Environmental Regulation of Yersinia Pathophysiology

Abstract

Hallmarks of Yersinia pathogenesis include the ability to form biofilms on surfaces, the ability to establish close contact with eukaryotic target cells and the ability to hijack eukaryotic cell signaling and take over control of strategic cellular processes. Many of these virulence traits are already well-described. However, of equal importance is knowledge of both confined and global regulatory networks that collaborate together to dictate spatial and temporal control of virulence gene expression. This review has the purpose to incorporate historical observations with new discoveries to provide molecular insight into how some of these regulatory mechanisms respond rapidly to environmental flux to govern tight control of virulence gene expression by pathogenic Yersinia.

Toxin–Antitoxin Systems and their Role in Maintaining the Pathogenic Potential of Causative Agents of Sapronoses

“…Sapronoses (from Greek sapros, meaning "putrid", and nosos, "disease") are diseases transmitted to humans from abiotic substrates of the environment (soil, water, decaying plants, animal feces, etc.) [1].…”

“…The issue of survival of pathogenic microorganisms and the ways of their existence in the environment has become one of the most urgent problems in modern microbiology. The endemism of sapronoses (from Greek "sapros" = decaying; "sapron" -in ecology -a decaying organic substrate) is associated with the ability of their causative agents to survive in natural ecosystems [1,2]. The most important characteristics of causative agents of the sapronoses are -The ability of the pathogens to grow and replicate in these substrata (i.e saprophytically) [2].…”

“…Thus these microorganisms are a distinctive type of infectious agent: they carry on dual ways of life: parasitic (pathogenic, at the temperature of a host organism) and saprophytic (in an abiotic substrate at ambient temperature) [1,2].…”

Urease Expression in Pathogenic Yersinia enterocolitica Strains of Bio-Serotypes 2/O:9 and 1B/O:8 Is Differentially Regulated by the OmpR Regulator

“…Yersinia enterocolitica synthesizes numerous virulence factors that are active at different stages of an infection and whose expression is altered according to the diverse growth conditions experienced by these bacteria in mammalian hosts (Straley and Perry, 1995;Marceau, 2005;Erhardt and Dersch, 2015;Chen et al, 2016). It was previously demonstrated that a functional urease is essential for the survival of Y. enterocolitica O:9 during passage through the stomach (De Koning-Ward and Robins-Browne, 1995;Young et al, 1996), and is also necessary for full virulence in oral infections in the rat model (Gripenberg-Lerche et al, 2000).…”

The Cyclic AMP Receptor Protein Regulates Quorum Sensing and Global Gene Expression in Yersinia pestis During Planktonic Growth and Growth in Biofilms

“…To interpret changes in these environments, Y. pestis encodes more than two dozen two-component systems (2), three quorum sensing systems (3), and additional transcriptional regulators with specialized functions. This sensor network allows Y. pestis to translate changes in its extracellular environment into altered gene expression to promote growth and pathogenesis (4,5). The 3',5'-cyclic adenosine monophosphate (cAMP) receptor protein (Crp) is required for Y. pestis virulence in mice (6).…”