Impaired gut barrier function has been reported in some functional gastrointestinal (GI) disorders.Evidences suggest that gut microbiota affects GI motility in particular Lactobacillus species ...elicits anti‐inflammatory activity and exerts protective effects on damage induced by pathogen Gram negative‐derived lipopolysaccharide(LPS). LPS produced an oxidative imbalance in human colonic smooth muscle cells (SMC) that persists after LPS‐washout and contributes to SMC morphofunctional alterations. Aim: evaluate if supernatants harvested from LGG cultures protect SMC from LPS‐induced myogenic damage.Methods:L. rhamnosus GG (ATCC 53103 strain) was grown in MRS medium and samples were collected from bacterial cultures in middle exponential phase, in early, in middle and late stationary phase (overnight).Supernatants were recovered, filtered and stored at ‐20 °C. Highly pure human SMC culture was then exposed for 24 h to highly purified LPS (1 μg/ml) of E.coli (O111:B4) in the absence and presence of the supernatants.Their effects were evaluated on LPS‐induced SMC morphofunctional alterations and pro‐inflammatory IL‐6 production. Data are expressed as mean ± SE (p < 0.05 significant).Results:LPS induced persistent significant 20.7% ± 1.2 cell shortening and 35.2% ± 2.6 decrease in contraction of human colonic SMC. These alterations were paralleled to a 238.5% ± 82.5 increase in IL‐6 production.These effects disappeared in the presence of LGG‐supernatants, following a progression related to LGG growth curve phases. Supernatants collected in the middle exponential phase already significantly partially restored LPS‐induced cell shortening by 43.4% ± 10.2 and IL6 increase by 47.6% ± 13.1 but had no effect on LPS‐induced inhibition of contraction. Supernatants collected later, in the early and middle stationary phase, further counteract LPS‐induced damage, including inhibition of contraction. Maximal protective effects were observed with supernatants of the late stationary phase where LPS‐induced cell shortening was reversed by 86% ± 4.7, inhibition of contraction by 98.2% ± 1.8 and IL6 basal production by 91.3% ± 0.6.Conclusions: LGG secreted products are substances/byproducts able to directly protect human SMC from LPS‐induced myogenic damage. Novel insights are then provided about the possibility that LGG‐derived products could reduce the risk of progression to a post‐infective motor disorder.
The term ‘functional gastrointestinal disorder (FGID)’ is used to define several variable combinations of chronic or recurrent gastrointestinal (GI) symptoms that do not have an identified underlying ...pathophysiology. In the absence of any objective marker, the identification and classification of FGIDs are based on symptoms. The most widely accepted classification is based on the ‘Rome diagnostic criteria,’ which have classified 24 FGIDs into oesophageal, gastroduodenal, bowel, biliary, anorectal and abdominal pain subcategories. Classification into mutually exclusive categories has been useful for performing epidemiological studies in homogeneous populations, but has inevitably lead to disregarding subjects with overlapping FGIDs, or with a not sufficiently standardised symptom presentation. The epidemiology of FGID is still in its infancy, as indicated by the lack of epidemiological data for many FGIDs and the widely different incidence and prevalence rates reported for the most frequently occurring and investigated FGIDs: irritable bowel syndrome (IBS), dyspepsia, constipation and oesophageal disorders. Epidemiological studies and the definitions of the various FGIDs need to be further improved and standardised.
The term “dysfunction” defines the motor disorders of the gall bladder and the sphincter of Oddi (SO) without note of the potential etiologic factors for the difficulty to differentiate purely ...functional alterations from subtle structural changes. Dysfunction of the gall bladder and/or SO produces similar patterns of biliopancreatic pain and SO dysfunction may occur in the presence of the gall bladder. The symptom-based diagnostic criteria of gall bladder and SO dysfunction are episodes of severe steady pain located in the epigastrium and right upper abdominal quadrant which last at least 30 minutes. Gall bladder and SO dysfunctions can cause significant clinical symptoms but do not explain many instances of biliopancreatic type of pain. The syndrome of functional abdominal pain should be differentiated from gall bladder and SO dysfunction. In the diagnostic workup, invasive investigations should be performed only in the presence of compelling clinical evidence and after non-invasive testing has yielded negative findings. Gall bladder dysfunction is suspected when laboratory, ultrasonographic, and microscopic bile examination have excluded the presence of gallstones and other structural abnormalities. The finding of decreased gall bladder emptying at cholecystokinin-cholescintigraphy is the only objective characteristic of gall bladder dysfunction. Symptomatic manifestation of SO dysfunction may be accompanied by features of biliary obstruction (biliary-type SO dysfunction) or significant elevation of pancreatic enzymes and pancreatitis (pancreatic-type SO dysfunction). Biliary-type SO dysfunction occurs more frequently in postcholecystectomy patients who are categorized into three types. Types I and II, but not type III, have biochemical and cholangiographic features of biliary obstruction. Pancreatic-type SO dysfunction is less well classified into types. When non-invasive investigations and endoscopic retrograde cholangiopanreatography show no structural abnormality, manometry of both biliary and pancreatic sphincter may be considered.
Subjects with irritable bowel syndrome may undergo an excess of cholecystectomy. It is not known, however, whether the cholecystectomy rate parallels an increased risk of gallstones.
Aim was to ...assess the prevalence and the incidence of gallstones and cholecystectomy in subjects with irritable bowel syndrome symptoms.
In this population-based study, 29,139 subjects (63.2% of 46,139 randomly selected subjects, age 30-69 years) underwent a physical examination, an interview on gastrointestinal symptoms and an upper abdominal ultrasonography. An identical survey was carried out 7.8+/-1.0 (M+/-S.D.) years later on 8460 gallstone-free subjects at the first survey. Prevalence and incidence of gallstones and cholecystectomy were assessed in subjects with (1) irritable bowel syndrome; (2) abdominal pain and normal bowel; (3) altered bowel and no abdominal pain and (4) asymptomatic controls; univariate and multivariate regression logistic models were used for statistical analysis.
Prevalence odds of gallstones and cholecystectomy were significantly higher in irritable bowel syndrome and abdominal pain and normal bowel than in controls. Irritable bowel syndrome and abdominal pain and normal bowel subjects were more aware of gallstones than controls (p<0.001), and the prevalence of gallstones in irritable bowel syndrome subjects unaware of their gallbladder status was not significantly different from the controls. The incidence of gallstone disease in irritable bowel syndrome, abdominal pain and normal bowel, and altered bowel and no abdominal pain subjects did not differ from the controls. The incidence of cholecystectomy was higher in irritable bowel syndrome and abdominal pain and normal bowel groups than in controls and altered bowel and no abdominal pain group.
Irritable bowel syndrome subjects have an increased risk of cholecystectomy that is not due to an increased risk of gallstones, but rather to abdominal pain, awareness of having gallstones, and inappropriate surgical indications.
Idiopathic achalasia is a rare disorder of the oesophagus of unknown aetio‐pathogenesis characterized by a myenteric inflammation, aperistalsis and insufficient lower oesophageal sphincter ...relaxation. Vasoactive intestinal peptide (VIP), present in the myenteric plexus, is involved in smooth muscle relaxation and acts as an anti‐inflammatory cytokine. The human VIP receptor 1 gene (VIPR1) is highly polymorphic and may play a role in idiopathic achalasia. One hundred and four consecutive patients and 300 random controls from the same geographic area were typed for five SNPs mapping in the VIPR1 gene. Patients with idiopathic achalasia show a significant difference in allele, genotype and phenotype distribution of SNP rs437876 mapping in intron 4. This association, however, was almost entirely due to the group of patients with late disease onset (P = 0.0005). These results strongly suggest that idiopathic achalasia is a heterogeneous disease with a different aetiology in cases with early or late disease onset.
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