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Enteric glial-derived S100B protein stimulates nitric oxide production in celiac disease.
Gastroenterology. 2007 Sep; 133(3):918-25.G

Abstract

BACKGROUND & AIMS

Enteric glia participates to the homeostasis of the gastrointestinal tract. In the central nervous system, increased expression of astroglial-derived S100B protein has been associated with the onset and maintaining of inflammation. The role of enteric glial-derived S100B protein in gastrointestinal inflammation has never been investigated in humans. In this study, we evaluated the expression of S100B and its relationship with nitric oxide production in celiac disease.

METHODS

Duodenal biopsy specimens from untreated and on gluten-free diet patients with celiac disease and controls were respectively processed for S100B and inducible nitric oxide synthase (iNOS) protein expression and nitrite production. To evaluate the direct involvement of S100B in the inflammation, control biopsy specimens were exposed to exogenous S100B, and iNOS protein expression and nitrite production were measured. We also tested gliadin induction of S100B-dependent inflammation in cultured biopsy specimens deriving from on gluten-free diet patients in the absence or presence of the specific S100B antibody.

RESULTS

S100B messenger RNA and protein expression, iNOS protein expression, and nitrite production were significantly increased in untreated patients but not in on gluten-free diet patients vs controls. Addition of S100B to control biopsy specimens resulted in a significant increase of iNOS protein expression and nitrite production. In celiac disease patients but not in controls biopsy specimens, gliadin challenge significantly increased S100B messenger RNA and protein expression, iNOS protein expression, and nitrite production, but these effects were completely inhibited by S100B antibody.

CONCLUSIONS

Enteric glial-derived S100B is increased in the duodenum of patients with celiac disease and plays a role in nitric oxide production.

Authors+Show Affiliations

Department of Experimental Pharmacology, University Federico II, Naples, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17678654

Citation

Esposito, Giuseppe, et al. "Enteric Glial-derived S100B Protein Stimulates Nitric Oxide Production in Celiac Disease." Gastroenterology, vol. 133, no. 3, 2007, pp. 918-25.
Esposito G, Cirillo C, Sarnelli G, et al. Enteric glial-derived S100B protein stimulates nitric oxide production in celiac disease. Gastroenterology. 2007;133(3):918-25.
Esposito, G., Cirillo, C., Sarnelli, G., De Filippis, D., D'Armiento, F. P., Rocco, A., Nardone, G., Petruzzelli, R., Grosso, M., Izzo, P., Iuvone, T., & Cuomo, R. (2007). Enteric glial-derived S100B protein stimulates nitric oxide production in celiac disease. Gastroenterology, 133(3), 918-25.
Esposito G, et al. Enteric Glial-derived S100B Protein Stimulates Nitric Oxide Production in Celiac Disease. Gastroenterology. 2007;133(3):918-25. PubMed PMID: 17678654.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Enteric glial-derived S100B protein stimulates nitric oxide production in celiac disease. AU - Esposito,Giuseppe, AU - Cirillo,Carla, AU - Sarnelli,Giovanni, AU - De Filippis,Daniele, AU - D'Armiento,Francesco Paolo, AU - Rocco,Alba, AU - Nardone,Gerardo, AU - Petruzzelli,Raffaella, AU - Grosso,Michela, AU - Izzo,Paola, AU - Iuvone,Teresa, AU - Cuomo,Rosario, Y1 - 2007/06/20/ PY - 2006/02/16/received PY - 2007/05/31/accepted PY - 2007/8/7/pubmed PY - 2007/10/24/medline PY - 2007/8/7/entrez SP - 918 EP - 25 JF - Gastroenterology JO - Gastroenterology VL - 133 IS - 3 N2 - BACKGROUND & AIMS: Enteric glia participates to the homeostasis of the gastrointestinal tract. In the central nervous system, increased expression of astroglial-derived S100B protein has been associated with the onset and maintaining of inflammation. The role of enteric glial-derived S100B protein in gastrointestinal inflammation has never been investigated in humans. In this study, we evaluated the expression of S100B and its relationship with nitric oxide production in celiac disease. METHODS: Duodenal biopsy specimens from untreated and on gluten-free diet patients with celiac disease and controls were respectively processed for S100B and inducible nitric oxide synthase (iNOS) protein expression and nitrite production. To evaluate the direct involvement of S100B in the inflammation, control biopsy specimens were exposed to exogenous S100B, and iNOS protein expression and nitrite production were measured. We also tested gliadin induction of S100B-dependent inflammation in cultured biopsy specimens deriving from on gluten-free diet patients in the absence or presence of the specific S100B antibody. RESULTS: S100B messenger RNA and protein expression, iNOS protein expression, and nitrite production were significantly increased in untreated patients but not in on gluten-free diet patients vs controls. Addition of S100B to control biopsy specimens resulted in a significant increase of iNOS protein expression and nitrite production. In celiac disease patients but not in controls biopsy specimens, gliadin challenge significantly increased S100B messenger RNA and protein expression, iNOS protein expression, and nitrite production, but these effects were completely inhibited by S100B antibody. CONCLUSIONS: Enteric glial-derived S100B is increased in the duodenum of patients with celiac disease and plays a role in nitric oxide production. SN - 0016-5085 UR - https://www.unboundmedicine.com/medline/citation/17678654/Enteric_glial_derived_S100B_protein_stimulates_nitric_oxide_production_in_celiac_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0016-5085(07)01150-X DB - PRIME DP - Unbound Medicine ER -