Toll-like receptors, pathogenesis and immune response to Helicobacter pylori

Norma Angélica Sánchez-Zauco, Silvia Giono-Cerezo, Carmen Maldonado-Bernal

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Helicobacter pylori colonize the gastric epithelial, most infected people are asymptomatic, 10 to 20% develop atrophic gastritis, peptic ulcer and less than 3% gastric cancer. These diseases are determined by the relationship between virulence factors of bacteria, host factors such as, genetic predisposition, and immune response. The innate immune response mainly represented by Toll-like receptors and Nod-like receptors that recognize their specific ligands, activate transcription factors as NF-κB, AP-1, CREB-1, inducing production of inflammatory cytokines such as IL -8, IL-12, IL-6, IL-1β, IL-18, TNF-α and IL-10. Chronic inflammation promotes gastric morphological changes, prevents apoptosis and allows angiogenesis generating neoplasic lesions and cancer. The aim of this review is to analyze the mechanisms proposed to date of the innate and adaptative immune response involved in H. pylori infection; remarking the mechanisms related in the elimination or persistence.
Original languageAmerican English
Pages (from-to)447-454
Number of pages401
JournalSalud Publica de Mexico
StatePublished - 15 Nov 2010

Fingerprint

Toll-Like Receptors
Innate Immunity
Helicobacter pylori
Stomach
Atrophic Gastritis
Interleukin-18
Transcription Factor AP-1
Helicobacter Infections
Virulence Factors
Genetic Predisposition to Disease
Interleukin-12
Peptic Ulcer
Interleukin-8
Interleukin-1
Interleukin-10
Stomach Neoplasms
Interleukin-6
Transcription Factors
Apoptosis
Cytokines

Cite this

Sánchez-Zauco, Norma Angélica ; Giono-Cerezo, Silvia ; Maldonado-Bernal, Carmen. / Toll-like receptors, pathogenesis and immune response to Helicobacter pylori. In: Salud Publica de Mexico. 2010 ; pp. 447-454.
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Toll-like receptors, pathogenesis and immune response to Helicobacter pylori. / Sánchez-Zauco, Norma Angélica; Giono-Cerezo, Silvia; Maldonado-Bernal, Carmen.

In: Salud Publica de Mexico, 15.11.2010, p. 447-454.

Research output: Contribution to journalArticle

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AB - Helicobacter pylori colonize the gastric epithelial, most infected people are asymptomatic, 10 to 20% develop atrophic gastritis, peptic ulcer and less than 3% gastric cancer. These diseases are determined by the relationship between virulence factors of bacteria, host factors such as, genetic predisposition, and immune response. The innate immune response mainly represented by Toll-like receptors and Nod-like receptors that recognize their specific ligands, activate transcription factors as NF-κB, AP-1, CREB-1, inducing production of inflammatory cytokines such as IL -8, IL-12, IL-6, IL-1β, IL-18, TNF-α and IL-10. Chronic inflammation promotes gastric morphological changes, prevents apoptosis and allows angiogenesis generating neoplasic lesions and cancer. The aim of this review is to analyze the mechanisms proposed to date of the innate and adaptative immune response involved in H. pylori infection; remarking the mechanisms related in the elimination or persistence.

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