Gastric expression of IL-17A and IFNγ in Helicobacter pylori infected individuals is related to symptoms

Adamsson, Jenni; Ottsjo, Louise Sjökvist; Lundin, Samuel; Svennerholm, Ann Mari; Raghavan, Sukanya

doi:10.1016/j.cyto.2017.06.013

Cited by 28 publications

(21 citation statements)

References 13 publications

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“…As expected, the severity of the gastritis was positively correlated with the production of IL‐17 . However, two studies showed that the number of infiltrating Th17 cells is higher in H. pylori ‐infected patients with peptic ulcers compared to individuals with H. pylori gastritis . To converse, Cremniter et al described that the same level of IL17A mRNA is found in patients with gastritis, ulcer, or precancerous and cancerous lesions …”

Section: Immunologymentioning

confidence: 69%

“…In the last year, clinical investigations emphasized that Th1 and Th17 responses are elicited during H. pylori infection. Adamsson et al reported that the level of expression of the genes encoding the prototype Th17 cytokine IL‐17A and the Th1 lymphokine IFN‐γ is enhanced in the corpus and antrum of Swedish patients with H. pylori infection compared to uninfected individuals; more importantly they confirmed by immunofluorescence that the number of IL‐17A + and IFN‐γ + cells is also increased in H. pylori ‐infected patients . Similar to that, a significant increase in IL17A mRNA transcripts was observed in the gastric tissue of H. pylori ‐infected patients from Iran and France compared to uninfected ones.…”

Section: Immunologymentioning

confidence: 71%

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Helicobacter: Inflammation, immunology, and vaccines

et al. 2018

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Helicobacter pylori infection induces a chronic gastric inflammation which can lead to gastric ulcers and cancer. The mucosal immune response to H. pylori is first initiated by the activation of gastric epithelial cells that respond to numerous bacterial factors, such as the cytotoxin-associated gene A or the lipopolysaccharide intermediate heptose-1,7-bisphosphate. The response of these cells is orchestrated by different receptors including the intracellular nucleotide-binding oligomerization domain-containing protein 1 or the extracellular epidermal growth factor receptor. This nonspecific response leads to recruitment and activation of various myeloid (macrophages and dendritic cells) and T cells (T helper-17 and mucosal-associated invariant T cells), which magnify and maintain inflammation. In this review, we summarize the major advances made in the past year regarding the induction, the regulation, and the role of the innate and adaptive immune responses to H. pylori infection. We also recapitulate efforts that have been made to develop efficient vaccine strategies.

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Section: Immunologymentioning

confidence: 69%

Section: Immunologymentioning

confidence: 71%

Helicobacter: Inflammation, immunology, and vaccines

et al. 2018

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“…CD4+ and CD8+ T‐cell concentration also increases compared to the preinfection state. The secretion of cytokines (interferon‐γ [IFN‐γ], tumor necrosis factor‐α [TNF‐α], and interleukins [IL‐1, IL‐6, IL‐7, IL‐8, IL‐10, IL‐17, and IL‐17A]) from the immune cells is frequently increased in the H. pylori ‐infected individuals compared to uninfected individuals …”

Section: Ureasementioning

confidence: 99%

“…The secretion of cytokines (interferon-γ [IFN-γ], tumor necrosis factorα [TNF-α], and interleukins [IL-1, IL-6, IL-7, IL-8, IL-10, IL-17, and IL-17A]) from the immune cells is frequently increased in the H. pylori-infected individuals compared to uninfected individuals. 8,70,71 In some previous studies, the relationship between the host and H. pylori has been shown to be two-sided and during this relationship in thousands of years, H. pylori has adapted or modulated itself for persistence. 72 Overall, the persistence phenomenon can only occur when H. pylori coadapts and evades the immune system.…”

Section: Immunological Responses and Immune Evasionmentioning

confidence: 99%

Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

Gupta

Maurya

Verma

et al. 2019

J of Cellular Biochemistry

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Helicobacter pylori and humans have one of the most complex relationships in nature. How a bacterium manages to live in one of the harshest and hostile environments is a topic of unraveling mysteries. H. pylori is a prevalent species and it colonizes the human gut of more than 50% of the world population. It infects the epithelial region of antrum and persists there for a long period. Over the time of evolution, H. pylori has developed complex strategies to extend the degree of inflammation in gastric mucosa. H. pylori needs specific adaptations for initial colonization into the host environment like helical shape, flagellar movement, chemotaxis, and the production of urease enzyme that neutralizes acidic environment of the stomach. There are several factors from the bacterium as well as from the host that participate in these complex interactions. On the other hand, to establish the persistent infection, H. pylori escapes the immune system by mimicking the host antigens. This pathogen has the ability to dodge the immune system and then persist there in the form of host cell, which leads to immune tolerance. H. pylori has an ability to manipulate its own pathogen‐associated molecular patterns, which leads to an inhibition in the binding with specific pattern recognition receptors of the host to avoid immune cell detection. Also, it manipulates the host metabolic homeostasis in the gastric epithelium. Besides, it has several genes, which may get involved in the acquisition of nutrition from the host to survive longer in the host. Due to the persistence of H. pylori, it causes chronic inflammation and raises the chances of gastric cancer. This review highlights the important elements, which are certainly responsible for the persistence of H. pylori in the human host.

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“…Thus, an increased rate of proliferation is associated with TRPM-6 and TRPM-7 complex formation, in which magnesium enters the cell to fulfill magnesium-dependent enzymes for energy production and energy consumption, protein synthesis, fatty acids, phospholipids etc. By the way, magnesium ions optimize conditions for a normal blood flow in organs and tissues [1,3].…”

Section: оригинальные исследованияmentioning

confidence: 99%

Interrelation of endothelial nitric oxides synthase activity in tissues of the stomach and magnesium balance in the period of erosive-ulcerative acid-induced lesion development in rats with different resistance to stress

Nikolaevna¹,

Nikolaevna²

2017

Medical news of the North Caucasus

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Волгоградский государственный медицинский университет, Российская ФедерацияAcetate stomach ulcer was experimentally modeled in stress resistant and stress nonresistant rats for immunohistochemical identifying a specific number and expression intensity of eNOS-positive cells and determination of the magnesium level in biological media. The content of intra-erythrocyte magnesium in reaction with titanium yellow was reduced in rats with different resistance to stress in low eNOS activity in the gastric mucosa, in the muscular layer in stress nonresistant animals and almost complete absence of antigen-positive cells in the submucosa. A positive correlation was found between the level of intra-erythrocyte magnesium and the specific number of eNOS-positive cells in the gastric mucosa in both groups of animals and also between expression intensity in the submucosa of stress nonresistant rats. A relationship was established between the magnesium content, specific number and expression intensity of eNOS in stress nonresistant rats in the stomach submucosa.

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Gastric expression of IL-17A and IFNγ in Helicobacter pylori infected individuals is related to symptoms

Cited by 28 publications

References 13 publications

Helicobacter: Inflammation, immunology, and vaccines

Helicobacter: Inflammation, immunology, and vaccines

Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

Interrelation of endothelial nitric oxides synthase activity in tissues of the stomach and magnesium balance in the period of erosive-ulcerative acid-induced lesion development in rats with different resistance to stress

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