Differential Immune Phenotypes in Human Monocytes Induced by Non-Host-Adapted Salmonella enterica Serovar Choleraesuis and Host-Adapted . Typhimurium.

We studied the effects of two serovar Typhimurium (host-adapted) strains (14028 and 4/74) and three Choleraesuis (non-host-adapted) strains (A50, A45, and B195) in human monocytes between 2 and 24 h postinfection (p.i.) to investigate whether differences in immune response may explain the much higher prevalence of sepsis in individuals infected with Choleraesuis.

Inhibited Production of iNOS by Murine J774 Macrophages Occurs via a phoP-Regulated Differential Expression of NFκB and AP-1.

Background. There are no reported data to explain how Salmonella suppress nitrite ion production in macrophages or whether this phenomenon is unique to typhoidal or non-typhoidal serovars. The aims of this study were, therefore, to investigate these phenomena.

Analysis of the role of 13 major fimbrial subunits in colonisation of the chicken intestines by Salmonella enterica serovar Enteritidis reveals a role for a novel locus.

Background: Salmonella enterica is a facultative intracellular pathogen of worldwide importance. Over 2,500 serovars exist and infections in humans and animals may produce a spectrum of symptoms from enteritis to typhoid depending on serovar- and host-specific factors. S.

The Salmonella pathogenicity island 1 and Salmonella pathogenicity island 2 type III secretion systems play a major role in pathogenesis of systemic disease and gastrointestinal tract colonization of Salmonella enterica serovar Typhimurium in the chicken.

Salmonella enterica serovar Typhimurium infection of chickens is a major public and animal health problem. In young chicks, S. Typhimurium infection results in severe systemic infection; in older chicks, infection results in prolonged gastrointestinal tract colonization.

Macrophages isolated from chickens genetically resistant or susceptible to systemic salmonellosis show magnitudinal and temporal differential expression of cytokines and chemokines following Salmonella enterica challenge.

Macrophages from inbred chickens that are resistant to salmonellosis show greater and more rapid expression of proinflammatory chemokines and cytokines, including the key Th1-inducing cytokine interleukin-18, upon Salmonella challenge than those from susceptible birds. This suggests the possibility that salmonellosis resistant-line macrophages signal more effectively and rapidly and are more able to induce protective Th1 adaptive responses.

Oral infection with the Salmonella enterica serovar Gallinarum 9R attenuated live vaccine as a model to characterise immunity to fowl typhoid in the chicken.

Background: Salmonella enterica serovar Gallinarum (S. Gallinarum) is the causative agent of fowl typhoid, a severe systemic disease of chickens that results in high mortality amongst infected flocks. Due to its virulence, the immune response to S.

Stimulation of gp91 phagocytic oxidase and reactive oxygen species in neutrophils by an avirulent Salmonella enterica serovar infantis strain protects gnotobiotic piglets from lethal challenge with serovar Typhimurium strain F98 without inducing intestinal pathology.

Preinoculation of susceptible 5-day-old gnotobiotic piglets with Salmonella enterica serovar Infantis strain 1326/28Phi(r) stimulates neutrophil migration into the intestine, which rapidly protects the pigs against a subsequent (normally lethal) challenge with S. enterica serovar Typhimurium strain F98. Here we show that inoculation with either 1326/28Phi(r) or F98 activated reactive oxygen species (ROS) in neutrophils via NADPH pathways in vivo and in vitro and that the survival of both Salmonella strains was increased if neutrophils were cocultured with the ROS inhibitor N-acetylcysteine (captopril).

Infection of the reproductive tract and eggs with Salmonella enterica serovar pullorum in the chicken is associated with suppression of cellular immunity at sexual maturity.

Salmonella enterica serovar Pullorum causes persistent infections in laying hens. Splenic macrophages are the main site of persistence. At sexual maturity, numbers of bacteria increase and spread to the reproductive tract, which may result in vertical transmission to eggs or chicks.

Inhibition of IFN-gamma-stimulated proinflammatory cytokines by vasoactive intestinal peptide (VIP) correlates with increased survival of Salmonella enterica serovar typhimurium phoP in murine macrophages.

Vasoactive intestinal peptide (VIP)is a novel Th2 cytokine that has been shown previously to rescue rats and mice from the lethal effect of bacterial lipopolysaccharide (LPS). We report that VIP inhibited production of the proinflammatory cytokines, tumor necrosis factor-alpha(TNF-alpha)and interleukin-1beta (IL-1beta), at the mRNA level and that the inhibitory effect of VIP was maintained when macrophages were cocultured with an immunostimulatory concentration of interferon-gamma (IFN-gamma)(100 U/ml). The concentration of VIP that had optimal inhibitory effect was (1010) M.

In vivo and in vitro studies of genetic resistance to systemic salmonellosis in the chicken encoded by the SAL1 locus.

A number of inbred lines of chickens have been shown to be resistant or susceptible to systemic salmonellosis caused by Salmonella enterica serovar Gallinarum in adult birds, or by S. enterica serovar Enteritidis and S. enterica serovar Typhimurium in young chicks.

Phagocytic and oxidative burst activity of chicken thrombocytes to Salmonella, Escherichia coli and other bacteria.

The potential role of chicken thrombocytes in immune responses to Salmonella, Escherichia coli and other bacteria was investigated by in vitro assays of phagocytosis and respiratory burst activity. Thrombocytes were found to phagocytose bacteria, but were found to be less phagocytic than heterophils. Oxidative burst activity was generated upon challenge of thrombocytes with various Salmonella strains, E.