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Dive into the research topics where G. Sarnelli is active.

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Featured researches published by G. Sarnelli.


Neurogastroenterology and Motility | 2009

Increased mucosal nitric oxide production in ulcerative colitis is mediated in part by the enteroglial‐derived S100B protein

Carla Cirillo; G. Sarnelli; Giuseppe Esposito; Michela Grosso; Raffaella Petruzzelli; Paola Izzo; Gaetano Calì; Francesco Paolo D'Armiento; Alba Rocco; Gerardo Nardone; Teresa Iuvone; Luca Steardo; Rosario Cuomo

Abstract  In the central nervous system glial‐derived S100B protein has been associated with inflammation via nitric oxide (NO) production. As the role of enteroglial cells in inflammatory bowel disease has been poorly investigated in humans, we evaluated the association of S100B and NO production in ulcerative colitis (UC). S100B mRNA and protein expression, inducible NO synthase (iNOS) expression, and NO production were evaluated in rectal biopsies from 30 controls and 35 UC patients. To verify the correlation between S100B and NO production, biopsies were exposed to S100B, in the presence or absence of specific receptor for advanced glycation end‐products (RAGE) blocking antibody, to measure iNOS expression and nitrite production. S100B and iNOS expression were evaluated after incubation of biopsies with lipopolysaccharides (LPS) + interferon‐gamma (IFN‐γ) in the presence of anti‐RAGE or anti‐S100B antibodies or budesonide. S100B mRNA and protein expression, iNOS expression and NO production were significantly higher in the rectal mucosa of patients compared to that of controls. Exogenous S100B induced a significant increase in both iNOS expression and NO production in controls and UC patients; this increase was inhibited by specific anti‐RAGE blocking antibody. Incubation with LPS + IFN‐γ induced a significant increase in S100B mRNA and protein expression, together with increased iNOS expression and NO production. LPS + IFN‐γ‐induced S100B up‐regulation was not affected by budesonide, while iNOS expression and NO production were significantly inhibited by both specific anti‐RAGE and anti‐S100B blocking antibodies. Enteroglial‐derived S100B up‐regulation in UC participates in NO production, involving RAGE in a steroid insensitive pathway.


Neurogastroenterology and Motility | 2007

The hallucinogenic herb Salvia divinorum and its active ingredient salvinorin A reduce inflammation‐induced hypermotility in mice

Raffaele Capasso; Francesca Borrelli; Jordan K. Zjawiony; L. Kutrzeba; Gabriella Aviello; G. Sarnelli; Francesco Capasso; Angelo A. Izzo

Abstract  The hallucinogenic plant Salvia divinorum has been used for medical treatments of gastrointestinal disorders. Here, we evaluated the effect of a standardized extract from the leaves of Salvia divinorum (SDE) and of its active ingredient salvinorin A on motility in vivo, both in physiological states and during croton oil‐induced intestinal inflammation. SDE (1–100 mg kg−1) significantly inhibited motility only in inflamed, but not in control, mice. In control mice, salvinorin A (0.01–10 mg kg−1) significantly inhibited motility only at the highest doses tested (3 and 10 mg kg−1) and this effect was not counteracted by naloxone or by the κ‐opioid receptor (KOR) antagonist nor‐binaltorphimine. Inflammation significantly increased the potency of salvinorin A (but not of the KOR agonist U‐50488) in reducing motility. The inhibitory effects of both salvinorin A and U‐50488 in inflamed mice were counteracted by naloxone or by nor‐binaltorphimine. We conclude that salvinorin A may reduce motility through activation of different targets. In physiological states, salvinorin A, at high doses, inhibited motility through a non‐KOR mediated mechanism. Gut inflammation increased the potency of salvinorin A; this effect was mediated by KOR, but it was not shared by U‐50488, thus suggesting that salvinorin A may have target(s) other than KOR in the inflamed gut.


Alimentary Pharmacology & Therapeutics | 2006

Oesophageal acid exposure and altered neurocardiac function in patients with GERD and idiopathic cardiac dysrhythmias.

Rosario Cuomo; F De Giorgi; L Adinolfi; G. Sarnelli; F Loffredo; Eleonora Efficie; Clelia Verde; Mf Savarese; Paolo Usai; Gabriele Budillon

Oesophageal sensory stimuli alter neurocardiac function through autonomic reflexes.


Neurogastroenterology and Motility | 2008

Tissue ghrelin level and gastric emptying rate in adult patients with celiac disease.

Alba Rocco; G. Sarnelli; Debora Compare; P. De Colibus; P. Micheli; P. Somma; B. Marotti; Rosario Cuomo; G. Nardone

Abstract  Celiac disease (CD) patients show a number of gastrointestinal motor abnormalities. Ghrelin, a gastric peptide implicated in short‐term feeding control and long‐term body weight regulation, has been recently considered a key regulator of gastric motility. The aim of this study was to evaluate the gastric emptying rate of solids and the density of ghrelin‐immunopositive cells in adult CD patients before and at least 1 year after starting a gluten‐free diet. Twenty CD patients (M 8/F 12; mean age 36 years) and 10 controls underwent endoscopy with gastric and duodenal biopsies and 13C‐octanoic acid breath test to measure gastric emptying of solids. Celiac disease patients repeated the protocol at least 1 year after starting gluten‐free diet. Ghrelin tissue levels were evaluated by immunohistochemistry on gastric mucosa specimens. Gastric emptying time was normal in all control subjects (t1/2 = 89 ± 16 min) while it was delayed in CD patients prior to gluten‐free diet (t1/2 = 252 ± 101 min; P < 0.005). The mean number of ghrelin‐positive cells/field (×400) was 14.4 ± 2.7 in controls and 25.3 ± 5.7 in CD patients respectively (P < 0.0001). Gluten withdrawal was effective in normalizing gastric emptying time in all CD patients (97 ± 14 min; P < 0.0001) and resulted in a significant reduction of the density of ghrelin‐immunopositive cells (19.8 ± 5.4; P < 0.0001). The density of ghrelin‐positive cells correlated directly with the degree of duodenal damage (P < 0.001) and inversely with the body mass index of CD patients (P < 0.0001). However, in neither CD patients nor controls, a correlation between tissue ghrelin levels and gastric emptying rate was detected. In conclusion, tissue ghrelin level does not correlate with gastric emptying rate in adult CD patients and in controls.


Neurogastroenterology and Motility | 2013

Increased severity of dyspeptic symptoms related to mental stress is associated with sympathetic hyperactivity and enhanced endocrine response in patients with postprandial distress syndrome

F. De Giorgi; G. Sarnelli; Carla Cirillo; Ivana Giusy Savino; Fabio Turco; G. Nardone; Alba Rocco; Rosario Cuomo

Background  Mental stress (MS) may alter gastric sensory‐motor function. The aim of the study was to assess postprandial autonomic nervous system activity and stress hormones in response to acute mental stress in dyspeptic patients.


Digestive and Liver Disease | 2003

Acid exposure and altered acid clearance in GERD patients treated for Helicobacter pylori infection

G. Sarnelli; Enzo Ierardi; Raffaella Grasso; Clelia Verde; Maria Ermina Bottiglieri; Gerardo Nardone; Gabriele Budillon; Rosario Cuomo

BACKGROUND After the eradication of Helicobacter pylori, an increased incidence of gastroesophageal reflux disease and acid gastric secretion have been reported. AIM To evaluate the effect of Helicobacter pylori-eradication on proximal and distal gastroesophageal reflux and acid clearance in patients with gastroesophageal reflux disease. PATIENTS AND METHODS Sixty-eight gastroesophageal reflux disease patients (age range 18-61 years) were studied by upper endoscopy. All underwent esophageal manometry and dual probe 24-h pH-metry. RESULTS Percent of time at pH<4 was significantly increased in the proximal esophagus of Helicobacter pylori-eradicated patients compared to Helicobacter pylori-negative (2.4+/-0.5 vs. 1.0+/-0.2; p<0.01); no differences were found in the distal esophagus (14.0+/-3.7 vs. 9.0+/-1.4%, NS). The total number of reflux episodes was significantly higher in the proximal oesophagus of Helicobacter pylori-eradicated patients (37+/-3 vs. 22+/-3, p<0.05). In the distal esophagus, acid clearance was significantly longer, both during total time (1.4+/-0.2 vs. 0.8+/-0.7 min, p<0.01), and in the supine period (8.5+/-2.7 vs. 2.7+/-0.4 min, p<0.05). No differences were reported in the manometric parameters of the two groups of patients. CONCLUSION In patients with gastroesophageal reflux disease, Helicobacter pylori eradication is associated with increased acid exposure of the proximal esophagus and delayed distal acid clearance.


Brain Behavior and Immunity | 2018

Antibiotic-induced microbiota perturbation causes gut endocannabinoidome changes, hippocampal neuroglial reorganization and depression in mice

Francesca Guida; F. Turco; Monica Iannotta; D. De Gregorio; Ilaria Palumbo; G. Sarnelli; Anna Furiano; F. Napolitano; Serena Boccella; Livio Luongo; Mariacristina Mazzitelli; Alessandro Usiello; F. De Filippis; Fabio Arturo Iannotti; Francesco Piscitelli; Danilo Ercolini; V. de Novellis; V. Di Marzo; Rosario Cuomo; Sabatino Maione

The microbiota-gut-brain axis (MGBA) regulates the reciprocal interaction between chronic inflammatory bowel and psychiatric disorders. This interaction involves multiple pathways that are highly debated. We examined the behavioural, biochemical and electrophysiological alterations, as well as gut microbiota composition in a model of antibiotic-induced experimental dysbiosis. Inflammation of the small intestine was also assessed. Mice were exposed to a mixture of antimicrobials for 2weeks. Afterwards, they received Lactobacillus casei DG (LCDG) or a vehicle for up to 7days via oral gavage. Perturbation of microbiota was accompanied by a general inflammatory state and alteration of some endocannabinoidome members in the gut. Behavioural changes, including increased immobility in the tail suspension test and reduced social recognition were observed, and were associated with altered BDNF/TrkB signalling, TRPV1 phosphorylation and neuronal firing in the hippocampus. Moreover, morphological rearrangements of non-neuronal cells in brain areas controlling emotional behaviour were detected. Subsequent probiotic administration, compared with vehicle, counteracted most of these gut inflammatory, behavioural, biochemical and functional alterations. Interestingly, levels of Lachnospiraceae were found to significantly correlate with the behavioural changes observed in dysbiotic mice. Our findings clarify some of the biomolecular and functional modifications leading to the development of affective disorders associated with gut microbiota alterations.


International Journal of Immunopathology and Pharmacology | 2015

Enteric glia: A new player in inflammatory bowel diseases

Elena Capoccia; Carla Cirillo; Stefano Gigli; Marcella Pesce; Alessandra D'Alessandro; Rosario Cuomo; G. Sarnelli; Luca Steardo; Giuseppe Esposito

In addition to the well-known involvement of macrophages and neutrophils, other cell types have been recently reported to substantially contribute to the onset and progression of inflammatory bowel diseases (IBD). Enteric glial cells (EGC) are the equivalent cell type of astrocyte in the central nervous system (CNS) and share with them many neurotrophic and neuro-immunomodulatory properties. This short review highlights the role of EGC in IBD, describing the role played by these cells in the maintenance of gut homeostasis, and their modulation of enteric neuronal activities. In pathological conditions, EGC have been reported to trigger and support bowel inflammation through the specific over-secretion of S100B protein, a pivotal neurotrophic factor able to induce chronic inflammatory changes in gut mucosa. New pharmacological tools that may improve the current therapeutic strategies for inflammatory bowel diseases (IBD), lowering side effects (i.e. corticosteroids) and costs (i.e. anti-TNFα monoclonal antibodies) represent a very important challenge for gastroenterologists and pharmacologists. Novel drugs capable to modulate enteric glia reactivity, limiting the pro-inflammatory release of S100B, may thus represent a significant innovation in the field of pharmacological interventions for inflammatory bowel diseases.


United European gastroenterology journal | 2017

Specific dyspeptic symptoms are associated with poor response to therapy in patients with gastroesophageal reflux disease

Alessandra D’Alessandro; Francesco Paolo Zito; Marcella Pesce; Paolo Andreozzi; E Efficie; Martina Cargiolli; Francesco Maione; G.D. De Palma; Rosario Cuomo; G. Sarnelli

Introduction In patients with gastroesophageal reflux disease (GORD), co-existence of functional dyspepsia (FD) is known to be associated with poor response to proton pump inhibitors (PPIs), but the contribution of specific dyspepsia symptoms has not yet been systematically investigated. Objective We aimed to characterize the impact of dyspepsia symptoms on response to PPIs in patients with GORD. Methods The enrolled subjects were consecutive patients with a diagnosis of GORD. All patients underwent a 24 hour pH–impedance test, while on PPI therapy. Patients were divided into two groups, refractory and responders, according to the persistence of GORD symptoms. A standardized questionnaire for FD was also administered to assess presence of dyspepsia symptoms. Results In the subgroup of refractory patients FD was more prevalent than in responders, with post-prandial fullness, nausea, vomiting, early satiation and epigastric pain being significantly prevalent in refractory GORD patients. In the multivariate analysis only early satiation and vomiting were significantly associated with poor response to PPIs. Conclusion Co-existence of FD is associated with refractory GORD. We showed that only early satiation and vomiting are risk factors for poor response to therapy with PPIs. Our findings suggest that symptoms of early satiation and vomiting would help to identify the subset of PPI-refractory GORD patients.


Digestive and Liver Disease | 2011

P.1.147: RAGE-DEPENDENT S100B PROTEIN MODULATION OF PERIPHERAL AND MUCOSAL IMMUNE CELLS' FUNCTIONS IN PATIENTS WITH ULCERATIVE COLITIS (UC)

Carla Cirillo; G. Sarnelli; Fabio Turco; Alessandra D'Alessandro; Annamaria Mango; Rosario Cuomo

colitis (mortality; clinical scores, weight loss) was significantly greater in TPH2 KO than in WT animals. The enhanced severity was also evident in enteric histological scores, leukocyte infiltration, and cytokine expression. These data are compatible with the ideas that by promoting inflammation, mucosal 5-HT enhances the defense of the bowel against infection, while neuronal 5-HT makes such an effect less damaging by protecting the ENS from inflammation. Mucosal and neuronal 5-HT may thus exert antagonistic effects on inflammation that are functionally synergistic. Supported by a clinical and translational pilot grant from Columbia University (KGM) and NS12969 (MDG).

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Rosario Cuomo

University of Naples Federico II

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Carla Cirillo

Katholieke Universiteit Leuven

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Marcella Pesce

University of Naples Federico II

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Gabriele Budillon

University of Naples Federico II

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Alessandra D'Alessandro

University of Naples Federico II

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Alba Rocco

University of Naples Federico II

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Giuseppe Esposito

Sapienza University of Rome

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Maria Savarese

University of Naples Federico II

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Eleonora Efficie

University of Naples Federico II

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Fabio Turco

University of Naples Federico II

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