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Abstract
Microbes with the capability to survive in the host tissue and efficiently subvert its innate immune responses can cause various health hazards. There is an inherent need to understand microbial infection patterns and mechanisms in order to develop efficient therapeutics. Microbial pathogens display host specificity through a complex network of molecular interactions that aid their survival and propagation. Co-infection states further lead to complications by increasing the microbial burden and risk factors. Quantitative proteomics based approaches and post-translational modification analysis can be efficiently applied to gain an insight into the molecular mechanisms involved. The measurement of the proteome and post-translationally modified proteome dynamics using mass spectrometry, results in a wide array of information, such as significant changes in protein expression, protein abundance, the modification status, the site occupancy level, interactors, functional significance of key players, potential drug targets, etc. This mini review discusses the potential of proteomics to investigate the involvement of post-translational modifications in bacterial pathogenesis and host–pathogen interactions.
Highlights
Diverse microorganisms such as bacteria, viruses or protozoans commonly pose as “pathogens.” They have the capacity to survive in the host tissue, adapt to and suppress the host innate immune responses, constantly challenging human health and welfare
The following sections in this review describe the implications of various post-translational modifications (PTMs) on bacterial virulence and the proteomics technologies available to investigate such events along with the associated technical challenges
Pathogenic strains such as Streptococcus spp., Pseudomonas aeruginosa, Mycobacteria, Yersinia spp., to name a few, employ Ser/Thr kinasemediated host–pathogen interactions to mediate diverse cellular networks required for adhesion to and invasion of the host
Summary
Diverse microorganisms such as bacteria, viruses or protozoans commonly pose as “pathogens.” They have the capacity to survive in the host tissue, adapt to and suppress the host innate immune responses, constantly challenging human health and welfare. The existence of Hanks-type Ser/Thr kinases in bacteria has generated a huge interest in the field of infection biology Pathogenic strains such as Streptococcus spp., Pseudomonas aeruginosa, Mycobacteria, Yersinia spp., to name a few, employ Ser/Thr kinasemediated host–pathogen interactions to mediate diverse cellular networks required for adhesion to and invasion of the host. To control the timing of effector proteinmediated functions, S. enterica SopE, that targets RHO-GTPases leading to membrane ruffling, is ubiquitinated and degraded earlier than the protein SptP that prevents membrane ruffling after invasion (Kubori and Galan, 2003). Shigella flexneri effector protein OspF, a phosphothreonine lyase, interferes with host signaling by irreversibly dephosphorylating MAP kinases In this PTM termed eliminylation, the phosphate and the hydroxyl group of threonine is removed, thereby preventing any future phosphorylation. In a systematic study of H. pylori glycoproteins, 26 proteins with diverse roles in pathogenesis were identified, arguably indicating a broader array of mechanisms for glycosylation-based virulence (Champasa et al, 2013)
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