Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IL-4, IL-5, tryptase and eosinophil cationic protein levels were measured in nasal lavage fluid from 15 pollen allergic rhinitis beyond pollen season. Allergy was proved by prick test. There were 15 non allergic children in the control group. Specific nasal allergen provocation was performed on the rhinitic group. Nasal lavage were done before, 1 and 12 hours after the provocation. Before the nasal provocation the ECP and IL-4 levels were significantly higher in the allergic group compared to the non allergic group. The levels of tryptase, ECP and IL-4 rose significantly after the provocation. The results reflect to the possibility of an activated immune status in allergic rhinitis even without the presence of the triggering pollens. After the specific provocation elevated tryptase levels were measured, referring to the activity of the early phase of the I. type hypersensitivity reaction, while the ECP and IL-5 elevation to its late phase. According to our examinations it can be said, that tryptase, ECP and IL-5 might be used to detect the activation of the early and late phases of the IgE mediated hypersensitive reaction.
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PMID:[Levels of interleukin-4, interleukin-5, tryptase and eosinophil cationic protein of nasal lavage fluid in pollen allergic rhinitis]. 1101 93

Since asthma has been recognized as a chronic inflammatory airway disease, inflammatory markers are useful tools to show the degree of allergic airway inflammation. Asthmatic airway is characterized with infiltration of activated Th2 lymphocyte, eosinophils and mast cells/basophils. Eosinophil derived proteins such as ECP, MBP and EDN are important markers indicating eosinophilic inflammation. Histamine and tryptase are the products of mast cell/basophil activation. These markers are detected in sputum, BALF, serum and urine, and increased in asthmatics. In addition to these markers, NO concentration in exhaled air, cytokines such as IL-4, IL-5, chemokines such as RANTES, eotaxin, LTE4, MMP are inflammatory markers to indicate the quality and quantity of asthmatic airway inflammation. Assessment of these markers, therefore, contributes to better control of asthmatic symptoms with appropriate therapy.
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PMID:[Airway inflammatory marker]. 1167 35

Allergen specific immunotherapy (IT) represents a cornerstone of allergic rhinitis treatment and his efficacy has been confirmed, through open and double blind trials and meta-analysis. In the last few years non invasive routs for IT (oromucosal, nasal) were developed gained general acceptation mainly in children and were validated by WHO. The efficacy of IT could be markers, the pattern of specific antibody response or by the effect on sequential nasal challenges. We have evaluated the effect of IT in allergic rhinitis by different methods. Nasal IT decreased mean symptoms and pharmacological scores as well as in seasonal as in perennial rhinitis. The same decrease has been observed after oromucosal IT. The effect of IT in allergic inflammation has been confirmed by a decrease in the level of soluble adhesion molecule sVCAM-1 which is related to eosinophilic inflammation but not statistically for sICAM-1. We have also evaluated the immunoblotting pattern or specific IgE after oromucosal IT for house dust mites. For D. pteronyssinus in 4 patients the bands intensity decreased and in 3 patients the bands decreased and in 10 disappeared. IT decreases tryptase and ECP in nasal lavage after sequential nasal challenges. Therefore IT decreases clinical scores, inflammation markers, specific IgE immunoblotting bands and response to allergen challenge. These different results confirm his efficacy and usefulness in allergic rhinitis.
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PMID:Immunotherapy in allergic rhinitis. 1176 23

Specific vasomotorial rhinopathy, or allergic rhinitis is to be seen as a systemic pathology characterized by a condition of hyperactivity, the target organ of which is the nose. Particular attention, among the diagnostic tests, should be reserved to the specific nasal provocative test (sNPT), which has been part of the clinical routine for years but has nonetheless failed to achieve a suitable level of standardization. With this intent, we have devoted the present work to the assay of several phlogosis mediators (tryptase, specific IgE and ECP) before and after performing the sNPT. We have studied 20 patients affected by allergic rhinitis, aged between 13 and 61, with single or multiple allergen sensitivities, but in any case with a predominant sensitization, who underwent sNPT between October 2000 and July 2001. In every patients we performed ECP, tryptase and specific IgE assay via direct incubation in the nasal mucosa, before and after specific nasal provocation. The results of the sNPT (rhinomanometry and symptoms score) were compared with the variations in the phlogosis mediators assayed at nasal level. On the basis of the variations in the rhinomanometric resistance and symptoms score, the sNPT was positive in 10 patients (50%). Tryptase and specific IgE increased to a statistically significant degree (respectively, p = 0.01 and p < 0.05) in all of the patients; the ECP variations, instead, were not significant (p > 0.05). Overall, the simultaneous assay of ECP, tryptase and specific IgE, increasing the sensibility of the sNPT, enabled a positive result to be ascertained in 60% of the subjects examined. The method is furthermore based on the principle of local reactivity in that it assays the phlogosis mediators not at systemic level, but directly in the target organ, showing itself to be more specific than level I and II tests.
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PMID:[Specific nasal provocative test in allergic rhinitis diagnosis: reliability and standardization]. 1237 41

The specific Nasal Provocation Test (sNPT) is a third level diagnostic tool. Fitted to reproduce natural exposure condition to pick the responsible allergen for nasal symptoms out, it is applied when prick test and RAST responses are doubtful. SNPT results have been evaluated measuring nasal resistance (anterior rhinomanometry) and nasal symptoms (clinical score), reaching 50% of sensitivity. This study focused on the determination of allergic response markers, triggered by nasal challenge: tryptase levels in the nose, specific IgE and ECP (Eosinophil Cationic Protein). The aim was to increase sNPT sensitivity. Twenty patients suffering from allergic rhinitis and 16 age-matched-nonallergic subjects were enrolled in the study. Tryptase, specific IgE and ECP were determined in nasal mucosa applying a new method, based on in situ incubation, before and after sNPT. The latter was performed following a standardized method. Tryptase levels increased in 13 patients (65%), were unchanged in four patients (20%), and slightly decreased in three patients (15%). The increase recorded was significant in mite allergic patients (p=0.005), but not significant (p> 0.05) in pollen allergic patients. ECP values increased in 13 patients (65%), were unchanged in two patients (10%), and highly decreased in five patients (25%). ECP increase was not significant (p> 0.05). Specific IgE levels increased in seven patients (35%), were unchanged in 11 patients (55%) and decreased in two patients (10%). The IgE increase was significant in pollen-allergic patients (p<0.05), while it was not significant in mite-allergic patients (p>0.05). Tryptase, ECP, and specific IgE were not detected in the control group. The data obtained showed a positive sNPT response in 12 patients (60%). Comparing our results with those derived from classical-parameter employment, we gathered an improvement of 10%. On the basis of the usual parameters, in fact, we recorded 50% positivity, while the use of mediators provided an additional 10% improvement in sNPT sensitivity: taking together the usual parameters and nasal allergic mediators values, we reached an sNPT over-all sensitivity of 85%.
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PMID:Do tryptase, ECP and specific IgE measurement by nasal incubation increase the specific nasal provocation test sensitivity? 1517 21

To probe ionic contacts of skeletal muscle myosin with negatively charged residues located beyond the N-terminal part of actin, myosin subfragment 1 (S1) and actin split by ECP32 protease (ECP-actin) were cross-linked with 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC). We have found that unmodified S1 can be cross-linked not only to the N-terminal part, but also to the C-terminal 36 kDa fragment of ECP-actin. Subsequent experiments performed on S1 cleaved by elastase or trypsin indicate that the cross-linking site in S1 is located within loop 2. This site is composed of Lys-636 and Lys-637 and can interact with negatively charged residues of the 36 kDa actin fragment, most probably with Glu-99 and Glu-100. Cross-links are formed both in the absence and presence of MgATP.P(i) analog, although the addition of nucleotide decreases the efficiency of the cross-linking reaction.
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PMID:Ionic interaction of myosin loop 2 with residues located beyond the N-terminal part of actin probed by chemical cross-linking. 1805 41

Nasal obstruction is the main symptom in patients with allergic rhinitis and may be measured by rhinomanometry. Rupatadine is a new antihistamine with potential antiallergic activities. The aim of this pilot study is to evaluate nasal symptoms, nasal airflow and nasal mediators in patients with persistent allergic rhinitis, before and after treatment with rupatadine. Twenty patients with persistent allergic rhinitis were evaluated, 15 males and 5 females (mean age 35 +/- 9.1 years), all of whom received rupatadine (10 mg/daily) for 3 weeks. Nasal and ocular symptoms (measured by VAS), rhinomanometry, and nasal mediators (ECP and tryptase) were assessed in all subjects before and after treatment. Rupatadine treatment induced significant symptom relief (both nasal and ocular, respectively p=0.005 and p=0.0004), including obstruction (p=0.0015) and significant increase of nasal airflow (p=0.0025). Moreover, there was a significant difference of nasal mediators. In conclusion, this pilot study demonstrates the effectiveness of rupatadine treatment in: i) improving nasal and ocular symptoms, ii) increasing nasal airflow, iii) exerting antiallergic activity in patients with persistent allergic rhinitis. These positive results could explain the effectiveness of rupatadine in the treatment of persistent allergic rhinitis, as reported in a previous study Further controlled studies need to be conducted to confirm these preliminary findings.
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PMID:Rupatadine improves nasal symptoms, airflow and inflammation in patients with persistent allergic rhinitis: a pilot study. 2048 31

The identification of inflammatory mediators in the tear fluid have been extensively used in ocular allergy to find either a 'disease marker', to better understand the immune mechanisms involved in the ocular surface inflammation, or to identify potential targets for therapeutic interventions. While the clinical characteristics allow a relatively convincing diagnosis of ocular allergic diseases, in the initial, non active phases, or in the chronic stages, the diagnosis may not be clear. Although not highly specific, total tear IgE can be measured with local tests by inserting a paper strip in the lower meniscus. The measurement of tear specific inflammatory markers, such as histamine, tryptase, ECP, IL-4, IL-5 and eotaxin, may be useful for the diagnosis or monitoring ocular allergy. New technologies such as multiplex bead assays, membrane-bound antibody array and proteomic techniques can characterize the distribution of a wide range of bioactive trace proteins in tears. Dozens of mediators, cytokines, chemokines, growth factors, angiogenic modulators, enzymes and inhibitors were thus identified in small tear samples using these techniques, providing the possible identification of specific biomarker for either specific disease or disease activity. However, to date, there is no a single specific laboratory test suitable for the diagnosis and monitoring of allergic conjunctivitis.
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PMID:Allergy and allergic mediators in tears. 2389 62


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