Abstract
Some bacterial pathogens modulate signaling pathways of eukaryotic cells in order to subvert the host response for their own benefit, leading to successful colonization and invasion. Pathogenic bacteria produce multiple compounds that generate favorable conditions to their survival and growth during infection in eukaryotic hosts. Many bacterial toxins can alter the cell cycle progression of host cells, impairing essential cellular functions and impeding host cell division. This review summarizes current knowledge regarding cyclomodulins, a heterogeneous family of bacterial effectors that induce eukaryotic cell cycle alterations. We discuss the mechanisms of actions of cyclomodulins according to their biochemical properties, providing examples of various cyclomodulins such as cycle inhibiting factor, γ-glutamyltranspeptidase, cytolethal distending toxins, shiga toxin, subtilase toxin, anthrax toxin, cholera toxin, adenylate cyclase toxins, vacuolating cytotoxin, cytotoxic necrotizing factor, Panton-Valentine leukocidin, phenol soluble modulins, and mycolactone. Special attention is paid to the benefit provided by cyclomodulins to bacteria during colonization of the host.
Highlights
We discuss the mechanisms of actions of cyclomodulins according to their biochemical properties, providing examples of various cyclomodulins such as cycle inhibiting factor, γ-glutamyltranspeptidase, cytolethal distending toxins, shiga toxin, subtilase toxin, anthrax toxin, cholera toxin, adenylate cyclase toxins, vacuolating cytotoxin, cytotoxic necrotizing factor, Panton-Valentine leukocidin, phenol soluble modulins, and mycolactone
An exposure of cells to a recombinant Vacuolating cytotoxin (VacA) was associated with the inhibition of cell growth and resulted in morphological changes and DNA fragmentation; a cell cycle analysis revealed a prolongation of the cell cycle progression in the gap phase 1 (G1) phase (Kimura et al, 1999; Cho et al, 2003). These findings indicate that VacA of H. pylori induces apoptosis in gastric epithelial cells and suggests that VacA might mediate the development of gastric diseases through a cell cycle arrest in the G1 phase (Cho et al, 2003)
Cyclomodulin structures and the mechanisms of bacteriainduced cell cycle alterations dramatically vary depending on the type of bacteria
Summary
Many pathogenic bacteria use sophisticated mechanisms to interfere with eukaryotic cells, to subvert the host response for their own benefit, and to colonize and invade the host tissues (Bhavsar et al, 2007; Alto and Orth, 2012). Tomato) as well as animal or human pathogens (e.g., Escherichia coli or Citrobacter rodentium) (Huibregtse and Rohde, 2014) They can interact with eukaryotic modulating factors involved in the assembly of actin filaments, as was shown for the Rho GTPases-activating toxins such as the Cytotoxic Necrotizing Factor 1 described in E. coli (Bhavsar et al, 2007; Lemichez and Aktories, 2013). Their activity can hijack host response despite the negative pressure of the host immune system and induce a belated apoptosis of host cells bearing pathogens, which results in an extension of the time lapse for their replication. Despite the importance of such findings, until recently, not much attention was paid to the investigation of the capacity of bacteria to alter the host cell cycle and to the analysis of this alteration on the outcome of the infection
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