Susceptibility of Desulfovibrio desulfuricans intestinal strains to sulfasalazine and its biotransformation products.

BACKGROUND: Desulfovibrio desulfuricans intestinal bacteria may contribute to toxic hydrogen sulfide production in the human gut. Our objective was to examine whether the D. desulfuricans strains isolated from the human body are susceptible to sulfasalazine (SAS) and the products of its biotransformation, i.e. 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP), in order to determine the relationship between the strains' susceptibility to SAS and their ability to reduce the azo bond within this drug. MATERIAL/METHODS: Six wild strains of D. desulfuricans (isolated from feces and biopsy specimens from patients with colitis ulcerosa, Crohn's disease, irritable bowel syndrome, colonic diverticula, primary biliary cirrhosis, or tubular adenomas of the colon) were cultured in the presence of SAS, 5-ASA, and SP. Growth inhibition coefficients were compared with coefficients of inhibition of the azo-bond reduction in SAS. RESULTS: The D. desulfuricans strains present in the human digestive tract were susceptible to a small degree to SAS and to 5-ASA and SP. CONCLUSIONS: The intestinal D. desulfuricans strains differed in their susceptibility to SAS and its biotransformation products. The strains showing higher susceptibility to SAS lost the ability to reduce the azo bond in this drug, which may be attributed to the lower metabolic activity of the bacteria. The presence of D. desulfuricans in the large intestines of patients with ulcerative colitis and the confirmed diversity of the biological activity of the isolated strains demonstrate the need for clinical examination of the role of these bacteria in the development of some inflammatory disorders.

Desulfovibrio desulfuricans lipopolysaccharides induce endothelial cell IL-6 and IL-8 secretion and E-selectin and VCAM-1 expression.

The aim of this study was to determine whether Desulfovibrio desulfuricans-derived LPS stimulate the release of IL-6 and IL-8 from ECs and the expression of their adhesion molecules at the transcriptional level. Confluent monolayers of HUVEC were incubated in the absence or presence of 20 microg/ml and 60 microg/ml LPSs derived from the DdT and DdA bacterial strains. Also, the simultaneous stimulation of cells with LPSs and IL-1beta was evaluated. The levels of cytokines released were measured using ELISA. LPS-activated HUVEC increased the secretion of both IL-6 and IL-8, which was not LPS dose dependent. The expression of E-selectin and VCAM-1 was assessed by TR-PCR. The transcripts were detectable at all the concentrations (20, 40, 60 microg/ml) of LPSs used. These results suggest that D. desulfuricans LPS may activate immune functions in endothelial cells and influence the inflammatory response during bacteremia caused by these bacteria.