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      A plausible explanation for male dominance in typhoid ileal perforation

      article-commentary
      Clinical and Experimental Gastroenterology
      Dove Medical Press
      explanation, dominance, male, perforation, ileum, typhoid

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          Abstract

          The phenomenon of consistent male dominance in typhoid ileal perforation (TIP) is not well understood. It cannot be explained on the basis of microbial virulence, Peyer’s patch anatomy, ileal wall thickness, gastric acidity, host genetic factors, or sex-linked bias in hospital attendance. The cytokine response to an intestinal infection in males is predominantly proinflammatory as compared with that in females, presumably due to differences in the sex hormonal milieu. Sex hormone receptors have been detected on lymphocytes and macrophages, including on Peyer’s patches, inflammation of which (probably similar to the Shwartzman reaction/Koch phenomenon) is the forerunner of TIP, and is not excluded from the regulatory effects of sex hormones. Hormonal control of host-pathogen interaction may override genetic control. Environmental exposure to Salmonella typhi may be more frequent in males, presumably due to sex-linked differences in hygiene practices and dining-out behavior. A plausible explanation of male dominance in TIP could include sex-linked differences in the degree of natural exposure of Peyer’s patches to S. typhi. An alternative explanation may include sexual dimorphism in host inflammatory response patterns in Peyer’s patches that have been induced by S. typhi. Both hypotheses are testable.

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          Most cited references61

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          Persistent bacterial infections: the interface of the pathogen and the host immune system.

          Persistent bacterial infections involving Mycobacterium tuberculosis, Salmonella enterica serovar Typhi (S. typhi) and Helicobacter pylori pose significant public-health problems. Multidrug-resistant strains of M. tuberculosis and S. typhi are on the increase, and M. tuberculosis and S. typhi infections are often associated with HIV infection. This review discusses the strategies used by these bacteria during persistent infections that allow them to colonize specific sites in the host and evade immune surveillance. The nature of the host immune response to this type of infection and the balance between clearance of the pathogen and avoidance of damage to host tissues are also discussed.
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            Salmonella typhimurium Persists within Macrophages in the Mesenteric Lymph Nodes of Chronically Infected Nramp1+/+ Mice and Can Be Reactivated by IFNγ Neutralization

            Host-adapted strains of Salmonella are capable of establishing a persistent infection in their host often in the absence of clinical disease. The mouse model of Salmonella infection has primarily been used as a model for the acute systemic disease. Therefore, the sites of long-term S. typhimurium persistence in the mouse are not known nor are the mechanisms of persistent infection clearly understood. Here, we show that S. typhimurium can persist for as long as 1 yr in the mesenteric lymph nodes (MLNs) of 129sv Nramp1 + / + (Slc11a1 + / +) mice despite the presence of high levels of anti–S. typhimurium antibody. Tissues from 129sv mice colonized for 60 d contain numerous inflammatory foci and lesions with features resembling S. typhi granulomas. Tissues from mice infected for 365 d have very few organized inflammatory lesions, but the bacteria continue to persist within macrophages in the MLN and the animals generally remain disease-free. Finally, chronically infected mice treated with an interferon-γ neutralizing antibody exhibited symptoms of acute systemic infection, with evidence of high levels of bacterial replication in most tissues and high levels of fecal shedding. Thus, interferon-γ, which may affect the level of macrophage activation, plays an essential role in the control of the persistent S. typhimurium infection in mice.
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              Animal models of Salmonella infections: enteritis versus typhoid fever.

              The most common disease syndromes caused by Salmonella serotypes in humans, typhoid fever and enteritis, can be modeled using Salmonella enterica serotype Typhimurium infections in mice and calves, respectively. This article reviews murine typhoid and bovine enteritis and discusses strengths, limitations and distinctive features of these animal models.
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                Author and article information

                Journal
                Clin Exp Gastroenterol
                Clin Exp Gastroenterol
                Clinical and Experimental Gastroenterology
                Clinical and Experimental Gastroenterology
                Dove Medical Press
                1178-7023
                2012
                12 November 2012
                : 5
                : 213-217
                Affiliations
                Department of Microbiology, College of Medicine, Chichiri, Blantyre, Malawi
                Author notes
                Correspondence: Mohammad Khan, Department of Microbiology, Microbiology Building, Room 431, College of Medicine, PO Box 360, Chichiri, Blantyre 3, Malawi, Tel +26 5187 1911 ext 224, Fax +26 5187 4700, Email moh_kahn@ 123456yahoo.com
                Article
                ceg-5-213
                10.2147/CEG.S36569
                3501370
                23180972
                196f0afa-7e22-4a59-aa80-0471796a1e6a
                © 2012 Khan, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

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                Gastroenterology & Hepatology
                explanation,ileum,male,typhoid,perforation,dominance
                Gastroenterology & Hepatology
                explanation, ileum, male, typhoid, perforation, dominance

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