Abstract
Our organism is exposed to pathogens on a daily basis. Owing to this age-old interaction, both pathogen and host evolved strategies to cope with these encounters. Here, we focus on the consequences of the direct encounter of cells of the innate immune system with bacteria. First, we will discuss the bacterial strategies to counteract powerful reactive species. Our emphasis lies on the effects of hypochlorous acid (HOCl), arguably the most powerful oxidant produced inside the phagolysosome of professional phagocytes. We will highlight individual examples of proteins in gram-negative bacteria activated by HOCl via thiol-disulfide switches, methionine sulfoxidation, and N-chlorination of basic amino acid side chains. Second, we will discuss the effects of HOCl on proteins of the host. Recent studies have shown that both host and bacteria address failing protein homeostasis by activation of chaperone-like holdases through N-chlorination. After discussing the role of individual proteins in the HOCl-defense, we will turn our attention to the examination of effects on host and pathogen on a systemic level. Recent studies using genetically encoded redox probes and redox proteomics highlight differences in redox homeostasis in host and pathogen and give first hints at potential cellular HOCl signaling beyond thiol-disulfide switch mechanisms.
Highlights
Bacteria, and especially pathogenic bacteria, have to be able to effectively counter a number of different obstacles in order to survive
hypochlorous acid (HOCl) can be generated by immune cells, and we found cysteines of OxyR significantly more oxidized in phagocytized E. coli, when compared to non-phagocytized E. coli (Xie et al 2019)
The change in the cytosolic redox state of the immune cells was not dependent on HOCl, it was not sufficient to induce effective NETosis: Neutrophils treated with an MPO-inhibitor and activated with PMA or E. coli did still experience a change in their cellular redox potential, but were significantly less effective in NET formation
Summary
Especially pathogenic bacteria, have to be able to effectively counter a number of different obstacles in order to survive. Recent studies have shown that both host and bacteria address failing protein homeostasis by activation of chaperone-like holdases through N-chlorination.
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