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Salmonella infect humans and animals world-wide causing a spectrum of diseases including enteric fever, gastroenteritis and septicaemia. A number of mechanisms of host resistance to salmonellosis have been identified in the mouse typhoid model. In mice, salmonellae usually reside inside phagocytes and dendritic cells localized within discrete pathological lesions surrounded by normal tissue. Bacterial growth in the tissues is controlled by NADPH oxidase-dependent and iNOS-dependent anti-microbial functions of resident and inflammatory phagocytes and is under the control of H-2 genes and the Nramp1 gene. The concerted action of a number of cytokines (TNFα, IFNγ, IL-12, IL-18, IL-15), the contribution of CD4 TCR-α/β T-cells, the presence of B-cells and antibodies are essential for host resistance to this bacterium. Observations on the increased incidence of Salmonella infections in immunocompromised patients have revealed some effector mechanisms that control these infections in humans. Deficiencies in components of the innate immune system including gastric secretion, neutrophil and macrophage functions predispose individuals to salmonellosis. A higher incidence of salmonellosis is seen also in patients with antibody deficiencies, defects in cell-mediated immunity and deficiencies in Th1 cytokines (IL-12, IFNγ) or cytokine receptors (IL-12R β1 subunit, IFNγR chains 1 and 2).