Vulnificus Research Paper

V. vulnificus is a gram-negative marine bacterium that is present in high numbers of seafood (shellfish, raw oysters, clams, etc). Inflammation seen in wound infections, endotoxic shock, and tissue necrosis are characteristic symptoms associated with V. Vulnificus. These symptoms are attributed to the endotoxic activity of lipopolysaccharides (LPS) lending itself as a primary virulence factor in V. vulnificus. LPS is a fever-inducing polypeptide that also produces metabolic changes in the hypothalamus. In addition, LPS engenders a cytokine response in mice that contributes to the release and overproduction of tumor necrosis factor (TNF-a). In V. vulnificus cytokines are known to arouse inflammatory responses in the host; and it has been suggested that overactive cytokine induction to the site of infection may cause septic shock, trademark sign of V. vulnificus disease.
vulnificus via proinflammatories interleukin 6 (IL-6), IL-8, and tumor necrosis factor alpha, dominantly expressed during infection. In V. vulnificus when toll-like receptor 2 (TLR2) binds to the surface of a lipoprotein its is associated with the production of TNF-alpha and IL-6 (proinflammatories correlated with infection). Based on research conducted by McPherson, Watts, Simpson, and Oliver (cited in both review articles); direct, intravenous injection of V. Vulnificus LPS in mice resulted in a decrease in “mean arterial pressure and rapid death of the animal, implicating its role in symptom development and lethality” (1). Interestingly, when mice are introduced to LPS along with a nitric oxide synthase inhibitor (such as LDL cholesterol or estrogen), it is reported to diminish the endotoxic activity of LPS. This suggests nitric oxide production (dependent on TNF-alpha stimulation) is responsible for endotoxic shock seen in response to Vibrio vulnificus