Isolation of a Human Erythrocyte-Adapted Substrain of Babesia rodhaini and Analysis of the Merozoite Surface Protein Gene Sequences

Kawabuchi, Takako; Tsuji, Masayoshi; Kuwahara, Satoko; Nishida, Atsumi; Shimofurutachi, Tadahisa; Oka, Hideki; Ishihara, Chiaki

doi:10.1292/jvms.67.901

Cited by 4 publications

(3 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This protection is mainly due to T-cell-mediated immunity in the spleen (28,44). In contrast, B. rodhaini causes a more severe disease, resulting in 100% mortality (34). Interestingly, mice that had a prior infection with B. microti are known to be protected against challenge infection by B. rodhaini Antwerp strain, with a survival rate of up to 83% (58).…”

mentioning

confidence: 99%

Macrophages Are Critical for Cross-Protective Immunity Conferred by Babesia microti against Babesia rodhaini Infection in Mice

Terkawi

Nishikawa

et al. 2012

Infect Immun

View full text Add to dashboard Cite

Although primary infection of mice with Babesia microti has been shown to protect mice against subsequent lethal infection by Babesia rodhaini, the mechanism behind the cross-protection is unknown. To unravel this mechanism, we investigated the influence of primary infection of mice with nonlethal B. microti using different time courses on the outcome of subsequent lethal B. rodhaini infection. Simultaneous infections of mice with these parasites resulted in rapid increases in parasitemia, with 100% mortality in BALB/c mice, as observed with control mice infected with B. rodhaini alone. In contrast, mice with acute, resolving, and chronic-phase B. microti infections were completely protected against B. rodhaini, resulting in low parasitemia and no mor-

show abstract

mentioning

confidence: 99%

Macrophages Are Critical for Cross-Protective Immunity Conferred by Babesia microti against Babesia rodhaini Infection in Mice

Terkawi

Nishikawa

et al. 2012

Infect Immun

View full text Add to dashboard Cite

show abstract

“…Babesia rodhaini is known to be a lethal rodent Babesia that has been used in many studies as economically laboratory model to understand the host immune response as well as the requirements of an effective vaccine (5). Human erythrocytes are susceptible to infection by this parasite (6).…”

Section: Research Notementioning

confidence: 99%

C3 contributes to the cross‐protective immunity induced by Babesia gibsoni phosphoriboprotein P0 against a lethal B. rodhaini infection

Terkawi

Zhang

Jia

et al. 2008

Parasite Immunology

View full text Add to dashboard Cite

We have studied the impact of complement component 3 (C3) deficiency on the progression of lethal Babesia rodhaini infection in immune mice. A B. gibsoni ribosomal phosphoprotein P0 (BgP0) previously reported to be a cross-protective antigen against Babesia infection was used to immunize C57BL/6 wild-type (WT) and C3-deficient (C3-/-) mice. Test mice were immunized intraperitoneally (i.p.) with recombinant BgP0 (rBgP0), while controls either were immunized with PBS or did not receive any immunization. Following the immunization regime, test WT mice induced a specifically strong humoral response consisting of mixed immunoglobulins IgG1 and IgG2 associated with high production of IFN-gamma in the supernatant of splenocytes. While test C3-/- mice had significantly decreased total IgG, IgG1 and IgG2b responses, the secretions of IL-12 and IFN-gamma tended to be lower than those in WT mice. Furthermore, partial protection was only observed in rBgP0-immunized WT mice but not in C3-/- mice or controls. Indeed, rBgP0-immunized WT mice showed significant reductions in the initiation of parasitaemia correlated with delayed mortalities and considerable survival rates. Taken together, our results indicate that cross-protection was impaired in C3-/- mice in view of the decrease in the antibody responses and cytokine production and the high susceptibility to infection.

show abstract

“…Both species belong to the “small group” of Babesia , characterized by the relatively smaller size (1.0-2.5 µm) of trophozoites ( Homer et al., 2000 ). Babesia rodhaini has the potential to infect human erythrocytes ( Kawabuchi et al., 2005 ) and inoculation of even a single parasite leads to 100% mortality in mice ( Clark, 2001 ). In contrast, B. microti (Munich strain) causes a self-limiting disease in mice that resolves eventually ( Igarashi et al., 1999 ).…”

Section: Introductionmentioning

confidence: 99%

The Cross-Species Immunity During Acute Babesia Co-Infection in Mice

Zafar

Galon

Kondoh

et al. 2022

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

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.

show abstract

Isolation of a Human Erythrocyte-Adapted Substrain of Babesia rodhaini and Analysis of the Merozoite Surface Protein Gene Sequences

Cited by 4 publications

References 35 publications

Macrophages Are Critical for Cross-Protective Immunity Conferred by Babesia microti against Babesia rodhaini Infection in Mice

Macrophages Are Critical for Cross-Protective Immunity Conferred by Babesia microti against Babesia rodhaini Infection in Mice

C3 contributes to the cross‐protective immunity induced by Babesia gibsoni phosphoriboprotein P0 against a lethal B. rodhaini infection

The Cross-Species Immunity During Acute Babesia Co-Infection in Mice

Contact Info

Product

Resources

About