Correlation between IL-8 induction,   status and   genotypes in 153 French   isolates

Audibert, Céline; Janvier, Blandine; Grignon, B.; Salaüna, Laurence; Burucoa, Christophe; Lecron, Jean‐Claude; Fauchère, Jean-Louis

doi:10.1016/s0923-2508(00)00139-x

Cited by 34 publications

(27 citation statements)

References 43 publications

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“…The ability of H. pylori to induce IL-8 secretion by eucaryotic cells was investigated by using 138 of the 153 isolates. A cutoff value of 71 pg/ml was established using the Tx30a reference strain, which is known as a non-IL-8 inducer (4). Among the 138 strains tested, 81 (58.7%) induced IL-8 secretion by the HEp-2 cells (from 71 to 4,071 pg/ml) while 57 (41.3%) induced no or low IL-8 secretion (from 0 to 71 pg/ml).…”

Section: Resultsmentioning

confidence: 99%

“…In this work, the proinflammatory power of a strain was evaluated by its ability to induce IL-8 secretion from HEp-2 cells. This method has been validated previously (4,10) and assesses for the intrinsic virulence of the strain independently of the patient response.…”

Section: Discussionmentioning

confidence: 99%

“…IL-8 induction by H. pylori strains. The IL-8 induction ability of H. pylori was investigated on HEp-2 cells as previously described (4). Briefly, we cocultured HEp-2 cells for 24 h with an H. pylori suspension containing 5 ϫ 10 8 bacteria/ml.…”

Section: Methodsmentioning

confidence: 99%

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Implication of the Structure of theHelicobacter pylori cagPathogenicity Island in Induction of Interleukin-8 Secretion

Audibert¹,

Burucoa²,

Janvier³

et al. 2001

Infect Immun

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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.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Implication of the Structure of theHelicobacter pylori cagPathogenicity Island in Induction of Interleukin-8 Secretion

Audibert¹,

Burucoa²,

Janvier³

et al. 2001

Infect Immun

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“…Our results are consistent with previous observations, in which CagA elicited high neutrophil accumulation, measured as inflammation activity in gastric mucosa (29). According to some studies, this can be related to strong stimulation of IL-8 production by CagA positive strains (34,35). There are no data on the association of seropositivity to proteins p30 (OMP), p33, and p19 (OMP) and different patterns of gastritis.…”

Section: Discussionmentioning

confidence: 99%

Serum Antibodies Positivity to 12 Helicobacter pylori Virulence Antigens in Patients with Benign or Malignant Gastroduodenal Diseases – Cross-sectional Study

et al. 2009

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Aim To investigate the association of gastric histological and endoscopic findings in patients with Helicobacter pylori (H. pylori), according to presence of seropositivity to 12 bacterial virulence antigens.Methods This is a cross-sectional single-center study of 360 consecutive outpatients referred in the period of one year to upper gastrointestinal endoscopy because of dyspeptic complaints. Patients sera were tested by Western blot method to determine the presence of serum antibodies to bacterial virulence antigens -p120 (CagA -cytotoxin-associated antigen), p95 (VacA -vacuolating cytotoxin), p67 (FSH -flagellar sheath protein), p66 (UreB -urease enzyme heavy subunit), p57 (HSP homologue -heath shock protein homologue), p54 (flagellin), p33, p30 (OMP -outer membrane protein), p29 (UreA -urease enzyme light subunit), p26, p19, and p17. Upper gastrointestinal endoscopy was performed, endoscopic diagnosis recorded, and 4 mucosal biopsy samples were obtained and assessed according to Updated Sydney protocol. ResultsThe sera of 207 patients were analyzed. Thirty patients had gastric adenocarcinoma, 126 peptic ulcers, and 51 normal finding. p120 (CagA) seropositivity was significantly more often present in patients with higher activity grade in the antrum (P = 0.025), p30 in patients with greater inflammation in the antrum (P = 0.025) and the corpus (P = 0.010), p33 in patients with greater inflammation in the corpus (P = 0.050), and p19 (OMP) in patients with lower intestinal metaplasia grades in the corpus (P = 0.025). Seroreactivity to all other bacterial proteins showed no association with the histological status of the stomach mucosa. Except for the seropositivity to protein p95 (VacA), which was more often present in patients with duodenal ulcer (P = 0.006), there was no difference in seroreactivity to other bacterial proteins and upper gastrointestinal endoscopic findings.Conclusions p120 (CagA), p33, p 30 (OMP), and p19 (OMP) seropositivity was more often present in patients with higher grades of the histological parameters of gastritis and seropositivity to protein p95 (VacA) with endoscopic presence of duodenal ulcer. Histological parameters of gastritis are more associated with bacterial virulence than endoscopic findings.

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“…Although many studies have shown that the presence of either cagA or vacAs1 or both is associated with a more severe inflammatory response and more pronounced pathological changes (2,33,35,44,55), there have also been a number of reports suggesting that the expression levels of some cytokines, such as IL-7, IL-10, IL-16, and tumor necrosis factor alpha (TNF-␣), are independent of the presence of cagA or vacAs1 (3,21,22,40,48,49). Moreover, it has also been shown that expression of IFN-␥, TNF-␣, and IL-12R ␤2 was similar in biopsies from patients carrying triple-negative and biopsies from patients carrying triple-positive strains, although the latter showed a higher level of bacterial colonization and granulocyte infiltration (36).…”

Section: Discussionmentioning

confidence: 99%

Expression of Helicobacter pylori Virulence Factors and Associated Expression Profiles of Inflammatory Genes in the Human Gastric Mucosa

et al. 2007

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Helicobacter pylori virulence factors have been suggested to be important in determining the outcome of infection. The H. pylori adhesion protein BabA2 is thought to play a crucial role in bacterial colonization and in induction of severe gastric inflammation, particularly in combination with expression of CagA and VacA. However, the influence of these virulence factors on the pathogenesis of H. pylori infection is still poorly understood. To address this question, the inflammatory gene expression profiles for two groups of patients infected with triple-negative strains (lacking expression of cagA, babA2, and vacAs1 but expressing vacAs2) and triple-positive strains (expressing cagA, vacAs1, and babA2 but lacking expression of vacAs2) were investigated. The gene expression patterns in the antrum gastric mucosa from patients infected with different H. pylori strains were very similar, and no differentially expressed genes could be identified by pairwise comparisons. Our data thus suggest that there is a lack of correlation between the host inflammatory responses in the gastric mucosa and expression of the babA2, cagA, and vacAs1 genes.Helicobacter pylori infection is widespread in humans; it is present in 20 to 50% of the population in developed countries and 80% of the population in developing countries (43). Most infected individuals display only asymptomatic gastritis, whereas a small proportion develop severe disease, including peptic ulceration and gastric malignancy. Although the factors that determine the outcome of the infection are not well understood, bacterial virulence factors have been suggested to play important roles.One of the major virulence factors of H. pylori is the vacuolating cytotoxin (VacA), which causes cytoplasmic vacuolization in gastric epithelial cells (41). Another well-characterized virulence factor is the cytotoxin-associated antigen (CagA), which is encoded by one of the genes located in the cag pathogenicity island (PAI) (8). Strains expressing vacAs1 and/or cagA are present at a higher frequency in patients with duodenal ulcers, atrophic gastritis, and gastric carcinoma (2,5,13,17,23) and are referred to as type I strains. In contrast, type II strains, which lack the cagA gene, present a nontoxic form of VacA and are considered less virulent (37, 46). The blood group antigen binding adhesin (BabA), encoded by the babA2 gene, has previously been shown to mediate adherence of H. pylori to the Lewis b blood group antigen on human gastric epithelial cells (6,7,19). The attachment may facilitate H. pylori colonization and efficient delivery of virulence factors such as VacA or CagA to the host cells, resulting in severe gastric inflammation. It has indeed been shown that strains with babA2, particularly when it is present together with cagA and vacAs1 (referred to as triple-positive strains here), are more often associated with duodenal ulcers and adenocarcinoma than the strains without babA2 (15). Moreover, triplepositive strains are detected more frequently in patients with severe ...

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Correlation between IL-8 induction, status and genotypes in 153 French isolates

Cited by 34 publications

References 43 publications

Implication of the Structure of theHelicobacter pylori cagPathogenicity Island in Induction of Interleukin-8 Secretion

Implication of the Structure of theHelicobacter pylori cagPathogenicity Island in Induction of Interleukin-8 Secretion

Serum Antibodies Positivity to 12 Helicobacter pylori Virulence Antigens in Patients with Benign or Malignant Gastroduodenal Diseases – Cross-sectional Study

Expression of Helicobacter pylori Virulence Factors and Associated Expression Profiles of Inflammatory Genes in the Human Gastric Mucosa

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