Impact of Taurine on Innate and Adaptive Immunity as the Result of HOCl Neutralization.

Abstract

Taurine, the most abundant free amino-acid in the human body, reaches particularly high concentrations in inflammatory cells, such as neutrophils. At the site of inflammation, taurine is a major scavenger of hypochlorous acid (HOCl) generated by activated neutrophils. This reaction results in formation of taurine chloramine (TauCl), the less toxic agent with anti-inflammatory and anti-microbial properties. Therefore, the primary role of taurine in inflammation is protecting self-components of the immune system from HOCl-mediated oxidative damage. HOCl, the major product of the neutrophil myeloperoxidase (MPO)–halide system, is not only a key molecule of the host defense against microbes but it is also responsible for tissue injury, when generated in excess. Importantly, HOCl-oxidative modification of enzymes alters their biological functions. Moreover, chlorination of proteins enhances their immunogenecity, suggesting adjuvant-like effect of HOCl. Herein, we investigated biological effects of taurine interaction with HOCl in two experimental systems. In vitro we tested the impact of taurine on HOCl-dependent inhibition of alpha1-antitrypsin (A1AT), an inhibitor of neutrophil enzymes involved in inflammation. In vivo we measured humoral response to non-self, and self-proteins, chlorinated in the presence of taurine. Our results indicate that taurine conversion of HOCl to TauCl is associated with amelioration of biological effects of protein chlorination. In conclusion, a number of data indicate that taurine is a pivotal component of innate and adaptive immune system. However, immunoregulatory activities of endogenous taurine and TauCl are masked in vivo due to the redundancy of the immune system.