Abstract
Ubiquitination of proteins, like phosphorylation and acetylation, is an important regulatory aspect influencing numerous and various cell processes, such as immune response signaling and autophagy. The study of ubiquitination has become essential to learning about host–pathogen interactions, and a better understanding of the detailed mechanisms through which pathogens affect ubiquitination processes in host cell will contribute to vaccine development and effective treatment of diseases. Pathogenic bacteria (e.g., Salmonella enterica, Legionella pneumophila and Shigella flexneri) encode many effector proteins, such as deubiquitinating enzymes (DUBs), targeting the host ubiquitin machinery and thus disrupting pertinent ubiquitin-dependent anti-bacterial response. We focus here upon the host ubiquitination system as an integral unit, its interconnection with the regulation of inflammation and autophagy, and primarily while examining pathogens manipulating the host ubiquitination system. Many bacterial effector proteins have already been described as being translocated into the host cell, where they directly regulate host defense processes. Due to their importance in pathogenic bacteria progression within the host, they are regarded as virulence factors essential for bacterial evasion. However, in some cases (e.g., Francisella tularensis) the host ubiquitination system is influenced by bacterial infection, although the responsible bacterial effectors are still unknown.
Highlights
Competition between host defense mechanisms and pathogens’ effective tools has been observed since ancient times
TNF binds tumor necrosis factor receptor 1 (TNFR1) to trigger a cascade of signaling reactions leading to activation of the nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, where Ub linkage is important for NF-κB functioning [40]
Ubiquitin and enzymes associated with ubiquitination machinery constitute an important component of signaling pathways in the immune host response to pathogen infection
Summary
Competition between host defense mechanisms and pathogens’ effective tools has been observed since ancient times. The immune system of the host organism is regulated by complex metabolic and signaling pathways, including, but not limited to, a network of post-translational modifications. Should any of these important pathways be impaired, such as by efficient mechanisms of pathogens, the immune balance is disrupted and pathogens may become more successful. During their development, pathogenic organisms have acquired several mechanisms by which they can influence the immune response of the host and escape their defense mechanisms and prevent themselves from destruction. The importance of investigating this post-translational modification in the context of the host–pathogen interaction is constantly increasing, due to the availability of new and sensitive approaches for analyzing ubiquitination
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