Showing papers by "Alessandra Carattoli published in 2000"

Multiple-Antibiotic Resistance Mediated by Structurally Related IncL/M Plasmids Carrying an Extended-Spectrum β-Lactamase Gene and a Class 1 Integron

Abstract: A conjugative IncL/M plasmid (pSEM) conferring resistance to gentamicin, amikacin, kanamycin, sulfonamides, and expanded-spectrum cephalosporins was found in pathogenic strains of Salmonella enterica serotype Typhimurium. Resistance to aminoglycosides was encoded by a sul1-type class 1 integron (In-t3). An extended-spectrum beta-lactamase gene, bla(SHV-5), was identified 3. 5 kb downstream of the integrase (intI1) gene of In-t3. Nucleotide sequence analysis of the 5.3-kb bla(SHV-5)-In-t3 region of pSEM highlighted striking similarities with IncL/M plasmids isolated from nosocomial gram-negative pathogens, conferring resistance to expanded-spectrum cephalosporins and aminoglycosides.

Cytotoxin-associated gene A and vacuolating cytotoxin A in human isolates of Helicobacter pylori and their association with the clinical status of ulcer disease.

Abstract: OBJECTIVE: The aim of this study was to evaluate whether different Helicobacter pylori genotypes are associated with different clinical stages of peptic ulcer disease (PUD). DESIGN: We assessed the virulence characteristics of H. pylori isolates from patients with active PUD (presence of an ulcer crater at endoscopy) and from those with PUD in remission (normal endoscopic findings or scar not induced by drugs in PUD patients). METHODS: H. pylori isolates from biopsies of the gastric antrum were examined for cagA and vacA genotypes by PCR amplification and Western blot analysis. Descriptive statistical techniques and multivariate polytomous logistic regression were used to estimate adjusted odds ratio (OR) for cagA and vacA genotypes in patients with active PUD or PUD in remission. Patients with non-ulcer dyspepsia (NUD) were used as negative controls. RESULTS: The cagA genotype and phenotype were found to be differently associated with disease status. In fact, the multivariate regression model showed that gastric colonization by CagA+ H. pylori strains was associated with an increased risk of active PUD (OR 2.58), whereas the OR for patients with PUD in remission was 0.94. CONCLUSIONS: Our data indicate that the active ulcer status is more strongly associated with H. pylori strains carrying the pathogenicity island (PAI) than remission status. These results support the hypothesis that a dynamic equilibrium exists among bacterial populations with or without the PAI, and that the relapse of the peptic ulcer could be consequent to expansion of the H. pylori population carrying the PAI.

Inhibition of HIV-1 transcription by cyclopentenone prostaglandin A1 in Jurkat T lymphocytes.

Abstract: Cyclopentenone prostaglandins inhibit virus replication in several DNA and RNA virus models. In this report we investigated the effect of prostaglandin A1 (PGA1) on HIV-1 transcription in human CD4+ Jurkat T lymphocyte cells. A dramatic reduction of HIV-1 RNA levels was detected up to seven days post infection in both unstimulated and phorbol 12-mystrate 13-acetate (PMA)-stimulated cells treated with PGA1- PGA1 treatment of cells was also effective in inhibiting the transcription of a chloramphenicol acetyltransferase (CAT) reporter gene, under the control of HIV-1 LTR, in Jurkat-Tat cells. We also show that PGA1 induced the synthesis of 70-kDa heat-shock protein (HSP70) in this cell system and the induction correlated with the drug-antiviral activity. PGA1 was also found to induce the loss of the tumor suppressor p53 protein, in the "proliferative" conformation, in a time correlation with the induction of the HSP70 As the "proliferative" p53 has been involved in the positive trans-activation of the HIV-1 LTR its depletion could contribute to the inhibitory mechanisms of PGA1 on virus transcription.