Vibrio vulnificus-induced cell death of human mononuclear cells requires ROS-dependent activation of p38 and ERK 1/2 MAPKs.

Vibrio vulnificus is a Gram-negative bacterium that multiplies rapidly in host tissue and causes extensive tissue damage. Human peripheral blood mononuclear cells (PBMC) were shown to be readily killed by exposure to live V. vulnificus.

Vibrio vulnificus-induced death of Jurkat T-cells requires activation of p38 mitogen-activated protein kinase by NADPH oxidase-derived reactive oxygen species.

Vibrio vulnificus, a pathogenic bacterium causing primary septicemia, exhibited cytotoxicity towards Jurkat cells of T-lymphocytes through intracellular reactive oxygen species (ROS) production. Pretreatment of Jurkat T-cells with diphenyleneiodonium chloride (DPI) abolished V. vulnificus-induced ROS generation and bacterial ability to cause cell death.

Vibrio vulnificus IlpA-induced cytokine production is mediated by Toll-like receptor 2.

Vibrio vulnificus is a pathogenic bacterium causing primary septicemia, which follows a classical septic shock pathway, including an overwhelming inflammatory cytokine response. In this study, we identified a putative lipoprotein of V. vulnificus, encoded by the ilpA gene, as one of the surface proteins that specifically reacted with the antibodies raised against outer membrane proteins of V.

Modification of serine 392 is a critical event in the regulation of p53 nuclear export and stability.

Although it has been shown that phosphorylations of p53 serine its residues are critical events for the regulation of their function, the specific biological effects of each of these phosphorylations, especially at serine 392, remain to be elucidated. Serine 392 has been proposed to play a role in the tetramerization of p53 and in the enhancement of its DNA-binding affinity. However, this is not consistent with other reports showing that substitution of serine 392 does not disrupt p53 function.