title: The immunobiology of avian systemic salmonellosis.
abstract: Avian systemic salmonellosis is primarily caused by Salmonella enterica serovar Gallinarum and serovar Pullorum causing the diseases Fowl Typhoid and Pullorum Disease respectively. During infection interaction with the immune system occurs in three main phases. First is invasion via the gastrointestinal tract. Infection with S. Pullorum or S. Gallinarum does not cause substantial inflammation, unlike S. Typhimurium or S. Enteritidis. Through in vitro models it was found that S. Gallinarum does not induce expression of CXC chemokines or pro-inflammatory cytokines such as IL-1beta or IL-6, whilst in an in vivo model S. Pullorum infection leads to down-regulation of CXCLi1 and CXCLi2 in the ileum. The absence of flagella in S. Gallinarum and S. Pullorum means they are not recognised by TLR5, which is believed to play a key role in the initiation of inflammatory responses, though other pathogen-factors are likely to be involved. The second phase is establishing systemic infection. Salmonella invade macrophages and probably dendritic cells and are translocated to the spleen and liver, where replication occurs. Salmonella survival is dependent on the Salmonella pathogenicity island 2 type III secretion system, which inhibits antimicrobial activity by preventing fusion of lysosymes with the phagocytic vacuole and by modulation of MHC and cytokine expression. Studies in resistant and susceptible chicken lines have shown that the interaction with macrophages is central to the progression of infection or immunological clearance. Primary macrophages from resistant animals are more efficient in killing Salmonella through respiratory burst and by induction of cytokine expression including the initiation of protective Th1 responses that leads to the third phase. Where replication of Salmonella is not controlled the death of the animal usually results. If the innate immune system is not able to control replication then cellular and humoral responses, primarily mediated through Th1-associated cytokines, are able to clear infection. In S. Pullorum a significant number of animals develop persistent infection of splenic macrophages. Here we show preliminary evidence of modulation of adaptive immunity away from a Th1 response to facilitate the development of the carrier state. In carrier animals persistence may lead to reproductive tract and egg infection associated with a decline in CD4+ T cell numbers and function associated with the onset of sexual maturity in hens.
authors.affiliation: Division of Immunology, Institute for Animal Health, Compton, Newbury, RG20 7NN, UK.
authors.forename: Lucy
authors.initials: L
authors.lastname: Chappell
authors.forename: Peter
authors.initials: P
authors.lastname: Kaiser
authors.forename: Paul
authors.initials: P
authors.lastname: Barrow
authors.forename: Michael A
authors.initials: MA
authors.lastname: Jones
authors.forename: Claire
authors.initials: C
authors.lastname: Johnston
authors.forename: Paul
authors.initials: P
authors.lastname: Wigley
mesh_terms: D000818:Animals; D002353:Carrier State / Q000276:immunology / Q000382:microbiology / Q000662:veterinary; D002645:Chickens; D007422:Intestines / Q000382:microbiology; D011201:Poultry Diseases / Q000276:immunology* / Q000382:microbiology*; D012481:Salmonella Infections, Animal / Q000276:immunology* / Q000382:microbiology; D019779:Salmonella enterica / Q000276:immunology / Q000502:physiology*