IL-26 mediated human cell activation and antimicrobial activity against Borrelia burgdorferi

Lyme disease is an inflammatory disease caused by infection with Borrelia burgdorferi (Bb). Inflammatory sequelae of Bb infection appear to be refractory to antibiotics. An antimicrobial peptide with the ability to bind the DNA in the tissue could serve as a viable option of treatment for chronic complications of Lyme borreliosis. DNA of Bb can remain in tissues causing a prolonged inflammatory response that lead to chronic joint pain. Here we examined the effect of IL-26, a newly reported antimicrobial protein, against Bb DNA.

An antimicrobial effect of IL-26 on the spirochete was observed. In human macrophages, IL-26 treated cells showed an increase in IRF activation upon Bb stimulation. Moreover, IL-26 treated macrophages showed an increased in phagocytic activity compared to untreated cells. Although no Bb DNA degradation was observed using a TUNEL assay run in an agarose gel, a Comet assay on whole bacteria showed cellular and Bb DNA degradation by IL-26.

Our results showed that IL-26 (monomer and dimer) has not only the potential to control Bb growth in vitro, but it also enhances the anti-borrelial response of human macrophages. Further research aiming to characterize the role of IL-26 in controlling other aspects of the inflammatory response that could provide insight of its potential therapeutic applications are needed.

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