Babesia bovis-Stimulated Macrophages Express Interleukin-1β, Interleukin-12, Tumor Necrosis Factor Alpha, and Nitric Oxide and Inhibit Parasite Replication In Vitro

Babesia bovis
DOI: 10.1128/iai.68.9.5139-5145.2000 Publication Date: 2002-07-27T09:58:18Z
ABSTRACT
The tick-transmitted hemoparasite Babesia bovis causes an acute infection that results in persistence and immunity against challenge cattle control the initial parasitemia. Resolution of with this protozoal pathogen is believed to be dependent on products activated macrophages (Mphi), including inflammatory cytokines nitric oxide (NO) its derivatives. B. stimulates inducible synthase (iNOS) production NO bovine Mphi, chemical donors inhibit growth vitro. However, induction Mphi by babesial parasites has not been described, antiparasitic activity produced bovis-stimulated definitively demonstrated. We report monocyte-derived expressed enhanced levels interleukin-1beta (IL-1beta), IL-12, tumor necrosis factor alpha are important for stimulating innate acquired pathogens. Furthermore, a lipid fraction bovis-infected erythrocytes stimulated iNOS expression Mphi. Cocultures either contact or physically separated resulted reduced parasite viability. response was only partially responsible inhibition, suggesting additional factors contribute inhibition replication. These findings demonstrate induces immune capable controlling replication could potentially result host survival persistence.
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