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Infection and Immunity, September 2000, p. 5139-5145, Vol. 68, No. 9
Program in Vector-Borne Diseases, Department
of Veterinary Microbiology and Pathology, Washington State University,
Pullman, Washington 99164-70401;
Institute of Neuroscience (CONICET), CC 137, RA-1663, San
Miguel, Argentina2; and Veterinary
Infectious Disease Organization, University of Saskatchewan, Saskatoon,
Saskatchewan, Canada3
Received 24 February 2000/Returned for modification 12 April
2000/Accepted 20 June 2000
The tick-transmitted hemoparasite Babesia bovis causes
an acute infection that results in persistence and immunity against challenge infection in cattle that control the initial parasitemia. Resolution of acute infection with this protozoal pathogen is believed
to be dependent on products of activated macrophages (M
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Babesia bovis-Stimulated Macrophages
Express Interleukin-1
, Interleukin-12, Tumor Necrosis Factor Alpha,
and Nitric Oxide and Inhibit Parasite Replication In
Vitro
), including
inflammatory cytokines and nitric oxide (NO) and its derivatives.
B. bovis stimulates inducible nitric oxide synthase (iNOS)
and production of NO in bovine M, and chemical donors of NO inhibit
the growth of B. bovis in vitro. However, the induction of
inflammatory cytokines in M by babesial parasites has not been
described, and the antiparasitic activity of NO produced by B. bovis-stimulated M has not been definitively demonstrated. We
report that monocyte-derived M activated by B. bovis
expressed enhanced levels of inflammatory cytokines interleukin-1
(IL-1), IL-12, and tumor necrosis factor alpha that are important
for stimulating innate and acquired immunity against protozoal
pathogens. Furthermore, a lipid fraction of B. bovis-infected erythrocytes stimulated iNOS expression and NO
production by M. Cocultures of M and B. bovis-infected erythrocytes either in contact or physically
separated resulted in reduced parasite viability. However, NO produced
by bovine M in response to B. bovis-infected
erythrocytes was only partially responsible for parasite growth
inhibition, suggesting that additional factors contribute to the
inhibition of B. bovis replication. These findings
demonstrate that B. bovis induces an innate immune response
that is capable of controlling parasite replication and that could
potentially result in host survival and parasite persistence.
*
Corresponding author. Mailing address: Program in
Vector-Borne Diseases, Department of Veterinary Microbiology and
Pathology, Washington State University, Pullman, WA 99164-7040. Phone:
(509) 335-6067. Fax: (509) 335-8529. E-mail:
wbrown{at}vetmed.wsu.edu.
Infection and Immunity, September 2000, p. 5139-5145, Vol. 68, No. 9
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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