergic asthma, and this effect relies on highly suppressed Tregs. The remote regulation of lung immune function by <i>H. pylori</i> is consistent with the gut-lung axis theory. Perhaps, <i>H. pylori</i> also protects against asthma by altering levels of stomach hormones, affecting the autonomic nervous system and lowering the expression of heat shock protein 70. Therapeutic products from <i>H. pylori</i> may be used to prevent and treat asthma. This paper reviews the possible protective influence of <i>H. pylori</i> on allergic asthma and the possible application of <i>H. pylori</i> in treating asthma.


2009 ◽  
Vol 7 (2) ◽  
pp. 13-22
Author(s):  
E A Varyushina ◽  
A S Simbirtsev

Helicobacter pylori is a Gram-negative bacterium that chronically infects the stomach of more than 50% of human population and represents the major cause of gastroduodenal pathologies. The H. pylori infection is followed by local inflammatory response in gastric mucosa and proinflammatory cytokine production, and preferably elicits a T-helper 1 (Thl) immune response. Bronchial asthma and allergic diseases are orchestrated by Th2 cytokines. A negative association between the H. pylori infection and frequency of allergic diseases was found. Investigations of possible molecular mechanisms of the association are required for research of novel strategies of prevention and treatment of allergic diseases.


2020 ◽  
Vol 9 (12) ◽  
pp. 3887
Author(s):  
Antonietta G. Gravina ◽  
Kateryna Priadko ◽  
Paola Ciamarra ◽  
Lucia Granata ◽  
Angela Facchiano ◽  
...  

Helicobacter Pylori (H. pylori) is a Gram-negative flagellated microorganism that has been extensively studied since its first isolation due to its widespread diffusion and association with numerous diseases. While the bacterium is proved to be a causative factor for a number of gastric diseases such as gastritis, gastric adenocarcinoma, and MALT-lymphoma, its role at other gastrointestinal levels and in other systems is being thoroughly studied. In this article, we reviewed the latest published clinical and laboratory studies that investigated associations of H. pylori with hematologic diseases such as Vitamin B12- and iron-deficiency anemia, primary immune thrombocytopenia, and with a number of dermatologic and ophthalmic diseases. In addition, the putative role of the bacterium in inflammatory bowel diseases, esophageal disorders, metabolic, diseases, neurologic diseases and allergy were outlined.


Pathogens ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 331
Author(s):  
Montserrat Palau ◽  
Núria Piqué ◽  
M. José Ramírez-Lázaro ◽  
Sergio Lario ◽  
Xavier Calvet ◽  
...  

Helicobacter pylori is a common pathogen associated with several severe digestive diseases. Although multiple virulence factors have been described, it is still unclear the role of virulence factors on H. pylori pathogenesis and disease progression. Whole genome sequencing could help to find genetic markers of virulence strains. In this work, we analyzed three complete genomes from isolates obtained at the same point in time from a stomach of a patient with adenocarcinoma, using multiple available bioinformatics tools. The genome analysis of the strains B508A-S1, B508A-T2A and B508A-T4 revealed that they were cagA, babA and sabB/hopO negative. The differences among the three genomes were mainly related to outer membrane proteins, methylases, restriction modification systems and flagellar biosynthesis proteins. The strain B508A-T2A was the only one presenting the genotype vacA s1, and had the most distinct genome as it exhibited fewer shared genes, higher number of unique genes, and more polymorphisms were found in this genome. With all the accumulated information, no significant differences were found among the isolates regarding virulence and origin of the isolates. Nevertheless, some B508A-T2A genome characteristics could be linked to the pathogenicity of H. pylori.


mBio ◽  
2014 ◽  
Vol 5 (4) ◽  
Author(s):  
Adria Carbo ◽  
Danyvid Olivares-Villagómez ◽  
Raquel Hontecillas ◽  
Josep Bassaganya-Riera ◽  
Rupesh Chaturvedi ◽  
...  

ABSTRACTThe development of gastritis duringHelicobacter pyloriinfection is dependent on an activated adaptive immune response orchestrated by T helper (Th) cells. However, the relative contributions of the Th1 and Th17 subsets to gastritis and control of infection are still under investigation. To investigate the role of interleukin-21 (IL-21) in the gastric mucosa duringH. pyloriinfection, we combined mathematical modeling of CD4+T cell differentiation within vivomechanistic studies. We infected IL-21-deficient and wild-type mice withH. pyloristrain SS1 and assessed colonization, gastric inflammation, cellular infiltration, and cytokine profiles. ChronicallyH. pylori-infected IL-21-deficient mice had higherH. pyloricolonization, significantly less gastritis, and reduced expression of proinflammatory cytokines and chemokines compared to these parameters in infected wild-type littermates. Thesein vivodata were used to calibrate anH. pyloriinfection-dependent, CD4+T cell-specific computational model, which then described the mechanism by which IL-21 activates the production of interferon gamma (IFN-γ) and IL-17 during chronicH. pyloriinfection. The model predicted activated expression of T-bet and RORγt and the phosphorylation of STAT3 and STAT1 and suggested a potential role of IL-21 in the modulation of IL-10. Driven by our modeling-derived predictions, we found reduced levels of CD4+splenocyte-specifictbx21androrcexpression, reduced phosphorylation of STAT1 and STAT3, and an increase in CD4+T cell-specific IL-10 expression inH. pylori-infected IL-21-deficient mice. Our results indicate that IL-21 regulates Th1 and Th17 effector responses during chronicH. pyloriinfection in a STAT1- and STAT3-dependent manner, therefore playing a major role controllingH. pyloriinfection and gastritis.IMPORTANCEHelicobacter pyloriis the dominant member of the gastric microbiota in more than 50% of the world’s population.H. pyloricolonization has been implicated in gastritis and gastric cancer, as infection withH. pyloriis the single most common risk factor for gastric cancer. Current data suggest that, in addition to bacterial virulence factors, the magnitude and types of immune responses influence the outcome of colonization and chronic infection. This study uses a combined computational and experimental approach to investigate how IL-21, a proinflammatory T cell-derived cytokine, maintains the chronic proinflammatory T cell immune response driving chronic gastritis duringH. pyloriinfection. This research will also provide insight into a myriad of other infectious and immune disorders in which IL-21 is increasingly recognized to play a central role. The use of IL-21-related therapies may provide treatment options for individuals chronically colonized withH. pylorias an alternative to aggressive antibiotics.


2017 ◽  
Vol 8 (2) ◽  
Author(s):  
Asieh Bolandi ◽  
Saam Torkan ◽  
Iman Alavi

In despite of the high clinical impact of Helicobacter pylori, its exact sources and routes of transmission are unknown. Dogs may play an imperative role in the transmission of H. pylori to humans. The current investigation was done to study the status of vacA and cagA genotypes in the H. pylori strains of dogs. One-hundred and fifty fecal samples were collected from healthy and complicated household dogs. Genomic DNA was extracted from fecal samples and presence of 16S rRNA gene was studied using the PCR amplification. Distribution of vacA and cagA genotypes were studied by the multiplex PCR. Thirteen out of 150 fecal samples (8.66%) were positive for H. pylori 16S rRNA gene. Prevalence of H. pylori in healthy and complicated dogs were 5.55% and 8.57%, respectively. Male had the higher prevalence of H. pylori (P=0.038). The most commonly detected genotypes among the H. pylori strains were vacAs1A (61.53%), cagA (38.46%), vacAm1a (38.46%), vacAs2 (30.76%) and vacAm2 (30.76%). The most commonly detected combined genotypes were s1aCagA (30.76%), s1am1a (23.07%), s2m1a (23.07%) and s2CagA (23.07%). Iranian household dogs harbor H. pylori in their fecal samples similar in genotypes of the vacA and cagA alleles which suggest that complicated and even healthy dogs may be the latent host of the H. pylori and its genotypes. However, supplementary studies are required to found the exact role of dogs as a definitive host of the H. pylori.


2001 ◽  
Vol 45 (1) ◽  
pp. 306-308 ◽  
Author(s):  
Dong H. Kwon ◽  
Miae Lee ◽  
J. J. Kim ◽  
J. G. Kim ◽  
F. A. K. El-Zaatari ◽  
...  

ABSTRACT The prevalence of furazolidone, nitrofurantoin, and metronidazole resistance among Helicobacter pylori strains was assessed with 431 clinical isolates. Fifty-two percent were metronidazole resistant, compared to 2% (7 of 431) with resistance to furazolidone and nitrofurantoin. All seven furazolidone- and nitrofurantoin-resistant isolates were also metronidazole resistant.rdxA, frxA, and fdxB knockouts did not result in furazolidone or nitrofurantoin resistance. These data suggest that furazolidone and nitrofurantoin may be good alternatives to metronidazole for treating H. pylori infection.


2000 ◽  
Vol 68 (9) ◽  
pp. 5225-5233 ◽  
Author(s):  
Véronique Hofman ◽  
Vittorio Ricci ◽  
Antoine Galmiche ◽  
Patrick Brest ◽  
Patrick Auberger ◽  
...  

ABSTRACT Helicobacter pylori infection can induce polymorphonuclear leukocyte (PMNL) infiltration of the gastric mucosa, which characterizes acute chronic gastritis. The mechanisms underlying this process are poorly documented. The lack of an in vitro model has considerably impaired the study of transepithelial migration of PMNL induced by H. pylori. In the present work, we used confluent polarized monolayers of the human intestinal cell line T84 grown on permeable filters to analyze the epithelial PMNL response induced by broth culture filtrates (BCFs) and bacterial suspensions from different strains of H. pylori. We have evaluated the role of the vacuolating cytotoxin VacA and of the cagpathogenicity island (PAI) of H. pylori in PMNL migration via their effects on T84 epithelial cells. We noted no difference in the rates of PMNL transepithelial migration after epithelial preincubation with bacterial suspensions or with BCFs of VacA-negative or VacA-positive H. pylori strains. In contrast, PMNL transepithelial migration was induced after incubation of the T84 cells with cag PAI-positive and cagE-positiveH. pylori strains. Finally, PMNL migration was correlated with a basolateral secretion of interleukin-8 by T84 cells, thus creating a subepithelial chemotactic gradient for PMNL. These data provide evidence that the vacuolating cytotoxin VacA is not involved in PMNL transepithelial migration and that the cag PAI, with a pivotal role for the cagE gene, provokes a transcellular signal across T84 monolayers, inducing a subepithelial PMNL response.


1970 ◽  
Vol 17 (2) ◽  
pp. 88-93
Author(s):  
K Ahsan ◽  
MZ Hossain ◽  
MR Uddin

Context: A cross-sectional study was carried out at the Department of Pathology, Dhaka Medical Collage, Dhaka and Immunology Laboratory, Laboratory Sciences Division of ICDDR,B, Dhaka during a period of 1 year from July, 2007 to June, 2008 to determine the efficacy of endoscopic crush cytology in the detection of Helicobacter pylori infection in gastroduodenal diseases. Clinically suspected cases of gastro-duodenal lesions and who had not taken antibiotics, omeprazole or bismuth salts for at least three weeks prior to endoscopy were selected. Patients who were clinically and endoscopically suspected of having malignancy were excluded from the study. A total of 110 such subjects were consecutively included in the study. The statistics used to analyze the data were descriptive statistics and components of accuracy test.Results: The sensitivity of crush cytology in correctly diagnosing H. pylori of those who had the disease was 89.3%, while the specificity of the test in correctly differentiating those who did not have H. pylori was 92.6% when compared against histopathological examination using Giemsa stain. However, a slightly low sensitivity (86.2%) without compromising with specificity (92.3%) was obtained when the crush cytology diagnosis was compared against histopathological examination using haematoxylin-eosin (H & E) stain.Conclusion: The study concludes that the diagnostic accuracy of crush smear cytology (sensitivity and specificity) for detection of Helicobacter pylori in gastric biopsy material is comparable to histopathology. Moreover, the technique is very simple, less expensive and less time consuming which gives clinicians added advantage in making a quicker decision.Key words: Cytology; Helicobacter pylori; Gastroduodenal disease. DOI: 10.3329/jdmc.v17i2.6589J Dhaka Med Coll. 2008; 17(2) : 88-93


Author(s):  
R. I. Khlynova ◽  
O. M. Khromtsova ◽  
R. B. Berdnikov ◽  
I. B. Khlynov

The aim is to study the effect of Helicobacter pylori infection on risk of developing gastroesophageal reflux disease. Materials and methods - cross-sectional observational study of 1007 patients with dyspepsia syndrome who underwent videoesophagogastroduodenoscopy with biopsy and histological examination of biopsy specimens of the gastric mucosa by OLGA-system. The age, gender, overweight, cigarette smoking, presence of Helicobacter pylori infection and gastritis stage were assessed. Results - the study showed a significant decrease in the incidence of gastroesophageal reflux disease in patients with positive H. Pylori status by 4% (RR 0,68; 95% CI, 0.49-0.94, p=0,041). The risk of developing gastroesophageal reflux disease significantly higher in overweight (RR 2,62; 95% CI 2,0-3,56; р<0,001) men (RR 1,76; 95% CI 1,33-2,32; р=0,0046) who smoked cigarettes (RR 3,23; 95% CI 2,45-4,24; р<0,001) and was not associated with the patient’s age and the stage of gastritis (р>0,05). Conclusion - a significant reduction in the frequency and risk of developing gastroesophageal reflux disease in patients with Helicobacter pylori infection is demonstrated.


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