Immunity & infection
Background: Salmonella enterica serovar Typhimurium (S. Typhimurium) is Gram-negative bacterium and an important is a worldwide problem that cause of bacterial foodborne and the leading cause of invasive non-typhoid disease, mainly in children. To infect the host, S. Typhimurium has several virulence factors encoded in chromosomal cluster known as Salmonella Pathogenicity Islands (SPI). The most important are SPI-1 and SPI-2, which allow the infection of intestinal epithelial cells and the survival inside phagocytic cells, respectively. The initial innate immune response is the migration of neutrophils to the site of infection playing an important role by restricting the bacterial growth and dissemination. These cells attack the bacteria using different mechanisms, however, these are not enough to avoid S. Typhimurium dissemination. For this reason, it is possible that S. Typhimurium evade the function of neutrophils. Objectives: To evaluate the neutrophil response against S. Typhimurium. Methods: We isolate bone marrow derived neutrophils from male and female C57BL/6 wild type mice and evaluate the infection of the neutrophils, intracellular bacterial survival and replication, ROS and cytokine production and NETs release against S. Typhimurium infection. We evaluate these parameters with the wild type strain, and two mutant strain: Dspi-1 and Dspi-2, in order to evaluate the immune response mediated by this type of cell and evaluate if the virulence factor encoded in this SPI are relevant during the infection of neutrophils. Conclusion: The immune response of Ly6G+ against S. Typhimurium infection depends on the SPI that the bacterium possess and the sex of the mice.