AIM: The interaction with fibronectin of dendritic cells (DC) from celiac disease (CD) patients and controls was investigated. In particular, the ability of these cells to interact with the substrate by analyzing their morphology and actin rearrangement when in contact with fibronectin, which is a physiological substrate for DC. Furthermore, we investigated the role of anti-tTg and anti-β1 integrin antibodies on the interaction of DC with fibronectin. DC from controls and from CD patients both in the active and remission phase of the disease were compared. MATERIALS AND METHODS: Immature DC were generated by extracting monocytes from peripheral blood and stimulating them with IL-4 and GM-CSF for 6 days. Cell shape and adhesion was determined by crystal violet staining. Confocal microscopy of phalloidin staining was used to highlight the actin cytoskeleton.RESULTS: We showed that cells of CD patients have a different shape when interacting with the substrate compared to controls cells, even without any treatment. This alteration is observed in patients in the active as well in the remission fase of the disease. Gliadin peptide P31-43 interferes with cells shape mainly in controls, inducing DC to make more dendrites. Gliadin peptide P56-68 has less effect on cell shape.Moreover we found that tTg antibodies can interfere with the shape of the cells, by making them round and small with almost no dendrite formation, both in CD patients and controls, without interfering with the possibility to adhere. This indicates a new biological role for these antibodies in the disease.Also anti-β1integrin antibodies interfere with the shape of the cells in the same way tTg antibodies does, suggesting a common mechanism for both antibodies. CONCLUSIONS: These results suggest that genetic background in CD patients seems to influence DC shape and actin cytoskeleton more than inflammatory state. Moreover the treatment of controls cells with gliadin peptides, mainly P31-43, are able to alter the shape of the cells by inducing them to generate more dendrites. Anti-tTg and Anti-β1 integrin antibodies can interfere with DC morphology both in CD patients and controls. The biological activity of these antibodies on DC may have a role in the CD pathogenesis.

CELL SHAPE DISCRIMINATES BETWEEN NORMAL AND CELIAC DISEASE (CD) DENDRITIC CELLS (DC).

Discepolo V.;SANTAGATA, SARA;ZANZI, DELIA;AURICCHIO, SALVATORE;TRONCONE, RICCARDO;BARONE, MARIA VITTORIA
2008

Abstract

AIM: The interaction with fibronectin of dendritic cells (DC) from celiac disease (CD) patients and controls was investigated. In particular, the ability of these cells to interact with the substrate by analyzing their morphology and actin rearrangement when in contact with fibronectin, which is a physiological substrate for DC. Furthermore, we investigated the role of anti-tTg and anti-β1 integrin antibodies on the interaction of DC with fibronectin. DC from controls and from CD patients both in the active and remission phase of the disease were compared. MATERIALS AND METHODS: Immature DC were generated by extracting monocytes from peripheral blood and stimulating them with IL-4 and GM-CSF for 6 days. Cell shape and adhesion was determined by crystal violet staining. Confocal microscopy of phalloidin staining was used to highlight the actin cytoskeleton.RESULTS: We showed that cells of CD patients have a different shape when interacting with the substrate compared to controls cells, even without any treatment. This alteration is observed in patients in the active as well in the remission fase of the disease. Gliadin peptide P31-43 interferes with cells shape mainly in controls, inducing DC to make more dendrites. Gliadin peptide P56-68 has less effect on cell shape.Moreover we found that tTg antibodies can interfere with the shape of the cells, by making them round and small with almost no dendrite formation, both in CD patients and controls, without interfering with the possibility to adhere. This indicates a new biological role for these antibodies in the disease.Also anti-β1integrin antibodies interfere with the shape of the cells in the same way tTg antibodies does, suggesting a common mechanism for both antibodies. CONCLUSIONS: These results suggest that genetic background in CD patients seems to influence DC shape and actin cytoskeleton more than inflammatory state. Moreover the treatment of controls cells with gliadin peptides, mainly P31-43, are able to alter the shape of the cells by inducing them to generate more dendrites. Anti-tTg and Anti-β1 integrin antibodies can interfere with DC morphology both in CD patients and controls. The biological activity of these antibodies on DC may have a role in the CD pathogenesis.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/362305
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