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Inflammatory Responses to Salmonella Infections Are Serotype-Specific

DOI: 10.1155/2013/168179

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Abstract:

The main purpose of this study was to investigate the profile of inflammatory response in patients with acute salmonellosis caused by two serotypes of Salmonella enterica, S. Enteritidis and S. Typhimurium, as well as in convalescent patients with previous acute disease caused by S. Enteritidis. Patients with acute disease showed significantly elevated levels of IL-1β, IL-17, IL-10, and calprotectin compared to healthy control subjects. In convalescent patients, these markers were also significantly elevated, with the exception of IL-1β. Multivariate statistical analyses with the use of these variables produced models with a good predictive accuracy resulting in excellent separation of the diseased and healthy cohorts studied. Overall, the results suggest that the profile of inflammatory response in this disease is determined, to a significant degree, by the serotype of Salmonella, and the profile of certain cytokines and calprotectin remains abnormal for a number of months following the acute disease stage. 1. Introduction Infections by various Salmonella species remain one of the leading causes of gastrointestinal disorders in the world resulting in significant morbidity and some mortality [1]. Infections by the two most common serotypes of Salmonella enterica, S. Enteritidis and S. Typhimurium, are the most frequent causes of acute gastroenteritis in humans worldwide. Although the members of the Salmonella genus are genetically close, they show wide variations in host-specificity, virulence, and disease manifestations [2]. Clinical picture of the disease depends on the host, the serotype of Salmonella, and the specificity of the interaction of certain serotypes with the host, but not all details of these complex interactions are fully understood. Under the normal physiological conditions of a healthy host, the gut defense system maintains several protective barriers to keep the bacteria at bay [3]. This network of defense mechanisms at mucosal surfaces is regulated by a number of regulatory signals, including cytokines, to maintain the controlled inflammation state under the normal circumstances. In the case of invasive pathogens such as Salmonella, the cytokines play an important protective role orchestrating a number of events leading to the local inflammatory response followed by its downregulation once the body is cleared from a pathogen [4]. The inflammatory response also includes the synthesis of antimicrobial peptides, some of which may possess a secondary role as regulatory molecules [5]. When the immune system detects the presence of a

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