Figure 1.

NTS intestinal immune response. NTS is a fecal‐oral pathogen, which thrives in the inflamed intestine. Tissue invasion in the distal intestine can be via direct invasion, uptake by M cells, or through paracellular spaces. Uptake by dendritic cells can initiate inflammation through the IL‐23/IL‐17 axis. Th17 cells promote neutrophil influx via the induction of neutrophil chemokines. NTS is able to persist within the Salmonella‐containing vacuole of macrophages, whereas neutrophils are efficient at NTS clearance. Systemic dissemination to draining lymph nodes is through CD18⁺ phagocytes. During experimental malaria, NTS colonization resistance is lowered, although it is unclear if there is an increase in tissue invasion. Regardless, inflammation (with reduced PMN influx) is reduced due to increased IL‐10 concentrations. However, the role of IL‐10, and potentially HO‐1, on intestinal neutrophil function and role for increased systemic dissemination are unclear