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  The cross-species immunity during acute Babesia co-infection in mice

Zafar, I., Galon, E. M., Kondoh, D., Efstratiou, A., Li, J., Ji, S., et al. (2022). The cross-species immunity during acute Babesia co-infection in mice. Frontiers in Cellular and Infection Microbiology, 12: 885985. doi:10.3389/fcimb.2022.885985.

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 Creators:
Zafar, Iqra, Author
Galon, Eloiza May, Author
Kondoh, Daisuke, Author
Efstratiou, Artemis1, 2, Author           
Li, Jixu, Author
Ji, Shengwei, Author
Liu, Mingming, Author
Li, Yongchang, Author
Hasegawa, Yae, Author
Zhou, Jinlin, Author
Xuan, Xuenan, Author
Affiliations:
1Emmy Noether Research Group Evolutionary Immunogenomics, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_2616693              
2IMPRS for Evolutionary Biology, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_1445639              

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Free keywords: Babesia microti,Babesia rodhaini, acute stage, co-infection, babesiosis, tick-borne infection, innateimmunity, oxidative stress
 Abstract: Babesiosis causes high morbidity and mortality in immunocompromised individuals. An earlier study suggested that lethal Babesia rodhaini infection in murine can be evaded by Babesia microti primary infection via activated macrophage-based immune response during the chronic stage of infection. However, whether the same immune dynamics occur during acute B. microti co-infection is not known. Hence, we used the mouse model to investigate the host immunity during simultaneous acute disease caused by two Babesia species of different pathogenicity. Results showed that B. microti primary infection attenuated parasitemia and conferred immunity in challenge-infected mice as early as day 4 post-primary infection. Likewise, acute Babesia co-infection undermined the splenic immune response, characterized by the significant decrease in splenic B and T cells leading to the reduction in antibody levels and decline in humoral immunity. Interestingly, increased macrophage and natural killer splenic cell populations were observed, depicting their subtle role in the protection. Pro-inflammatory cytokines (i.e. IFN-γ, TNF-α) were downregulated, while the anti-inflammatory cytokine IL-10 was upregulated in mouse sera during the acute phase of Babesia co-infection. Herein, the major cytokines implicated in the lethality caused by B. rodhaini infection were IFN- γ and IL-10. Surprisingly, significant differences in the levels of serum IFN- γ and IL-10 between co-infected survival groups (day 4 and 6 challenge) indicated that even a two-day delay in challenge infection was crucial for the resulting pathology. Additionally, oxidative stress in the form of reactive oxygen species contributed to the severity of pathology during acute babesiosis. Histopathological examination of the spleen showed that the erosion of the marginal zone was more pronounced during B. rodhaini infection, while the loss of cellularity of the marginal zone was less evident during co-infection. Future research warrants investigation of the roles of various immune cell subtypes in the mechanism involved in the protection of Babesia co-infected hosts.

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Language(s): eng - English
 Dates: 2022-02-282022-04-272022-05-27
 Publication Status: Published online
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: DOI: 10.3389/fcimb.2022.885985
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Title: Frontiers in Cellular and Infection Microbiology
  Other : Front. Cell. Infect. Microbiol.
  Abbreviation : fcimb
Source Genre: Journal
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Publ. Info: Lausanne : Frontiers Media
Pages: - Volume / Issue: 12 Sequence Number: 885985 Start / End Page: - Identifier: ISSN: 2235-2988
CoNE: https://pure.mpg.de/cone/journals/resource/2235-2988