NDLI: Macrophages Are the Determinant of Resistance to and Outcome of Nonlethal Babesia microti Infection in Mice

Content Provider	PubMed Central
Author	Alaa, Terkawi Mohamad Cao, Shinuo Herbas, Maria S. Nishimura, Maki Yan, Li Moumouni, Paul Franck Adjou Hamid, Pyarokhil Asadullah Kondoh, Daisuke Kitamura, Nobuo Nishikawa, Yoshifumi Kato, Kentaro Yokoyama, Naoaki Zhou, Jinlin Suzuki, Hiroshi Igarashi, Ikuo Xuan, Xuenan
Editor	Adams, J. H.
Copyright Year	2015
Abstract	In the present study, we examined the contributions of macrophages to the outcome of infection with Babesia microti, the etiological agent of human and rodent babesiosis, in BALB/c mice. Mice were treated with clodronate liposome at different times during the course of B. microti infection in order to deplete the macrophages. Notably, a depletion of host macrophages at the early and acute phases of infection caused a significant elevation of parasitemia associated with remarkable mortality in the mice. The depletion of macrophages at the resolving and latent phases of infection resulted in an immediate and temporal exacerbation of parasitemia coupled with mortality in mice. Reconstituting clodronate liposome-treated mice at the acute phase of infection with macrophages from naive mice resulted in a slight reduction in parasitemia with improved survival compared to that of mice that received the drug alone. These results indicate that macrophages play a crucial role in the control of and resistance to B. microti infection in mice. Moreover, analyses of host immune responses revealed that macrophage-depleted mice diminished their production of Th1 cell cytokines, including gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α). Furthermore, depletion of macrophages at different times exaggerated the pathogenesis of the infection in deficient IFN-γ−/− and severe combined immunodeficiency (SCID) mice. Collectively, our data provide important clues about the role of macrophages in the resistance and control of B. microti and imply that the severity of the infection in immunocompromised patients might be due to impairment of macrophage function.
Related Links	http://dx.doi.org/10.1128/iai.02128-14
Ending Page	16
Page Count	9
Starting Page	8
File Format	PDF
ISSN	00199567
e-ISSN	10985522
Journal	Infection and Immunity
Issue Number	1
Volume Number	83
Language	English
Publisher	American Society for Microbiology
Publisher Date	2015-01-01
Access Restriction	Open
Rights Holder	American Society for Microbiology
Subject Keyword	Immunology Microbiology Parasitology Infectious Diseases Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Infectious Diseases Parasitology Immunology Microbiology

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