Gastric mucosal secretion of interleukin-10: relations to histopathology, Helicobacter pylori status, and tumour necrosis factor-alpha secretion.

Bodger, Keith; Wyatt, Judy; Heatley, R. V.

doi:10.1136/gut.40.6.739

Cited by 99 publications

(91 citation statements)

References 27 publications

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“…Such fact may be due to the production of interleukin-10 (IL-10) that along with the tumor necrosis factor (TNF)-alpha are increased in H. pylori infections (2) . IL-10 may be a protective factor in limiting the tissue damage caused by inflammation that can contribute; however, to a failure of the immune response to eliminate the organism (2) , thus, great concentrations of H. pylori could inhibit the proliferation of mononuclear cells and stimulate a more intense compensatory inflammatory response at the expense of polymorphonuclear cells.…”

Section: Resultsmentioning

confidence: 99%

“…Table 1 shows the combination of histopathological findings, and Table 2 shows their combining frequency in the same biopsy related to the presence and concentration of H. pylori. (2) . However, some studies have reported that such isolated or combined histological findings have neither sensitive nor specific values enough to predict the diagnosis of this bacterium, and more specific techniques may be required for H. pylori detection as Giemsa staining or Warthin-Starry silver impregnation technique (16,18) .…”

Section: Resultsmentioning

confidence: 99%

“…In developed countries, the prevalence is influenced by age, race, and socioeconomic status of the population studied (14,16,22) . Histopathological findings of the gastric mucosa due to H. pylori infection are mononuclear infiltrate, infiltration by polymorphonuclear cells in the corium and epithelium (activity), presence of lymphoid follicles, intestinal metaplasia and regenerative cell atypias (2,3,4,5,8,9,11) . The inflammatory response is different in adults and children.…”

Section: Introductionmentioning

confidence: 99%

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Association between Helicobacter pylori concentration and the combining frequency of histopathological findings in gastric biopsies specimens

Nai¹,

Parizi

Barbosa

2007

Arq. Gastroenterol.

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-Background -Helicobacter pylori is the most prevalent infectious agent worldwide. About 90% of patients with chronic gastritis are infected with this bacterium. Some studies have shown a association between the H. pylori concentration and the scores of gastritis activity and severity. Aim -To evaluate the association between H. pylori concentration and the combining frequency of findings on histopathological examination. Methods -Two hundred consecutive gastric endoscopic biopsies diagnosed as chronic gastritis were retrospectively investigated. The Warthin-Starry silver stain was used to study H. pylori and the following parameters were assessed (according to the Sydney system): 1. infiltration by polymorphonuclear cells in chorio and epithelium (activity) graded as mild, moderate and marked; 2. presence of lymphoid follicles; 3. presence of intestinal metaplasia; 4. presence of regenerative cell atypias, graded as mild, moderate and marked; and 5. H. pylori concentration on the mucous covering the foveolar epithelium. Results -The most frequent association was chronic gastritis and activity, regardless of H. pylori concentration. The association of five histopathological findings in the same biopsy has not occurred in the cases of higher concentration of H. pylori. Conclusion -Our study has not revealed any association between H. pylori concentration and an increasing in the number of histopathological findings found in the gastric mucosa. Since referring to its presence is much more important than to its concentration. HEADINGS -Gastritis. Helicobacter pylori. Helicobacter infections. Biopsy.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association between Helicobacter pylori concentration and the combining frequency of histopathological findings in gastric biopsies specimens

Nai¹,

Parizi

Barbosa

2007

Arq. Gastroenterol.

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“…With this intention, we crossed IgA-onto IL-10-deficient C57BL/6 mice and obtained double and single gene knockout mice, IL-10 Ϫ/Ϫ /IgA Ϫ/Ϫ and IL-10 Ϫ/Ϫ /IgA ϩ/ϩ . Our choice of the IL-10 Ϫ/Ϫ mice was based on previous studies showing that these mice develop severe gastritis and that IL-10 is strongly produced in the gastric mucosa of patients as well as in mice infected with H. pylori (20,(25)(26)(27)(28)(29)(30)(31)(32). Also,…”

Section: Nfection Withmentioning

confidence: 99%

IgA Antibodies Impair Resistance againstHelicobacter pyloriInfection: Studies on Immune Evasion in IL-10-Deficient Mice

Akhiani

Stensson

Schön

et al. 2005

The Journal of Immunology

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We recently reported that Helicobacter pylori-specific Abs impair the development of gastritis and down-regulate resistance against H. pylori infection. In this study, we asked whether IgA Abs specifically can have an impact on H. pylori colonization and gastric inflammation. To obtain a sensitive model for the study of inflammation we crossed IgA- and IL-10-deficient mice. We found that IL-10−/−/IgA−/− mice were significantly less colonized than IL-10−/−/IgA+/+ mice, which in turn were less colonized than wild-type (WT) mice. The IL-10−/−/IgA−/− mice exhibited a 1.2-log reduction in bacterial counts compared with that in IL-10−/−/IgA+/+ mice, suggesting that IgA Abs rather promoted than prevented infection. The reduced colonization in IL-10−/−/IgA−/− mice was associated with the most severe gastritis observed, albeit all IL-10−/− mice demonstrated more severe gastric inflammation than wild-type mice. The gastritis score and the infiltration of CD4+ T cells into the gastric mucosa were significantly higher in IL-10−/−/IgA−/− mice than in IL-10−/−/IgA+/+ mice, arguing that IgA Abs counteracted inflammation. Moreover, following oral immunization, IL-10−/−/IgA−/− mice were significantly better protected against colonization than IL-10−/−/IgA+/+ mice. However, the stronger protection was associated with more severe postimmunization gastritis and gastric infiltration of CD4+ T cells. There was also a clear increase in complement receptor-expressing cells in IL-10−/−/IgA−/− mice, though C3b-fragment deposition in the gastric mucosa was comparable between the two. Finally, specific T cell responses to recall Ag demonstrated higher levels of IFN-γ production in IL-10−/−/IgA−/− as compared with IL-10−/−/IgA+/+ mice. Thus, it appears that IgA and IL-10 help H. pylori bacteria evade host resistance against infection.

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“…11 In this sense, it is noteworthy that the polymorphism in the genes encoding interleukins (IL) 1β, 1RN, 6, 8 and 10 are associated with increased susceptibility to gastric diseases. [12][13][14][15][16][17] The combined presence of environmental factors, such as, household crowding, inadequate eating habits, low socioeconomic conditions, poor hygienic, excessive alcohol consumption and smoking are related with H. pylori infection, especially when one takes into account aggravation of mucosal damage once the gastric infection with H. pylori induces the mucosal production of various pro-and anti-inflammatory cytokines in the host. The harmful role of environmental factors is related to poor socioeconomic conditions, salt intake, smoking and alcohol consumption.…”

Section: -9mentioning

confidence: 99%

Genes de patogenicidade de Helicobacter pylori, polimorfismos de citocinas e fatores ambientais afetam o desenvolvimento de doenças gástricas: uma visão geral

Vianna¹,

Silva²,

Ramis³

2016

Rev Epidemiol Control Infect

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Exceto onde especificado diferentemente, a matéria publicada neste periódico é licenciada sob forma de uma licença Creative Commons -Atribuição 4. pylori possui um conjunto de fatores de patogenicidade, tais como cagA, vacA, iceA, babA, para colonizar a mucosa gástrica e estabelecer infecção crônica. Estes fatores bacterianos são agentes essenciais em modular a resposta imune envolvida na iniciação da carcinogênesegástrica. Os fatores genéticos do hospedeiro contribuem para regular a resposta inflamatória e para o agravamento da lesão da mucosa gástrica uma vez que a infecção gástrica por H. pylori induz a produção de várias citocinas pró e anti-inflamatórias no hospedeiro. O papel prejudicial dos fatores ambientais está relacionado com as precárias condições socioeconômicas, com o consumo de sal, com o tabagismo e com o consumo de álcool. Conclusão: Ao decifrar as regras deterministas -se houver -dessa interação entre fatores da bactéria, do hospedeiro e variáveis ambientais, será possível prever, tratar e, finalmente, prevenir graves doenças gastroduodenais. Background and Objectives:Helicobacter pylori is a Gram-negative bacterium that colonizes the stomach of approximately 50% of the world´s human population. This microorganismis the major causal agent of gastritis and is an important risk factor for the development of peptic ulcer disease and gastric carcinoma. The factors that determine these diverse clinical outcomes are subject to continuous investigations and is thought to be determined by interaction of bacterial factors, host immune system and environmental variables. The aim of this review is to provide an overview of these factors that influence susceptibility to severe outcomes of H. pylori

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Gastric mucosal secretion of interleukin-10: relations to histopathology, Helicobacter pylori status, and tumour necrosis factor-alpha secretion.

Cited by 99 publications

References 27 publications

Association between Helicobacter pylori concentration and the combining frequency of histopathological findings in gastric biopsies specimens

Association between Helicobacter pylori concentration and the combining frequency of histopathological findings in gastric biopsies specimens

IgA Antibodies Impair Resistance againstHelicobacter pyloriInfection: Studies on Immune Evasion in IL-10-Deficient Mice

Genes de patogenicidade de Helicobacter pylori, polimorfismos de citocinas e fatores ambientais afetam o desenvolvimento de doenças gástricas: uma visão geral

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