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C Audibert

Publications and source records attributed to C Audibert.

8 recordsLinked to original sources
PubMed2004

[Imaging in acute toxic encephalopathy].

Neuroimaging, particularly MR imaging, plays a major role for the diagnosis of many acute toxic encephalopathies. Toxic disorders are related to drugs (immunosuppressive agents, chemotherapeutic agents, anti-epileptic drugs, heroin...), to metals (lead, manganese, mercury...), and to industrial and environmental chemicals (solvent, carbon monoxide...). MR imaging with diffusion and perfusion imaging provides information regarding brain lesions induced by the toxic agents (vasogenic edema, cytotoxic edema, infarction, hemorrhage, demyelination...).

Acute Disease↗
PubMed2001

implication of the structure of the Helicobacter pylori cag pathogenicity island in induction of interleukin-8 secretion.

Helicobacter pylori virulence is associated with the presence of the cag pathogenicity island (PAI). The cag PAI is involved in the ability to induce interleukin-8 (IL-8) secretion by human cells, which is implicated in the inflammatory response of the gastric mucosa to H. pylori infection. The aim of this study was to determine whether the genetic structure of the cag PAI is conserved and whether it is linked to IL-8 induction ability. Detection of specific markers (cagA, picB, cag13-cag14, virD4, and IS605) by PCR and dot blot hybridization and long-distance PCR determination of the presence of cagI, cagII, and the middle region of the cag PAI were performed on 153 strains isolated from adults suffering from ulcers (n = 79) or gastritis (n = 74). IL-8 induction ability was evaluated by coculture of the strains with HEp-2 cells. Eighty-three strains (54.3%) had an entire cag PAI, 12 strains (7.8%) had the cag PAI split in two, 49 strains (32%) had no cag PAI, and 9 strains exhibited other structural combinations. The presence of an entire cag PAI was statistically correlated with the presence of IS605 (P = 0.006) and the ability to induce IL-8 secretion but not with clinical presentation of the infection. The structure of the cag PAI appears to be rather conserved and is related to the proinflammatory power of a strain. The existence of strains inducing IL-8 secretion regardless of the cag PAI structure suggests that this region is not the only requirement for IL-8 secretion.

Adolescent↗
PubMed2000

Correlation between IL-8 induction, cagA status and vacA genotypes in 153 French Helicobacter pylori isolates.

The polymorphism of clinical presentations associated with Helicobacter pylori infection is potentially due to differences in the virulence of individual strains. H. pylori virulence has been associated with the ability to induce secretion of interleukin-8 (IL-8), the vacA genotypes, and the cagA status. The aim of this study was to determine the virulence profiles of 153 French H. pylori isolates on the basis of vacA genotypes, cagA status, and IL-8 induction ability. A total of 153 H. pylori isolates from patients with chronic gastritis (n = 74) or gastro-duodenal ulcers (n = 79) was examined for vacA genotypes and cagA status by polymerase chain reaction (PCR) and dot blot, and for their ability to induce IL-8 secretion by HEp-2 cells. The prevalence of vacA genotypes was: s1/m1 44.3%, s1/m2 24.9%, and s2/m2 23.5%. The cagA gene was present in 64% of the strains. IL-8 secretion was induced by 58.7% of the isolates. The presence of the cagA gene was significantly correlated with the s1/m1 vacA genotype and with the induction of IL-8. Thirty-four strains were atypical (cagA-positive/IL-8 noninducer or cagA-negative/IL-8 inducer). vacA genotypes, cagA status, and IL-8 induction ability are not correlated with the presence or absence of ulcer. The cagA status is not sufficient to predict the proinflammatory ability of H. pylori.

Adolescent↗
PubMed1999

Phenotypic changes of Helicobacter pylori components during an experimental infection in mice.

The bacterial pathogen Helicobacter pylori is highly adapted to the human stomach and the clinical isolates show a high diversity which could be due to adaptative changes of the strains passing from one host to another. In order to study these variations, experimental infection of mice was developed and provided three out of the eleven tested strains able to infect C57BL/6 mice: the Sydney strain which is known to be well adapted to mice and two freshly isolated strains from infected patients. Mice were orally infected with one of these three strains (infecting strains) and were killed 45 days later. H. pylori strains were isolated from the stomachs of mice (emerging strains). The three infecting strains were compared to the three emerging strains for protein and lipopolysaccharide profiles, antigenic profiles revealed by Western blot with monospecific sera and genetic status by testing for the cagA gene and the vacA genotype. During the 45 days of infection, H. pylori underwent phenotypic variations which may be attributed to the adaptation from a human to a mouse environment or from an in vitro to a mouse environment. Those variations consisted of an over-expression at the cell surface of a 180-kDa protein and of a decreased expression of proteins of 260 and 120 kDa. Moreover, antigenic variations were shown for the two freshly isolated strains from human: the CagA and VacA antigens were in the saline extracts of the infecting strains only while the UreA, UreB, HspA and HspB were in the saline extracts of both the infecting and the emerging strains. These variations may contribute to the adaptation of the strains to the mouse environment.

Animals↗
PubMed1998

Panmictic structure of Helicobacter pylori demonstrated by the comparative study of six genetic markers.

We compared the classifications of strains obtained by analysis of several genetic markers to demonstrate the panmictic structure of Helicobacter pylori, previously suggested by the study of multilocus enzyme electrophoresis. A series of 39 strains, including 37 clinical isolates from patients with gastritis or ulcers from two regions of France, reference strain CIP 101260 and the Sydney strain (strain SSI), were used. They were studied by restriction fragment length polymorphism analysis of ribosomal DNA (ribotyping) using HindIII and HaeIII, by polymorphism analysis of the ureA-ureB and flaA genes by PCR-RFLP using HaeIII and MboI, by vacA genotyping and by the presence or absence of the cagA gene and of the insertion sequence IS605 detected by PCR. There was a high level of genetic polymorphism over the studied strains, with 38 ribotypes, 38 restriction profiles for the ureA-ureB gene, 19 restriction profiles for the flaA gene and five combinations of the signal and mid-region sequences of the vacA gene. Factorial analysis of correspondence and hierarchical clustering performed using each marker revealed that the different classifications of the strains were not correlated. This suggests there is much genetic recombination between strains and supports the hypothesis of a panmictic structure for the H. pylori species.

Bacterial Proteins↗