Early hepatic immune response in rats infected
with <i>Fasciola hepatica</i>

Tliba, Omar; Moiré, Nathalie; Vern, Yves Le; Boulard, Chantal; Chauvin, Alain; Sibille, Pierre

doi:10.1051/vetres:2002014

Cited by 26 publications

(16 citation statements)

References 32 publications

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“…We hypothesize that F. hepatica exerts an active immunosuppression since PC recruitment still increased while the specific activity was being depressed (decreased cytotoxic response and NO production). This was in agreement with our observations showing a delayed hepatic immune response [29,30].…”

Section: Discussionsupporting

confidence: 94%

“…But these studies focused on the interactions between juvenile flukes and peritoneal cells from naive rats. Many modifications occurring both in the liver [28,30] and peritoneum in the early stages following an F. hepatica infection have been observed. In this work, we report an increase of cellular recruitment as well as macrophage oxidative burst, associated with a transient susceptibility of juvenile F. hepatica that were killed by the PC of rats infected 4 to 7 days before sacrifice.…”

Section: Introductionmentioning

confidence: 99%

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Early and transient cytotoxic response of peritoneal cells from Fasciola hepatica-infected rats

Sibille¹,

Tliba²,

Boulard³

2004

Vet. Res.

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-Experimental infection by F. hepatica was performed on rats. Early recruitment of the peritoneal cell population was observed and revealed transient parasite-killing activity, preceded and followed by a state of total unresponsiveness. The activation peaked at seven days postinfection (dpi) and was characterised by a massive peritoneal cell recruitment, a strong superoxide anion and nitric oxide (NO) production, that were coincident with the fasciolicide activity of these cells, as monitored by an in vitro decrease of juvenile fluke viability in a conditioned medium. The addition of L-NG-monomethyl arginine (LNMMA) to cell cultures abrogated both fasciolicide activity and NO production. Parasites started to die when NO production exceeded 25 µM and all juvenile flukes were killed by a 90 µM NO exposition (Lethal Dose 50 between 45.8 and 50.3 µM, 95% fiducial limits). However, when rat peritoneal cells were cultured in the presence of either infected or control rat serum, juvenile flukes were much more resistant to the oxidative burst, despite a massive attachment of rat peritoneal cells to the parasite tegument. These data suggest that a transient control of fasciolosis may take place in the peritoneum following the parasite intrusion but that the parasite efficiently scavenges the host cellular response to avoid destruction.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Early and transient cytotoxic response of peritoneal cells from Fasciola hepatica-infected rats

Sibille¹,

Tliba²,

Boulard³

2004

Vet. Res.

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“…Flow cytometry was performed as described previously (Tliba et al, 2002). Antibody used for CD38 expression was purchased from Santa Cruz Biotechnology.…”

Section: Methodsmentioning

confidence: 99%

CD38 Expression Is Insensitive to Steroid Action in Cells Treated with Tumor Necrosis Factor-α and Interferon-γ by a Mechanism Involving the Up-Regulation of the Glucocorticoid Receptor β Isoform

Tliba

Cidlowski²,

Amrani³

2005

Mol Pharmacol

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100

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Evidence shows that the CD38 molecule, recently involved in the two main features of asthma, bronchial hyper-responsiveness and airway inflammation, could represent a new potential therapeutic target for asthma. In this study, we investigated whether glucocorticoid (GC), the most effective treatment for lung diseases, can affect CD38 expression in human airway smooth muscle (ASM) cells treated with different pro-inflammatory cytokines, such as tumor necrosis factor-␣ (TNF␣) and interferons (IFNs). We found that CD38 expression induced by TNF␣ alone was completely abrogated by fluticasone (100 nM), dexamethasone (1 M), or budesonide (100 nM). In contrast, the synergistic induction of CD38 by the combination of TNF␣ with IFN␥ or IFN␤, but not with IL-1␤ or IL-13, was completely insensitive to the GC inhibitory effects. We also found that TNF␣ and IFN␥ impaired GC responsiveness by inhibiting steroid induced both 1) GR␣-DNA binding activity and 2) GCresponsive element-(GRE)-dependent gene transcription. Although levels of the GC receptor (GR) ␣ isoform remained unchanged, expression of GR␤, the dominant-negative GR isoform, was synergistically increased by TNF␣ and IFN␥ with a GR␣/GR␤ ratio of 1 to 3. More importantly, fluticasone failed to induce GRE-dependent gene transcription and to suppress TNF␣-induced CD38 expression in ASM cells transfected with constitutively active GR␤. We conclude that, upon pro-inflammatory cytokine stimulation, CD38 expression becomes insensitive to GC action by a mechanism involving the up-regulation of GR␤ isoform, thus providing a novel in vitro cellular model to dissect GC resistance in primary cells.

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“…Before intracellular cytokine staining, the cells were fixed with 2% paraformaldehyde, permeabilised with 0.5% saponin (Sigma). IL-2, IL-4 and IL-10 staining was performed as previously described [22] by incubating cells with A38-3, B11-3B and A5-6 (Becton Dickinson, Le Pont de Claix, France; 1/50, 1/300 and 1/50 dilutions, respectively) 45 min on ice followed by Streptavidin-FITC (Dako, Denmark) incubation for 15 min. IFNγ positive cells were directly stained with DB-1F (Serotec, 1/20 dilution) for 30 min on ice.…”

Section: Methodsmentioning

confidence: 99%

Evaluation of the hepatic NK cell response during the early phase of Fasciola hepatica infection in rats

Tliba

Chauvin²,

Vern

et al. 2002

Vet. Res.

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-The in situ distribution of NK cells in rat liver during the first 28 days of an experimental infection with F. hepatica was investigated. NK cells were distributed homogeneously throughout the hepatic parenchyma in uninfected animals. The total number of hepatic mononuclear cells increased significantly following infection, but the proportion of NK cells did not change. After infection, these cells were found around the portal space, around the centrolobular vein, in the periportal fibrosis and in the band of collagen. However, no NK cells could be detected in or around the granuloma during infection. The frequency of both IL-2-and IFNγ -producing NK cells was higher on day 7 postinfection (pi) but only the percentage of IFNγ + CD161 + subsets remained elevated thereafter, whereas the percentage of both IL-2 + CD161 + and IL-4 + CD161 + subsets returned to the baseline. The number of CD161 + IL10 + cells did not change significantly. These results suggest that NK cells could be another source for the early production of IFNγ but provide no evidence that these cells are involved in early events associated with granuloma formation. Fasciola hepatica / NK cells / cytokine / flow cytometry / immunohistochemistryRésumé -Évaluation de la réponse des cellules NK hépatiques pendant la phase précoce d'infestation par Fasciola hepatica chez le rat. Nous avons suivi la localisation et la distribution hépatique des cellules NK durant les 28 premiers jours d'une fasciolose expérimentale chez le rat. Chez les animaux non infestés, les cellules NK sont distribuées de façon homogène dans tout le foie. Chez les animaux infestés, ces cellules sont localisées préférentiellement au niveau des espaces portes, autour des veines centrolobulaires, dans les bandes de collagène et dans la zone de fibrose péri-portale. En revanche, aucune de ces cellules n'a été détectée ni autour ni au sein du granulome. Le

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Early hepatic immune response in rats infected with Fasciola hepatica

Cited by 26 publications

References 32 publications

Early and transient cytotoxic response of peritoneal cells from Fasciola hepatica-infected rats

Early and transient cytotoxic response of peritoneal cells from Fasciola hepatica-infected rats

CD38 Expression Is Insensitive to Steroid Action in Cells Treated with Tumor Necrosis Factor-α and Interferon-γ by a Mechanism Involving the Up-Regulation of the Glucocorticoid Receptor β Isoform

Evaluation of the hepatic NK cell response during the early phase of Fasciola hepatica infection in rats

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