Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Children who are destined to develop asthma are considered to be susceptible to a variety of respiratory pathogens. To elucidate respiratory inflammation among these children, we measured the levels of eosinophil cationic protein (ECP) and tryptase in sputum taken from three different groups of wheezy infants and young children: those with a first wheeze (n = 15); those with recurrent wheeze (n = 27); and those with recurrent wheeze with respiratory distress, namely asthma (n = 56). The numbers of eosinophils or metachromatic cells determined by microscopic analysis of sputum samples were also evaluated in combination with the ECP and tryptase levels. Although neither sputum ECP nor tryptase was a clear discriminative marker that differentiated the three different types of wheezy disease, ECP levels in sputum from the asthma group were significantly higher (2,269.2 +/- 6,216.8 ng/g) than those in the recurrent wheezy group (440.3 +/- 1,199.8 ng/g) or in the first-wheeze group (209.0 +/- 172.9 ng/g). A similar trend was observed with tryptase levels in sputum, but there were no significant differences among the three groups. Sputum taken from asthmatic children showed a marked accumulation of eosinophils. However, an accumulation of eosinophils in sputum (even in the presence of an elevated level of sputum ECP) was not identified in the asthmatic infants < 1 year of age. An accumlation of eosinophils in sputum was not evident until children became > 1 year old and thereafter the eosinophils rapidly increased in number until the children reached 5 years of age. It was noteworthy that sputa positive for pathogenic bacteria, taken from the 1- and 2-year-old asthmatic infants, had a tendency to show high levels of ECP but a reduced number of eosinophils. Along with the wheezy episodes induced by viral infection, primarily and occasionally in combination with secondary bacterial infection, eosinophil activation and infiltration may develop. These predestined immune reactions to various pathogens might be associated with triggering the onset of asthma.
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PMID:Analysis of sputum taken from wheezy and asthmatic infants and children, with special reference to respiratory infections. 1184 69

Antibacterial peptides were isolated from human peripheral granulocytes of a healthy donor who had been treated with granulocyte-colony stimulating factor (G-CSF) and cortisol. Peptides were solubilized in acidified chloroform/methanol, and partitioned in chloroform/methanol/water. Water- soluble polypeptides were separated by cation-exchange and reversed-phase chromatography. Several previously characterized antibacterial polypeptides were identified; defensins 1-3, defensin 4, lysozyme, eosinophil cationic protein, and calgranulin A. In addition, several histone fragments were isolated and exhibited activity against the Gram- positive bacterium Bacillus megaterium strain Bm11. These fragments included two C-terminal fragments of histone H1A, three C-terminal fragments of histone H1D, one fragment of histone H1B, and two fragments of histone H4. The molecular masses of both histone H1A fragments, as determined by electrospray (ES) MS, were 270 Da higher than those calculated from their amino acid sequences. The two histone H1A fragments corresponded to Lys152-Lys222 (7527 +/- 1 Da) and Lys167-Lys222 (6023 +/- 1 Da). Tandem MS (MS/MS) of the 7.5 kDa and 6.0 kDa fragments indicated that the post-translational modification is on Lys222, the epsilon-amino group of which was conjugated with the alpha-carboxyl group of the tripeptide Arg-Gly-Gly. This finding was substantiated by digestion of the 7.5-kDa polypeptide with trypsin and analysis of the resulting peptides by ES MS and MS/MS. The tripeptide Arg-Gly-Gly corresponded uniquely to the three C-terminal residues of ubiquitin, demonstrating the presence of ubiquitinated histone H1A.
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PMID:Antibacterial peptides in stimulated human granulocytes: characterization of ubiquitinated histone H1A. 1185 9

Tryptase is a specific marker of mast-cell activation and plays a part in the pathophysiology of various allergic diseases including asthma, but little is known of the spillover of this enzyme into the systemic circulation. Therefore, we measured serum levels of mast-cell-derived tryptase in 21 patients with mild to moderate asthma and 20 healthy, subjects, using a B12 monoclonal antibody-based immunofluoroassay that detects both monomers and tetramers of alpha- and beta-tryptases. There was a good correlation between serum and sputum tryptase levels, and, compared with healthy subjects (1.68 +/- 0.31 ng/ml), asthma patients had higher concentrations of serum tryptase (atopic asthma, 4.18 +/- 0.95 ng/ml, p = 0.022; nonatopic asthma, 3.93 +/- 0.82 ng/ml, p = 0.031). Although serum tryptase levels did not correlate with asthma symptom scores, peak expiratory flow, or forced expiratory volume in 1 s, they positively correlated with mast-cell and eosinophil counts (p = 0.041 and p = 0.025, respectively) and eosinophil cationic protein contents (p = 0.029) in induced sputum. These results suggest that serum tryptase detected with B12 antibody is a marker of allergic airway inflammation in asthma.
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PMID:Serum B12 tryptase level as a marker of allergic airway inflammation in asthma. 1209 81

Although asthma has been viewed mainly as an eosinophilic disease, and chronic obstructive pulmonary disease (COPD) as a neutrophilic disease, recent studies have shown increased neutrophil counts in severe asthma and sputum eosinophilia in some COPD patients. In an attempt to further characterise these two syndromes according to pathology, the current authors have conducted a study of induced sputum in 15 subjects with COPD, 17 asthmatics, and 17 nonatopic healthy individuals. Sputum was analysed for cytology and levels of eosinophil cationic protein (ECP), albumin, tryptase and soluble intercellular adhesion molecule-1. The COPD subjects differed from the asthmatics as they had higher sputum neutrophil and lower columnar epithelial cell counts, but there were no differences in any soluble marker studied. When compared to control subjects, both the asthmatic and COPD subjects had raised eosinophil counts and ECP levels. In a subset of COPD subjects with sputum eosinophilia (>3% of total cells), significantly increased levels of tryptase were detected. In conclusion, although chronic obstructive pulmonary disease is a more neutrophilic disease than asthma, the two diseases are difficult to distinguish on the basis of sputum levels of the soluble markers traditionally associated with asthma. However, a subset of patients with chronic obstructive pulmonary disease with airway eosinophilia and mast-cell activation might represent a distinct pathological phenotype.
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PMID:Evidence of mast-cell activation in a subset of patients with eosinophilic chronic obstructive pulmonary disease. 1221 63

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

Chronic rhinosinusitis with nasal polyposis usually develops in aspirin-sensitive patients with asthma Arachidonic acid metabolism appears to be abnormal in the nasal polyps of aspirin-sensitive patients with asthma. These abnormalities an characterized by a low production of prostaglandin E2 (PGE2) and a high release of cysteinyl leukotrienes. Moreover, cyclooxygenase-2 is markedly downregulated in polyps from aspirin-sensitive patients with asthma. This abnormality may explain the low production of PGE2 in nasal polyps and may account for the increased susceptibility to the inhibitory effects of aspirin. Nasal instillation or ingestion of aspirin induces a nasal reaction in most aspirin-sensitive patients with asthma. This reaction is accompanied by the influx of eosinophils and a concomitant increase in cysteinyl leukotrienes, tryptase, and eosinophil cationic protein release. The aspirin nasal challenge is a very safe test with a moderate sensibility and high specificity that can be used in the diagnosis of aspirin intolerance. The similarities in the reaction between the nose and airways in aspirin-sensitive patients provide compelling evidence for common pathogenic mechanisms for nasal polyps, chronic rhinosinusitis, and bronchial asthma.
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PMID:Aspirin intolerance and nasal polyposis. 1242 45

Eosinophil and mast cell infiltrations are consistent findings in nasal polyp tissue. Previous studies have shown that matrix metalloproteinases (MMPs) may be involved in eosinophil infiltration in airway mucosa of asthmatic patients, and that transforming growth factor-beta1 (TGF-beta1) induces extracellular matrix deposition in nasal polyp tissue. The aim of this study was to evaluate the role of MMPs and tissue-inhibitor of metalloproteinase-1 (TIMP-1) in association with TGF-beta1, eosinophils and mast cell activation in nasal polyp tissue. Nasal polyp tissues from 20 patients who underwent polypectomies were collected and prepared into tissue homogenate. Eosinophil cationic protein (ECP) and tryptase levels were measured by CAP system (Pharmacia, Sweden). MMP-2, MMP-9, TIMP-1 and TGF-beta1 levels were measured by enzyme-liked immunosorbent assay. MMP-2 was the predominant form of MMPs, followed by MMP-9 and TIMP-1. There were significant correlations between ECP, and MMP-9, MMP-2, TGF-beta1 and tryptase, but not with TIMP-1. Significant correlations were noted between tryptase, and MMP-2, MMP-9, and TGF-beta1, but not with TIMP-1. Close correlations were noted between TGF-beta1, and MMP-9 and MMP-2, but not with TIMP-1. MMP-2, MMP-9, and TGF-beta1 may contribute to eosinophil and mast cell migrations into nasal polyp tissue.
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PMID:Eosinophil inflammation of nasal polyp tissue: relationships with matrix metalloproteinases, tissue inhibitor of metalloproteinase-1, and transforming growth factor-beta1. 1258 95

Biological markers in nasal secretions provide valuable information on nasal pathophysiology. However, published data on biomarker concentrations in nasal fluids are remarkably inconsistent, and the bias due to different sampling techniques, has not yet been systematically evaluated. Concentrations of various protein were repeatedly determined in nasal secretions of 16 healthy volunteers. The proteins were detected by using: 1) alpha2-macroglobulin as a marker for plasma contamination; 2) lactoferrin as a marker for glandular secretion; 3) lactate dehydrogenase as a marker for tissue injury; and 4) interleukin (IL)-1beta, IL-8, tumour necrosis factor-alpha, and eosinophil cationic protein and tryptase as indicators for tissue inflammation. A total of four different sampling methods, including nasal lavage (NL) and a new polyurethane foam sampler technique (PFST) were employed. Analyte concentrations in NL were approximately 10-times lower than in specimens obtained by PFST. Due to the unpredictable dilution during NL, various analytes were below the detection limit of the high sensitivity assays employed. With PFST, concentrations below the detection limit rarely occurred. The specimens did not significantly differ regarding plasma contamination, glandular secretion or tissue injury. The considerable variability of reported analyte concentrations in nasal secretions mainly results from different sampling techniques. To collect nasal secretions, samplers are considered superior to nasal lavage techniques.
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PMID:Biological markers in nasal secretions. 1276 42

This article summarizes biological events in human and animal nasal epithelium after short- and long-term exposure to ozone, the principal agent in photochemical smog. Despite anatomical and histological interspecies differences, ozone exposures resulted in common nasal qualitative alterations with an anterior-posterior gradient of phenomena occurring immediately, and with a lag time postexposure: epithelial disruption and increased permeability, inflammatory cell influx, and proliferative and secretory responses. Described mechanisms of toxicity included a direct effect of ozone on epithelial lining fluid and cellular membranes and the subsequent release of cytokines and cyclooxygenase and lipoxygenase products. An indirect effect of ozone was indicated by a decreased mucociliary clearance, free radicals production interacting with a gene promoting factor, and increased DNA synthesis. Studies highlighted the pivotal role of activated neutrophils and mast cells leading to the release of deleterious enzymes (tryptase, eosinophil cationic protein) and numerous cytokines. Experiments performed with ozone exposure/allergen challenge reported that, besides the intrinsic deleterious properties of ozone, it also had a priming effect on the late-phase response to allergen challenge, providing new insights into the pathophysiology of respiratory allergic diseases.
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PMID:Nasal epithelial and inflammatory response to ozone exposure: a review of laboratory-based studies published since 1985. 1288 46


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