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Pathogenesis and Clinical Management of Gastric Infection

Abstract

() is a gram-negative bacterium that infects approximately 4.4 billion individuals worldwide. However, its prevalence varies among different geographic areas, and is influenced by several factors. The infection can be acquired by means of oral-oral or fecal-oral transmission, and the pathogen possesses various mechanisms that improve its capacity of mobility, adherence and manipulation of the gastric microenvironment, making possible the colonization of an organ with a highly acidic lumen. In addition, presents a large variety of virulence factors that improve its pathogenicity, of which we highlight cytotoxin associated antigen A, vacuolating cytotoxin, duodenal ulcer promoting gene A protein, outer inflammatory protein and gamma-glutamyl transpeptidase. The host immune system, mainly by means of a Th1-polarized response, also plays a crucial role in the infection course. Although most -positive individuals remain asymptomatic, the infection predisposes the development of various clinical conditions as peptic ulcers, gastric adenocarcinomas and mucosa-associated lymphoid tissue lymphomas. Invasive and non-invasive diagnostic methods, each of them with their related advantages and limitations, have been applied in detection. Moreover, bacterial resistance to antimicrobial therapy is a major challenge in the treatment of this infection, and new therapy alternatives are being tested to improve eradication. Last but not least, the development of effective vaccines against infection have been the aim of several research studies.

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References
1.
Walz A, Odenbreit S, Mahdavi J, Boren T, Ruhl S . Identification and characterization of binding properties of Helicobacter pylori by glycoconjugate arrays. Glycobiology. 2005; 15(7):700-8. DOI: 10.1093/glycob/cwi049. View

2.
Cutler A, Prasad V . Long-term follow-up of Helicobacter pylori serology after successful eradication. Am J Gastroenterol. 1996; 91(1):85-8. View

3.
Kanada R, Uchida T, Tsukamoto Y, Nguyen L, Hijiya N, Matsuura K . Genotyping of the cagA gene of Helicobacter pylori on immunohistochemistry with East Asian CagA-specific antibody. Pathol Int. 2008; 58(4):218-25. DOI: 10.1111/j.1440-1827.2008.02214.x. View

4.
Bamford K, Fan X, Crowe S, Leary J, Gourley W, Luthra G . Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype. Gastroenterology. 1998; 114(3):482-92. DOI: 10.1016/s0016-5085(98)70531-1. View

5.
Wilson K, Ramanujam K, Mobley H, Musselman R, James S, Meltzer S . Helicobacter pylori stimulates inducible nitric oxide synthase expression and activity in a murine macrophage cell line. Gastroenterology. 1996; 111(6):1524-33. DOI: 10.1016/s0016-5085(96)70014-8. View