Cellular Immunity, but Not Gamma Interferon, Is Essential for Resolution of<i>Babesia microti</i>Infection in BALB/c Mice

Clawson, Marion; Paciorkowski, Natalia; Rajan, T. V.; Vake, Carson La; Pope, Conny; Vake, Morgan La; Wikel, Stephen K.; Krause, Peter J.; Radolf, Justin D.

doi:10.1128/iai.70.9.5304-5306.2002

Cited by 41 publications

(45 citation statements)

References 24 publications

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“…The important roles of IFN-␥ and B and T lymphocytes as the key inducers of the immune effector mechanisms needed for initial control of the rodent Babesia infection are supported by the finding that IFN-␥ Ϫ/Ϫ and SCID mice are unable to resolve the primary infection (2,19,28,57). Here, IFN-␥ Ϫ/Ϫ and SCID mice were completely protected against the lethality of B. rodhaini infection, resulting in the survival of all mice.…”

Section: Discussionmentioning

confidence: 65%

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

Terkawi

Nishikawa

et al. 2012

Infect Immun

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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-

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Section: Discussionmentioning

confidence: 65%

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

Terkawi

Nishikawa

et al. 2012

Infect Immun

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“…33,[43][44][45] In P. chabaudi infection, ovariectomized female mice exhibit reduced production of the cytokines IL-12 and IFN-γ, leading to increased susceptibility. 24 However, in our study, ovariectomy in female mice caused low peak parasitemia and contributed to resistance against B. microti infection.…”

Section: Discussionmentioning

confidence: 66%

“…strain WA1, and susceptible mouse models. [23][24][25][26][27][28][29] Aguilar-Delfin and others reported a sex-related influence on resistance to acute Babesia sp. strain WA1 infection in C57BL/6 mice, with males being more resistant than females.…”

mentioning

confidence: 99%

Effect of Sex Steroids on Babesia microti Infection in Mice

Sasaki¹,

Fujii²,

Iwamoto³

et al. 2013

The American Society of Tropical Medicine and Hygiene

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Abstract. Sex-based-differences are known to affect susceptibility to protozoan infections, but their effects on parasitemia and clinical symptoms in Babesia infections remain unclear. We examined the sex-based susceptibility of various mouse strains to Babesia microti Munich strain infection. In all strains, male mice exhibited significantly higher peak parasitemia and more severe anemia than female mice. Testosterone and estradiol-17β treatment caused an increase in parasitemia and aggravation of anemia. Orchidectomized male mice receiving testosterone exhibited smaller splenic macrophage populations three days after infection, smaller B cell populations 10 days after infection, and reduced splenic tumor necrosis factor-α and interferon-γ mRNA expression than mice that did not receive testosterone. Mice receiving estradiol-17β did not exhibit immunosuppressive effects. Thus, a weakened and delayed innate immunity response may lead to acquired immunity failure. The results suggested that testosterone directly affects T or B cells, leading to delayed acquired immunity, dramatically increased parasitemia, and severe anemia.

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“…(24). More recently, it has been found that IFN-␥ is crucial for controlling parasitemia at early stages of infection in the model of KR1 B. microti in BALB/c mice (11).…”

Section: Discussionmentioning

confidence: 99%

Resistance to Acute Babesiosis Is Associated with Interleukin-12- and Gamma Interferon-Mediated Responses and Requires Macrophages and Natural Killer Cells

Aguilar-Delfín¹,

Wettstein

Persing

2003

Infect Immun

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We examined the role of the cytokines gamma interferon (IFN-γ) and interleukin-12 (IL-12) in the model of acute babesiosis with the WA1 Babesia. Mice genetically deficient in IFN-γ-mediated responses (IFNGR2KO mice) and IL-12-mediated responses (Stat4KO mice) were infected with the WA1 Babesia, and observations were made on the course of infection and cytokine responses. Levels of IFN-γ and IL-12 in serum increased 24 h after parasite inoculation. The augmented susceptibility observed in IFNGR2KO and Stat-4KO mice suggests that the early IL-12- and IFN-γ-mediated responses are involved in protection against acute babesiosis. Resistance appears to correlate with an increase in nitric oxide (NO) production. In order to assess the contribution of different cell subsets to resistance against the parasite, we also studied mice lacking B cells, CD4+ T cells, NK cells, and macrophages. Mice genetically deficient in B lymphocytes or CD4+ T lymphocytes were able to mount protective responses comparable to those of immunosufficient mice. In contrast, in vivo depletion of macrophages or NK cells resulted in elevated susceptibility to the infection. Our observations suggest that a crucial part of the response that protects from the pathogenic Babesia WA1 is mediated by macrophages and NK cells, probably through early production of IL-12 and IFN-γ, and induction of macrophage-derived effector molecules like NO

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Cellular Immunity, but Not Gamma Interferon, Is Essential for Resolution ofBabesia microtiInfection in BALB/c Mice

Cited by 41 publications

References 24 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

Effect of Sex Steroids on Babesia microti Infection in Mice

Resistance to Acute Babesiosis Is Associated with Interleukin-12- and Gamma Interferon-Mediated Responses and Requires Macrophages and Natural Killer Cells

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