Molecular Mechanisms of Salmonella Effector Proteins: A Comprehensive Review.

Pediatric Infections Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Students Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran. Clinical Microbiology Research Center, Ilam University of Medical Science, Ilam, Iran. Food Safety and Hygiene Division, Environmental health Department, School of Public Health, Tehran University of medical sciences, Tehran, Iran. Students Research Committee, Department of Food Sciences and Technology, Faculty of Nutrition and Food Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Department of Medical Microbiology, School of Medicine, Ilam University of Medical Science, Ilam, Iran.

Infection and drug resistance. 2020;:11-26
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Abstract

Salmonella can be categorized into many serotypes, which are specific to known hosts or broadhosts. It makes no difference which one of the serotypes would penetrate the gastrointestinal tract because they all face similar obstacles such as mucus and microbiome. However, following their penetration, some species remain in the gastrointestinal tract; yet, others spread to another organ like gallbladder. Salmonella is required to alter the immune response to sustain its intracellular life. Changing the host response requires particular effector proteins and vehicles to translocate them. To this end, a categorized gene called Salmonella pathogenicity island (SPI) was developed; genes like Salmonella pathogenicity island encode aggressive or modulating proteins. Initially, Salmonella needs to be attached and stabilized via adhesin factor, without which no further steps can be taken. In this review, an attempt has been made to elaborate on each factor attached to the host cell or to modulating and aggressive proteins that evade immune systems. This review includes four sections: (A) attachment factors or T3SS- independent entrance, (B) effector proteins or T3SS-dependent entrance, (c) regulation of invasive genes, and (D) regulation of immune responses.

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Publication Type : Review

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