[Mechanisms of immune and cytokine regulation in pathogenesis of ixodes tick-borne borreliosis].

BACKGROUND

Our aim was to identify the mechanisms of immune and cytokine regulation in different clinical forms of Ixodes tick-borne borreliosis.

METHODS

The clinical observations performed on 581 patients with erythemic (113 patients), non-eritemic (242 patients) forms of Ixodes tick- borne borreliosis and Borrelia co-infection tick-borne encephalitis (226 patients) in the manifestation of the disease. The examination included the determination of the levels of cytokines (interleukin 1β, 4, 8, and tumor necrosis factor α), indicators of cell immunity (CD3+, CD4+, CD8+) and phagocytosis (phagocytic index, the number of phagocytic neutrophils) during the height of the disease and during convalescence.

RESULTS

We established the correlations of cytokine production, lymphocyte subpopulations and phagocytosis. Revealed divergent immune-mediated mechanisms of pathogenesis, depending on the clinical forms of Ixodes tick-borne borreliosis and period of the disease, indicating the complexity and diversity of the immune system rearrangements. Cytokine regulation of immune response, mainly consists in the synthesis of the chemoattractant interleukin 8 production which is inversely correlated with the number of phagocytic neutrophils (r = -0.440, p < 0.001) with erythemic form of the disease, is directly correlated with the level of interleukin 4 (r = 0.313, p < 0.001) at non-eritemic form borreliosis, with the production of interleukin 1β (r = 0.367, p < 0.001) and interleukin 4 (r = 0.348, p < 0.001) in Borrelia co-infection tick-borne encephalitis.

CONCLUSION

In the manifestation of acute Borrelia infection, regardless of the clinicalform was typical Th1/Th2 type of immune response and then switches to the period of convalescence for Th1 (cellular) immune response in the form of erythemic Ixodes tick-borne borreliosis and Borrelia co-encephalitic tick-borne infection, and Th2 (humoral) immune response when non-eritemic form of the disease.