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Biomedical subjects

S Auricchio

Publications and source records attributed to S Auricchio.

At least 91 records · Page 5Linked to original sources
PubMed1987

Passage of gliadin into human breast milk.

Samples of breast milk were taken from 53 women following the ingestion of 20 g of gluten. The samples were analysed for the presence of gliadin by a double-antibody sandwich enzyme immunoassay. Gliadin (5-95 ng/ml) was detected in 54/80 samples collected at various stages of lactation. Maximum levels in milk were found 2-4 hours after ingestion; gliadin could not be detected in serum. The transfer of gliadin from mother to infant might be critical for the development of an appropriate specific immune response to gliadin later in life.

Administration, Oral↗
PubMed1987

Cisapride for gastro-oesophageal reflux and peptic oesophagitis.

Twenty children (age range 75 days-47 months) with reflux oesophagitis entered a random double blind trial in which they received either Cisapride (Janssen Pharmaceutical Ltd), a new prokinetic agent, or an identical placebo syrup. Diagnosis of gastro-oesophageal reflux was made by measurement of intraluminal oesophageal pH combined with manometry. Oesophagitis was assessed in all patients by histological examination of mucosal specimens taken during oesophagogastroduodenoscopy. Manometry, pH test, and endoscopy with biopsy examination were repeated at the end of the treatment period. Seventeen patients completed the trial, eight of whom were taking the drug and nine the placebo. Mean total clinical score and post-prandial reflux time (% of reflux) significantly improved in patients in the group given Cisapride but not in the group given placebo. Furthermore, there was a significant improvement of the histological oesophagitis score only in the children in the group given Cisapride, whereas placebo was ineffective. It is concluded that Cisapride is a useful agent both for the relief of symptoms of gastro-oesophageal reflux and for the healing of peptic oesophagitis in infancy.

Child, Preschool↗
PubMed1987

Prevention by mannan and other sugars of in vitro damage of rat fetal small intestine induced by cereal prolamin peptides toxic for human celiac intestine.

Peptic-tryptic-cotazym and peptic-tryptic digests were obtained, simulating in vivo protein digestion, from pure "bread" wheat gliadins and from rye, barley, and oats prolamine and tested on small intestine cultures from fetal rats. When tested at a concentration of 0.1 mg of peptides/ml of culture medium the peptic-tryptic-cotazym and peptic-tryptic digests of gliadin and prolamines were very active in slowing in vitro development of fetal rat intestine and in increasing the occurrence and severity of degenerative changes. The ability of some sugars to interfere with inhibition of fetal intestinal morphogenesis induced by these peptides was also tested. Mannan at a concentration of 0.1 mM was effective in allowing intestinal morphogenesis to take place in the presence of prolamine peptic-tryptic-cotazym and prolamine peptic-tryptic digests of the four toxic cereals. Some oligomers of N-acetyl-glucosamine were also effective in blocking the inhibitory effect of "bread" wheat gliadin peptides. These data are compatible with the hypothesis that some sugars may exert a protective effect on the toxic activity of cereal prolamin peptides on the human celiac intestine.

Animals↗
PubMed1987

In vitro gliadin antibody production by peripheral blood mononuclear cells from patients with coeliac disease.

In vitro spontaneous IgG gliadin antibody production was shown in peripheral blood mononuclear cell (PBMC) cultures from 12/14 patients with active coeliac disease; in most cases no increase and sometimes a marked reduction of the in vitro synthesis was observed after pokeweed mitogen (PWM) addition. Lower levels of gliadin antibodies were also detected in PBMC cultures from 7/12 coeliac patients in remission; in all the cases the synthesis was increased by PWM. In vitro production was confirmed by higher levels in 7-day culture supernatants than in 0-day frozen-thawed cell pellets and by the inhibitory effect of cycloheximide. Spontaneous release of antibodies occurred within the first 3 days of culture, while PWM-induced antibody production reached a plateau after 7-9 days. The analysis of the in vitro gliadin antibody production is a promising technique to assess the regulatory mechanisms involved in the humoral immune response to gliadin.

Adolescent↗
PubMed1986

On the primary site of control in the spontaneous development of small-intestinal sucrase-isomaltase after birth.

We have compared the appearance in the small intestine of baby rabbits, of sucrase and isomaltase activities and of the sucrase-isomaltase mRNA. For the latter we used a cDNA probe encompassing approximately 4.1 kb from the 5'-end of pro-sucrase-isomaltase cDNA [(1986) Cell 46, 227-234]. Sucrase-isomaltase mRNA and the enzyme activities developed simultaneously from the 15th day after birth onwards. Over two orders of magnitude the enzymatic activities and sucrase-isomaltase mRNA matched one another closely, thus ruling out translation as the main site of biosynthetic control during spontaneous development, while rendering very probable transcription as the primary site of control. However, we cannot rule out the possibility that, prior to day 15, sucrase-isomaltase mRNA might be degraded so rapidly that it is not translated.

Age Factors↗
PubMed1986

[Current concepts in the pathogenesis of celiac disease].

This paper is a critical appraisal of current hypotheses on the mechanisms of toxicity of wheat and other cereals in coeliac disease. The "primary immune defect" and the "gluten-lectin" hypotheses on the pathogenesis of coeliac disease are examined and critically reviewed.

Agglutination↗
PubMed1986

A sandwich enzyme immunoassay for wheat gliadin.

A sandwich double antibody solid-phase enzyme immunoassay (EIA) that can detect and quantitate gliadin is described. Quantitative analysis could be carried out in the range of 5-400 ng/ml and the assay was more sensitive than inhibition EIA. Gliadin possessed weak cross-reactivity with oats, maize and rice prolamines. In the presence of anti-gliadin antibody (serum from a patient with active coeliac disease) gliadin could not be detected, but the sensitivity of the assay was restored by heat treatment of the serum. This EIA can therefore be employed to assess the gliadin content of biological fluids where specific antibody may coexist.

Antibody Specificity↗
PubMed1986

Esophageal motor abnormalities in children with gastroesophageal reflux and peptic esophagitis.

Esophageal motility was studied in 26 children with gastroesophageal reflux. In 11 patients (group A), esophagitis was severe; in the remaining 15 (group B), either mild or no microscopic changes were found. Lower esophageal sphincter pressure and amplitude, as well as velocity and duration of esophageal pressure waves, were manometrically measured. All patients underwent a 12-week intensive antacid course. Manometric tracings, blindly read, were compared with those of 16 age-matched children with emesis without proven reflux (group C). Among the variables analyzed, amplitude of the motor waves was significantly lower in patients with severe esophagitis than in group B and C patients (P less than 0.01). Nonspecific motor defects (simultaneous, broad-based, double-peaked waves) were more commonly present in group A. At the end of therapy, symptoms had either disappeared or significantly improved. Endoscopic and histologic studies showed disappearance of the severe inflammatory changes. Manometry, repeated in patients with cured severe esophagitis, showed normalization of the amplitude and significant decrease of the nonspecific motility abnormalities. We conclude that severe gastroesophageal reflux disease in children causes esophageal motor dysfunction, resulting from esophageal inflammation. The occurrence of esophageal motility disorders only in patients with severe esophagitis and its disappearance after therapy may account for the favorable course of reflux disease in infancy.

Antacids↗
PubMed1986

In vitro activation of adenylate cyclase of atrophic celiac intestinal mucosa by wheat gliadin-derived peptides.

In order to demonstrate that gliadin peptides may interact with cell membranes of celiac small intestinal mucosa, the capacity of these peptides to activate the cell membrane enzyme adenylate cyclase was tested. The addition of peptides from bread wheat purified A-gliadin and whole gliadin (proteins that are toxic for celiac patients) enhanced the adenylate cyclase activity of crude cell membrane preparations obtained from atrophic small intestinal mucosa of celiac patients. No activation of adenylate cyclase of this tissue was observed with peptides from proteins nontoxic for celiac patients (bread wheat albumin and maize prolamin). Gliadin peptides did not activate adenylate cyclase of morphologically normal small intestinal mucosa from normal subjects or from celiac patients in remission. These results, therefore, suggest that peptides from bread wheat gliadin may interact with cell membrane of atrophic small intestinal mucosa of celiac patients.

Adenylyl Cyclases↗
PubMed1985

Gastrointestinal transit time, frequency of defecation, and anorectal manometry in healthy and constipated children.

Total gastrointestinal transit time (TGITT), frequency of defecation, and anorectal manometry were evaluated in 63 pediatric patients referred for chronic nonorganic constipation; in 39, segmental transit times of the right and left colon and rectum were also measured. TGITT was significantly longer in chronically constipated children than in matched normal controls. Although bowel frequency was highly significantly correlated with TGITT in patients with prolonged transit time, not all children with prolonged TGITT had reduced bowel frequency. Moreover, not all children with constipation had prolonged TGITT. In children with idiopathic chronic constipation, slowing of intestinal transit occurred most frequently at the level of the distal colon and rectum. Anorectal motility variables were not significantly different in children with functional chronic constipation and in normal children. Maximal resting and pressure and mean intrarectal distending volume causing threshold inhibition in constipated patients did not significantly differ from the control values. Therefore, anorectal manometry did not detect relevant motor abnormalities in constipated children.

Anal Canal↗
PubMed1985

The effect of early feeding on the onset of symptoms in celiac disease.

The appearance of celiac disease in infancy has often been related to the time when gluten is introduced into the diet, and more recently, to the kind of milk received in the early months. This retrospective study attempts to clarify the relation between breast-feeding and gluten introduction to the onset of symptoms of the disease. One hundred forty-six children with celiac disease, aged from 4 months to 11 years, were studied. The timing and types of feeds were recorded as well as the presenting symptoms of the disease. Data were analyzed by nonparametric statistical methods, as well as by parametric analysis after appropriate transformation. Children breast-fed for 3 months or more showed a marked delay in the onset of the disease and a longer latency time from gluten introduction to onset of disease, when compared with bottle-fed children. This relationship was present for both statistical analyses and was unrelated to the age at gluten introduction into the diet. Onset of disease was positively correlated to the duration of breast-feeding and not related to the age at gluten introduction.

Breast Feeding↗
PubMed1985

Isolation and characterization of two particle-bound oligoaminopeptidases from human meconium that are different from oligoaminopeptidase of adult small intestine.

Two oligoaminopeptidases (substrate L-leucyl-beta-naphthylamide) have been separated by ion exchange chromatography after Triton solubilization of meconial particles. The quantitatively major form (oligoaminopeptidase II) has been purified to apparent homogeneity. The two meconial oligoaminopeptidases differ from each other in their polyacrylamide gel electrophoretic mobility and isoelectric points. Both meconial enzymes differ from the adult enzyme by having more acidic isoelectric points and different affinities to Helix pomatia lectin-Sepharose columns. Oligoaminopeptidase II has a faster anodal electrophoretic mobility than the adult enzyme but a similar apparent molecular weight and subunit structure. Extensive neuraminidase digestion of meconial oligoaminopeptidase II does not modify the gel electrophoretic mobility of the enzyme. The charge difference between adult and meconial human brush border oligoaminopeptidases is therefore probably due, at least in part, to differences in the carbohydrate composition of these glycoproteins, and differences in the number of terminal or exposed sialic acid residues do not explain the observed charge differences.

Adult↗
PubMed1985

Toxicity mechanisms of wheat and other cereals in celiac disease and related enteropathies.

This paper is a critical appraisal of current theories on the mechanisms of toxicity of wheat and other cereals in celiac disease and some related enteropathies. The "peptidase deficiency," "primary immune defect," and "gluten-lectin" theories on celiac disease are examined and critically discussed on the basis of the relevant data available in 88 references. Special attention has been paid in this review to the nature of the cereal components triggering the appearance of toxic symptoms and signs in celiac disease as well as to underlying action mechanisms. The gluten-lectin theory is the one best able to explain, in addition to celiac disease, some secondary intolerances that may occur in temporarily predisposed individuals as a consequence of several causes, including viral hepatitis and intestinal infections, as well as the occurrence of intestinal lesions in healthy subjects administered very high amounts of gluten.

Animals↗
PubMed1985

Impaired suppressor activity in children affected by coeliac disease.

Immunoregulatory cells were enumerated in 19 coeliac disease children on a gluten free diet by means of monoclonal antibodies that define total T lymphocytes (T3), helper/inducer T cells (T4), suppressor/cytotoxic T cells (T8) and monocytes (M1), as well as by means of surface receptors for Fc fragments of IgM and IgG (T mu and T gamma, respectively). In addition, suppressor cell function was assessed in 17 coeliac disease patients by examining the ability of concanavalin-A (Con-A)-activated suppressor cells to inhibit autologous cell response to mitogenic stimulus as compared with age-matched controls. No statistically significant differences were found in the percentages of subsets defined by monoclonal antibodies between coeliac disease patients and age-matched controls, whereas coeliac disease patients had a significant decrease of the subpopulation bearing membrane receptor for Fc fragment of IgG. Mean value was 8.5% in coeliac patients versus 13.4% in age-matched controls. In the functional assay, mononuclear cells from 10 out of 17 coeliac disease patients either totally or partially failed to suppress responder cells after Con-A-activation. This defect is not related to HLA-DR status, because no difference was found between patients-HLA-matched and unmatched normal individuals. In this assay, mononuclear cells of three coeliac disease patients with low suppressor activity were able to inhibit responder cells to the same extent as controls, when indomethacin was used to block prostaglandin production in the induction phase of Con-A-activated suppressor cells. Our results suggest that an abnormality in immunoregulation may play a role in the pathogenesis of coeliac disease.

Adult↗
PubMed1984

Agglutinating activity of gliadin-derived peptides from bread wheat: implications for coeliac disease pathogenesis.

The PT-digest of bread wheat gliadin was very active in agglutinating undifferentiated human K562(S) cells. This activity was quantitatively, but not qualitatively, similar to that of Con A or WGA. Moreover, Con A-induced cell agglutination was inhibited by mannan and mannose, WGA-induced agglutination by NAG only, and cell agglutination induced by bread wheat gliadin peptides was inhibited by each of these three saccharides. Not only was mannan the most active saccharide in preventing cell agglutination induced by bread wheat gliadin peptides, but it was also able to dissociate agglutinated cells. As compared to the PT- digest of whole bread wheat gliadin, the digest obtained from purified A-gliadin was tenfold more active. The PT-digest of durum wheat gliadin did not show any agglutinating activity.

Agglutination Tests↗
PubMed1984

Does casomorphin have a functional role?

Degradation of buffalo beta-casein by various physiological enzymes was studied. Digestion with gastric and pancreatic proteases plus leucine aminopeptidase did not release casomorphins but a putative precursor (procasomorphin) which was further digested by brush border peptidases into peptides differing from casomorphins.

Amino Acids↗