Conti, J.; Gagliardi, T.; Arnaboldi, P.M.; Hale, S.J.; Skariah, S.; Sultan, A.A.; Mordue, D.G. Immune Mediators Important for a Protective Secondary Response to Babesia microti. Pathogens2024, 13, 123.
Conti, J.; Gagliardi, T.; Arnaboldi, P.M.; Hale, S.J.; Skariah, S.; Sultan, A.A.; Mordue, D.G. Immune Mediators Important for a Protective Secondary Response to Babesia microti. Pathogens 2024, 13, 123.
Conti, J.; Gagliardi, T.; Arnaboldi, P.M.; Hale, S.J.; Skariah, S.; Sultan, A.A.; Mordue, D.G. Immune Mediators Important for a Protective Secondary Response to Babesia microti. Pathogens2024, 13, 123.
Conti, J.; Gagliardi, T.; Arnaboldi, P.M.; Hale, S.J.; Skariah, S.; Sultan, A.A.; Mordue, D.G. Immune Mediators Important for a Protective Secondary Response to Babesia microti. Pathogens 2024, 13, 123.
Abstract
Babesia microti (B. microti), is a tick-transmitted protozoan parasite that infects red blood cells. It is the primary cause of human babesiosis in the US. It is also considered an emerging pathogen that continues to expand in terms of both numbers of cases and geograpical range. The severity of babesiosis can range from asymptomatic to fatal. Nevertheless, the mechanisms important for resolution of infection versus pathology remain largely unknown. In the current study we used a mouse model to evaluate factors important in protection from reinfection with B. microti following the clearance of a primary infection. Both B cell and CD4 T cell deficient mice failed to completely eliminate parasitemia 36 days post-infection following primary challenge. In the recall mouse model of infection, wild type or specific gene deleted mice were reinfected with the same strain of B. microti parasites 30-36 days after the initital primary infection, and the development of parasitemia was evaluated. Our results show that wild type mice were protected from reinfection with B. microti. In contrast, B cell and CD4 T cell deficient mice were only modestly impaired in their ability to protect against rechallenge as protection was more similar to reinfected wild type mice than naïve mice. However, one reinfected B cell deficient mice developed parasitemia levels similar to those observed in primary infection. Other factors including IFN-γ, inducible nitric oxide synthase (iNOS) and the adaptor protein MyD88 important for signling via IL-18 and IL-1 had no effect on rechallenge. Thus our study shows that infection with B. microti confers at least short term protection against rechallenge with the same parasite strain. Our data show that CD4 T cells make an important contribution to both primary and rechallenge infection with B. microti. They also suggest that antibody might play an important role in protection against reinfection or persistent infection. However, overall our results Our results suggest that no one aspect of the immune system is solely responsible for adequate protection against reinfection with B. microti.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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