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TNF–α, IL–6, and IL–10 in dogs with Babesia canis infection

Objective Canine babesiosis is a tick – borne disease of worldwide importance. Babesiosis can cause severe tissue hipoxia with consequent widespread tissue damage and probable release of inflammatory mediators (Lobetti, 1998). The systemic inflammatory response syndrome (SIRS) that precedes multiple organ dysfunction syndrome (MODS) is caused by excessive release of inflammatory mediators. The major mediators are cytokines, nitric oxide, free oxygen radicals, eicosanoids, and platelet – activating factor (Purvis and Kirby, 1994). Cytokines are low molecular weight, soluble proteins produced by immunocompetent cells that are divided on proinflammatory (such as TNF – α, IL – 1, IL – 6, IL -8) and antiinflammatory cytokines (IL – 4, IL – 10, IL – 13). Goris et al. (1985) hypothesized that MODS develops as the consequence of dysregulation of proinflammatory and anti-inflammatory mechanisms resulting in overwhelming auto-destructive inflammation. Markedly elevated serum concentrations of TNF, IFN-g, IL-2, IL-6, and adhesion molecules occur during the acute phase of human Babesia. microti infection (Shaio and Lin, 1998). We investigated the serum levels of the TNF – α, IL – 6, and IL – 10 in dogs naturally infected with Babesia canis. Although there are no significant differences between groups, results obtained in this study suggested that cytokines play important roles in pathophysiological events, and probably babesial symptoms are thought to be mediated by cytokines.

canine babesiosis; cytokines; TNF–α; IL–6; and IL–10

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