Cholera toxin differentially regulates nitric oxide synthesis, tumor necrosis factor-Î± production and respiratory burst in murine macrophages

Rodrı́guez, Boris L.; Rojas, Armando; Benítez, Jorge A.

doi:10.1111/j.1574-695x.1998.tb01206.x

Cited by 2 publications

(2 citation statements)

References 23 publications

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“…These data are in contradiction with previous reports indicating that an increase in cAMP levels in macrophage murine cellular lines augments NO production. In this case, the increase in NO production is related to an accumulation of NOS-2 mRNA [33][34][35][36][37][38]. Thus, CT may inhibit or induce NO production, depending on the cellular type studied.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide modulation of the immune response against cholera toxin-adjuvated ovalbumin administered by the intranasal route

et al. 2004

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Section: Discussionmentioning

confidence: 99%

Nitric oxide modulation of the immune response against cholera toxin-adjuvated ovalbumin administered by the intranasal route

et al. 2004

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“…Concomitant addition of cholera toxin and lipopolysaccharide to cell cultures enhanced the production of tumor necrosis factor-alpha. These effects were abrogated when cholera toxin was inactivated by heat or treated with a specific monoclonal antibody [18].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of human mitochondrial NADH dehydrogenase subunit 5 in intestinal epithelial cells is modulated by Vibrio cholerae pathogenesis

et al. 2005

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Cholera still remains an important global predicament especially in India and other developing countries. Vibrio cholerae, the etiologic agent of cholera, colonizes the small intestine and produces an enterotoxin that is largely responsible for the watery diarrheal symptoms of the disease. Using RNA arbitrarily primed PCR, ND5 a mitochondria encoded subunit of complex I of the mitochondrial respiratory chain was found to be upregulated in the human intestinal epithelial cell line Int407 following exposure to V. cholerae. The upregulation of ND5 was not observed when Int407 was infected with Escherichia coli strains. Incubation with heat-killed V. cholerae or cholera toxin or culture supernatant also showed no such upregulation indicating the involvement of live bacteria in the process. Infection of the monolayer with aflagellate non-motile mutant of V. cholerae O395 showed a very significant (59-fold) downregulation of ND5. In contrast, a remarkable upregulation of ND5 expression (200-fold) was observed in a hyperadherent icmF insertion mutant with reduced motility. V. cholerae cheY4 null mutant defective in adherence and motility also resulted in significantly reduced levels of ND5 expression while mutant with the cheY4 gene duplicated showing increased adherence and motility resulted in increased expression of ND5. These results clearly indicate that both motility and adherence to intestinal epithelial cells are possible triggering factors contributing to ND5 mRNA expression by V. cholerae. Interestingly infection with insertion mutant in the gene coding for ToxR, the master regulator of virulence in V. cholerae resulted in significant downregulation of ND5 expression. However, infection with ctxA or toxT insertion mutants did not show any significant changes in ND5 expression compared to wild-type. Almost no expression of ND5 was observed in case of mutation in the gene coding for OmpU, a ToxR activated protein. Thus, infection of Int407 with virulence mutant strains of V. cholerae revealed that the ND5 expression is modulated by the virulence of V. cholerae in a ToxT independent manner. Although no difference in the mitochondrial copy number could be detected between infected and uninfected cells, the modulation of the expression of other mitochondrial genes were also observed. Incidentally, upon V. cholerae infection, complex I activity was found to increase about 3-folds after 6 h. This is the first report of alteration in mitochondrial gene expression upon infection of a non-invasive enteric bacterium like V. cholerae showing its modulation with adherence, motility and virulence of the organism.

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Cholera toxin differentially regulates nitric oxide synthesis, tumor necrosis factor-Î± production and respiratory burst in murine macrophages

Cited by 2 publications

References 23 publications

Nitric oxide modulation of the immune response against cholera toxin-adjuvated ovalbumin administered by the intranasal route

Nitric oxide modulation of the immune response against cholera toxin-adjuvated ovalbumin administered by the intranasal route

Upregulation of human mitochondrial NADH dehydrogenase subunit 5 in intestinal epithelial cells is modulated by Vibrio cholerae pathogenesis

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