In this respect animal models of the disease process being caused by Salmonella have proved to be quite useful.
The process by which Salmonella invades and then onwards maintains itself in the host species is not only a complicated but indeed and intriguing process. It is also an example of adaptive evolution and selective preservation of a genotype. Given its prevalence across a range of warm blooded hosts it has been possible to study the infection and virulence factors in several species. For instance while, murine infection with Salmonella enterica serovar typhimurium has been used largely to replicate human typhoid (caused by Salmonella enterica serovar Typhi), bovine infection caused by Salmonella enterica serovar Dublin or S. enterica serovar Typhimurium has been the extensively used to model intestinal disease. The ability of Salmonella to exist within its host for months following the initial invasion requires it to resist any innate immunity or more likely evolve/adapt to resist the host resistance. Since these bacteria are well able to establish long term system infection in their hosts, the genetic factors responsible for such ability need to be well established to counteract any pathogeneicity.
While, Salmonella enterica serovar Typhi is a strictly human pathogen, Salmonella enterica serovar Typhimurium is a murine pathogen that is increasingly been used to model human typhoid (caused by Salmonella enterica serovar Typhi). ...
In the mouse model, S. Typhimurium invades epithelial cells and can survive and proliferate in macrophage before entering the blood stream and causing a systemic infection. The macrophages are ideal places for the bacteria as they are able to elude the host's immune response in this. Indeed it has been evidenced that the longest duration of stay for slamonella within the host occurs in the macrophages.
However for the most part understanding of the murine salmonella species has been limited to the Nramp1 susceptible (Nramp1s) mouse strains i.e. the BALB/c and C57Bl/6. Macrophages from Nramp1s mice permit a much higher rate of serovar Typhimurium replication in vitro as well as in vivo as compared to Nramp1r (Nramp1 is functional) macrophages. While this has upuntil date allowed for observation of the diseased condition, the hosts (mice) invariably are most severly affected by the bacteteria considerabily limiting the scope of study.
The paper here however focuses on the novel Salmonella persistence model based on the mouse strain 129X1/SvJ (Nramp1r), which are typically resistant to the replication of the bacteria not succumbing easily to the virulence. Consequently the bacteria can be obtained from systemic sites even up to an year post infection which would help to increase the time spectrum of study if need be.
Clearly as intricate an adaptive mechanism as seen in the samlonella species would require the contribution of several genes and virulence factors.The invasion-associated genes are required for intestinal secretory and inflammatory disease, that intracellular survival in both the intestinal epithelium and macrophages is essential for