In this paper, the researchers hypothesized that mast cells help protect against invasive Streptococcus skin infections by expression of the antimicrobial peptide cathelicidin. To test this hypothesis, the group challenged wild-type mice, mast cell deficient mice, and mast cell deficient mice that received either wild-type mast cells or cathelicidin mutant mast cells with invasive group A Streptococcus species. A small amount of the group A Streptococcus was injected into the skin of the mice and resulting lesion size was measured after 72 hours. The wild type mice and the mice that had reconstituted wild type mast cells had the smallest skin lesion size and had fewer instances of bacterial presence within the spleen. In contrast, the mast-cell deficient mice had much larger skin lesions when compared to wild type mice, along with an increased bacterial presence in the spleen. Most importantly, even with the introduction of cathelicidin mutant mast cells into mast cell deficient mice, the lesion size was larger in comparison to the wild type mice. This suggests that cathelicidin is important in the protection of the mice from group A Streptococcus infections because cathelicidin is an antimicrobial peptide that kills bacteria intercellularly and prevents the bacteria from entering the blood.
Figure 1. Size of GAS induced lesions of wild-type mice, mast cell deficient mice, and reconstituted mice visualized in (a) and compared in (b,c) demonstrate the importance of cathelcidin producing mast cells in protecting the blood (d) from bacteria after infection. As positive controls, wild-type mice and reconstituted wild-type mice were included in the assay to demonstrate the normal immune response to the infection. Mast cell deficient mice that were not reconstituted with mast cells served as the negative control, as they should respond to the infection as if the no mast cells were present.
This paper could have been improved by better defining the specific antimicrobial domain or function of cathelicidin; instead they referred to domains but did not provide a diagram. The research alluded to conflicting ideas of intracellular vs. extracellular killing of bacteria by cathelicidin, but claimed that their work supported intracellular mechanisms. In further research, it would be interesting to study mast cell produced cathelicidin’s domains in attempts to identify mechanism of action as well as the general effectiveness of the antimicrobial peptide as an extracellular agent.