Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible development of type-1 hypersensitivity reactions in the abomasal mucosa caused by soluble L3 products of Ostertagia ostertagi was studied in 4-month-old calves sensitized by repeated exposure to L3 over a 50-day period followed by anthelmintic treatment. Four groups each of 4 calves were used. Group 1 served as nonsensitized controls and group 2 as sensitized controls, group 3 was challenge exposed at 2-week intervals beginning at week 10 with a soluble L3 product (OAG), and group 4 was challenge exposed at 2-week intervals with an oral dose of L3, followed by anthelmintic treatment 3 days later. All calves infected with L3 became sensitized, as indicated by a positive reaction to an intradermal skin test. However, a passive cutaneous anaphylaxis was only partly effective in indicating the presence of homocytotropic antibody in the infected calves. Sensitized calves had significantly (P less than 0.05) higher eosinophil counts and plasma pepsinogen values for the entire 14 weeks than uninfected controls. Globule leukocyte and mast cell counts from the abomasal mucosa were also significantly (P less than 0.05) higher. Studies for possible immunomodulation revealed that lymphocyte counts decreased between every 2-week challenge-exposure period for groups-3 and -4 calves. A transient depression of blood lymphocyte (BL) responses to phytohemagglutinin (PHA), a T-cell mitogen, was observed over the first 8 weeks in the infected calves. Increases in BL responses to OAG were also observed. Differences were not observed in BL responses to pokeweed mitogen, a T- and B-cell mitogen. Blood lymphocyte responses to PHA in group-3 calves were low following the initial challenge exposure with OAG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse immune reactions and the pathogenesis of Ostertagia ostertagi infections in calves. 233 87

Serum pepsinogen concentrations rose more rapidly and to higher levels in adult sheep infected with Ostertagia circumcincta and treated orally with the mast cell stabilising agent sodium cromoglycate than they did in adult sheep infected with the parasite which remained untreated. Sodium cromoglycate did not affect the serum pepsinogen concentrations or abomasal pH in uninfected sheep.
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PMID:Effect of sodium cromoglycate on the response to Ostertagia circumcincta in adult sheep. 312 Feb 62

1. Evidence is given for the presence of at least five pepsinogens in a crude extract of mixed chicken stomachs. One of these was purified and could be activated to yield a single pepsin. 2. The molecular weights of the pepsinogen and pepsin were 36000 and 34000 respectively. The pepsin associated at low pH values and low ionic strength. 3. The amino acid analyses of both proteins are given. The pepsin was devoid of phosphate but contained carbohydrate. 4. The N-terminal amino acids of pepsinogen and pepsin were serine and threonine respectively. Five amino acids were released by carboxypeptidase A and it was deduced that serine may be the C-terminal one. 5. Each protein contained one thiol group per molecule as determined by titration with p-chloromercuribenzoate. The rate of the reaction was very rapid with pepsin, but much slower with pepsinogen, although the same group appeared to react in both instances. The enzymic activity of pepsin was unaffected by the modification. 6. The isoionic point of the pepsin was close to pH4.0 and the enzyme was stable for long periods at pH values up to 7.0. 7. The enzyme hydrolysed bisphenyl sulphite almost as rapidly as did pig pepsin A.
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PMID:The purification and properties of a single chicken pepsinogen fraction and the pepsin derived from it. 457 60

The effects on liveweight gain and development of immunity were studied in lambs trickle infected for 8 weeks with either a benzimidazole-resistant isolate (Moredun ovine resistant isolate, MORI), a multiple benzimidazole + ivermectin-resistant isolate (Moredun caprine resistant isolate, MCRI) or an unselected susceptible isolate (Moredun ovine susceptible isolate, MOSI) of Teladorsagia circumcincta. Plasma pepsinogen concentrations of infected groups were significantly elevated compared to an uninfected control group (P < 0.001) by day 14. The liveweight gains varied markedly but there were no statistical differences between the infected and uninfected control groups at any point in time during the study. Lambs infected with the MORI had significantly lower faecal consistency scores than the other challenged groups on days 7 and 14 (P < 0.05) but from day 21 onwards, faecal consistencies were similar in all of the groups. There was a notable difference in the pre-patent periods of the different isolates with the MOSI producing positive faecal egg counts (FECs) by day 14 of the study. The FECs remained reasonably low once infections had reached patency and there were no further differences between the groups. Following administration of anthelmintic to remove residual worms from the trickle infection, no differences between the infected groups in terms of worm burden or mucosal mast cell numbers were evident as a consequence of a single challenge infection. The changes in genetic code associated with enhanced resistance against anthelmintics do not appear to have resulted in any fundamental alteration of the pathogenicity and immunogenicity of these three isolates of Teladorsagia.
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PMID:Pathogenicity and immunogenicity of different isolates of Teladorsagia circumcincta. 965 94

It has been suggested that the periparturient breakdown of immunity to parasites has a nutritional basis. Our overall hypothesis is that it results from a prioritised scarce nutrient allocation to reproductive functions (e.g. milk production) rather than to immune functions. We tested this hypothesis by offering five levels of dietary metabolisable protein, ranging from 0.65 to 1.25 times their assumed requirements, for 4 weeks post-parturition to twin-rearing Greyface ewes, experimentally infected with Teladorsagia circumcincta. We hypothesised that the initial increments of metabolisable protein supply would increase milk production without affecting the degree of breakdown of immunity whilst later increments would reduce the degree of breakdown of immunity. The first two increments of metabolisable protein supply indeed increased milk production and did not affect final worm burdens, but in contrast to the expectation, reduced faecal egg counts and total egg output. The last two increments of metabolisable protein supply did not further affect milk production and egg output, but resulted in reduced final worm burdens. Metabolisable protein supply did not affect plasma IgG and IgE antibody against somatic L(3) antigen but the first three increments reduced plasma pepsinogen and plasma IgA antibody. The last increment did not further reduce plasma pepsinogen but increased plasma IgA. Metabolisable protein supply did not systematically affect abomasal mucosal mast cell, globule leukocyte and eosinophil counts. Our results support the view that the priority of scarce metabolisable protein allocation to milk production over immune functions may be gradual rather than absolute. The contrast between effects of metabolisable protein supply on faecal egg count and final worm burden points towards the possibility that if different effector responses regulate fecundity and worm expulsion, then they would differ in their sensitivity towards changes in the degree of nutrient scarcity.
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PMID:Is the allocation of metabolisable protein prioritised to milk production rather than to immune functions in Teladorsagia circumcincta-infected lactating ewes? 1267 May 17

Peptic ulcer is a common disorder of gastrointestinal system and its pathogenesis is multifactorial, where smoking and nicotine have significant adverse effects. Smoking and chronic nicotine treatment stimulate basal acid output which is more pronounced in the smokers having duodenal ulcer. This increased gastric acid secretion is mediated through the stimulation of H2-receptor by histamine released after mast cell degranulation and due to the increase of the functional parietal cell volume or secretory capacity in smokers. Smoking and nicotine stimulate pepsinogen secretion also by increasing chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Smoking also increases bile salt reflux rate and gastric bile salt concentration thereby increasing duodenogastric reflux that raises the risk of gastric ulcer in smokers. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H. pylori, alcohol, nonsteroidal anti-inflammatory drugs or cold restrain stress. Polymorphonuclear neutrophils (PMN) play an important role in ulcerogenesis through oxidative damage of the mucosa by increasing the generation of reactive oxygen intermediates (ROI), which is potentiated by nicotine and smoking. Nicotine by a cAMP-protein kinase A signaling system elevates the endogenous vasopressin level, which plays an aggressive role in the development of gastroduodenal lesions. Smoking increases production of platelet activating factor (PAF) and endothelin, which are potent gastric ulcerogens. Cigarette smoking and nicotine reduce the level of circulating epidermal growth factor (EGF) and decrease the secretion of EGF from the salivary gland, which are necessary for gastric mucosal cell renewal. Nicotine also decreases prostaglandin generation in the gastric mucosa of smokers, thereby making the mucosa susceptible to ulceration. ROI generation and ROI-mediated gastric mucosal cell apoptosis are also considered to be important mechanism for aggravation of ulcer by cigarette smoke or nicotine. Both smoking and nicotine reduce angiogenesis in the gastric mucosa through inhibition of nitric oxide synthesis thereby arresting cell renewal process. Smoking or smoke extract impairs both spontaneous and drug-induced healing of ulcer. Smoke extract also inhibits gastric mucosal cell proliferation by reducing ornithine decarboxylase activity, which synthesises growth-promoting polyamines. It is concluded that gastric mucosal integrity is maintained by an interplay of some aggressive and defensive factors controlling apoptotic cell death and cell proliferation and smoking potentiates ulcer by disturbing this balance.
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PMID:Smoking and the pathogenesis of gastroduodenal ulcer--recent mechanistic update. 1461 84

This study compared the immunological and biochemical responses of co-grazed Suffolk and Texel lambs to a natural gastrointestinal nematode infection. Variables analysed included serum pepsinogen, total protein, albumin, haematological variables and nematode-specific serum immunoglobulin activity, at 11, 14 and 17 weeks of age. At 17 weeks, randomly selected lambs were necropsied to determine worm burdens, nematode-specific mucosal abomasal and intestinal immunoglobulin activity. Nematode burden, faecal egg count and pepsinogen concentrations were significantly higher in Suffolks relative to Texels, at all 3 time-points investigated. Suffolks displayed significantly higher erythrocyte, total leukocyte, lymphocyte and neutrophil counts, mean cell volume and packed cell volume, than Texels (P<0.01). However, breed differences in eosinophil counts were not significant. While serum nematode-specific antibody activity levels were significantly higher (P<0.001) in Texels for all isotypes measured, antibody activity levels at a mucosal level were equivalent in both breeds. Correlation analysis of mucosal antibody levels and nematode variables highlighted a more consistent pattern of events in Texels, with more mucosal antibodies negatively correlated with FEC and worm burden, in comparison to Suffolks. In particular, an important role for mucosal IgE is proposed. In Texels, a significant and negative correlation was identified between IgE and faecal egg counts and worm burden (FEC: -0.48, P<0.005). This was not observed in Suffolks. The evidence suggests that susceptibility in Suffolks may be mediated through poor IgE affinity/avidity and/or through deficiencies in related mechanisms such as mast cell production, recruitment or activation.
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PMID:Breed differences in mucosal and systemic antibody response to nematode infection in sheep: an important role for IgE? 1790 17