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:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Allergic rhinitis is characterized by a profuse rhinorrhea in addition to paroxysms of sneezing, nasal congestion, and pruritus. To define better the sources of nasal secretion produced during rhinitis, nasal allergen challenges were performed on nine atopic subjects with seasonal rhinitis. A single dose of allergen was sprayed into one side of the nose, and nasal lavages were collected bilaterally for 7 hours. Nasal lavages were assayed for protein (total protein, albumin, lactoferrin, and lysozyme) and mediator (histamine and prostaglandin D2) content. Protein concentrations increased and remained elevated above baseline levels in both ipsilateral and contralateral secretions for up to 3 hours after allergen challenge. The proportion of albumin relative to total protein (the albumin percent) increased on the ipsilateral side, whereas the relative proportions of lactoferrin and lysozyme (the lactoferrin percent and lysozyme percent) increased on the contralateral side. Prostaglandin D2, but not histamine, increased selectively on the ipsilateral side. These data suggest that the ipsilateral protein secretory response is due to allergen-induced mast cell mediator release causing increased vascular permeability, whereas the contralateral protein secretory response is primarily a reflex-induced glandular secretion.
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PMID:The pathophysiology of rhinitis. V. Sources of protein in allergen-induced nasal secretions. 171 3

The mechanism of action of topical intranasal steroids is obscure. To investigate this, we have studied the effects of a topical intranasal corticosteroid, fluticasone propionate on nasal airflow resistance (Rnaw), secretions, cytological smears and symptoms. Fluticasone propionate aqueous nasal spray was given to 11 patients with perennial allergic rhinitis in a double-blind, placebo-controlled study. On each day, patients were challenged with ascending doses of histamine. Rnaw, secretion volume, total protein, mucin, lysozyme and albumin were measured. Nasal smears were taken and sneezes counted. Diary card data were collected for both treatment periods. There was a significant, dose-related increase in Rnaw and sneezing on histamine challenge. A single dose of fluticasone had no effect on any parameter. After 4 weeks of treatment, resistance measurements were reduced (post-challenge g.m.2.8 cmH2O/l/s, Q1-Q3 1.6-4.8; placebo 4.2, 2.9-5.3: P < 0.0001) as were baseline secretion volumes (mean 2.4 ml/5 min, c.i.1.9-3.0; placebo 3.3, 2.8-3.8: P < 0.05). Eosinophil counts were suppressed (fluticasone 5.8%, c.i. 4.0-15.7; placebo 23.3%, 12.4-34.1: P < 0.05) and the composite symptom score reduced (P < 0.05). Fluticasone has long-term effects on the nasal response to histamine in perennial allergic rhinitis and part of this effect is likely to be vascular.
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PMID:The effect of topical fluticasone propionate on intranasal histamine challenge in subjects with perennial allergic rhinitis. 755 27

Topical sodium cromoglycate is used to treat allergic diseases of the upper and lower airways. To investigate its mechanisms of action, intranasal histamine challenge was used in nine subjects with perennial allergic rhinitis. After a preliminary day where subjects' reactivity thresholds (D100) for histamine were determined, intranasal sodium cromoglycate was administered in a double-blind, placebo-controlled fashion. Graded (D100/3, D100, D100X3), sequential challenges were performed on days 1 and 21 of each course, and responses measured by changes in nasal airway resistance, sneezes, secretion volume and secretion content: total protein, lysozyme and mucin. After a single dose of sodium cromoglycate, there was no change in resistance, but secretion volumes fell significantly (3.12 ml/5 min c.i. 2.83-3.4; placebo 3.61, c.i. 3.32-3.90: P = 0.026). After a 3-week-course, there was a significant fall in resistance (4.29 cm H2O/l/s, c.i. 3.85-4.72; placebo 5.45, c.i. 5.01-5.88: P < 0.0001). No change in other parameters was observed. Thus, in perennial allergic rhinitis, intranasal sodium cromoglycate has both short- and long-term effects on nasal reactivity to histamine challenge. Acutely, there is a reduction in nasal lavage fluid volume which may be the result of reduced irritant receptor activity. After a 3-week course, there is a reduction in nasal resistance responses, a possible anti-inflammatory effect.
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PMID:The effect of topical sodium cromoglycate on intranasal histamine challenge in allergic rhinitis. 789 84

Bradykinin (BK) induces albumin exudation and glandular secretion in chronic allergic rhinitis subjects. Since bradykinin may stimulate nociceptive sensory nerves, neural reflex arcs could contribute to the secretion process. Six chronic allergic rhinitis subjects received 1000 nM bradykinin by unilateral nasal provocation using the method of Raphael et al. This dose induces optimal contralateral glandular secretion. Ipratropium bromide (80 micrograms) or saline were applied topically before the challenges. Total protein, albumin, glycoconjugate, and lysozyme were measured in lavage fluids. On the ipsilateral side, bradykinin induced significant total protein, glycoconjugate, and albumin secretion. None of these were affected by ipratropium. On the contralateral side, total protein and glycoconjugates were increased by bradykinin, while albumin and lysozyme were not significantly affected. Ipratropium bromide completely ablated total protein and glycoconjugate secretion on the contralateral side indicating that cholinergic reflexes mediated the glandular secretion. In chronic allergic rhinitis, bradykinin directly stimulated albumin secretion, but also stimulates nociceptive neuron--parasympathetic nerve reflexes to induce glandular secretion. The reflex loop was apparent on the contralateral side to the unilateral bradykinin challenge. This loop induced mucoglycoconjugate, but not serous cell, secretion in chronic allergic rhinitis subjects and can be inhibited by iptratropium bromide.
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PMID:Effects of ipratropium bromide on bradykinin nasal provocation in chronic allergic rhinitis. 798 21

There is little information about specific changes in submucosal gland exocytosis in diseases such as allergic rhinitis (AR), nonallergic rhinitis (NAR), and cystic fibrosis (CF). Nasal lavage fluids were collected from normal, AR, NAR, and CF subjects. Concentrations of lysozyme, Alcian blue-staining mucoglycoconjugate material (AB + m), and human high-molecular-weight mucoglycoconjugates recognized by the 7F10 murine monoclonal antibody [7F10-immunoreactive mucoglycoconjugates (7F10-irm)] were measured. AB + m and 7F10-irm were characterized by Sepharose-2B column chromatography and glycosidase digestion. 7F10-irm was increased in CF (2.4-fold; P = 0.001) and AR (12.7-fold; P = 0.00007) subjects. AB + m was increased in CF (1.8-fold; P = 0.049) and AR (1.2-fold; P = 0.07) subjects. There were no changes in NAR subjects. On Sepharose-2B columns, AB + m peaks were at 1.3-3.0 x 10(6) and 0.36-0.65 x 10(6) Da. 7F10-irm showed four distinct peaks at 1.5, 1.2, 0.85, and 0.53 x 10(6) Da that were nearly identical in both normal and CF samples. Sialic acid was present in both 7F10-irm and AB + m. 7F10-irm and AB + m are mutually exclusive sialylated mucoglycoproteins that are significantly induced in AR and CF but not in NAR.
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PMID:Mucoglycoprotein hypersecretion in allergic rhinitis and cystic fibrosis. 943 75

We have previously shown that capsaicin nasal challenge in subjects with allergic rhinitis produces a dose-dependent increase in the albumin content of nasal lavage fluids. In the present set of studies, we determined whether this observation represents plasma extravasation that is neuronally mediated. To evaluate whether glandular secretions contribute to the albumin increase in nasal lavage fluids, volunteers with allergic rhinitis were pretreated with atropine or placebo before capsaicin challenge. Atropine significantly reduced the volume of returned lavage fluids and their lysozyme content but increased their albumin and fibrinogen content. To assess the contribution of sensory nerve stimulation, subjects with allergic rhinitis were pretreated in a second study with lidocaine or placebo before capsaicin challenge. Lidocaine significantly attenuated the capsaicin-induced increases in the volume of nasal lavage fluids, as well as their lysozyme and albumin content. To rule out the possibility of a direct effect of lidocaine on blood vessels rather than on nerves, healthy subjects were pretreated in a third study with lidocaine or placebo before bradykinin nasal challenge. Lidocaine did not affect the bradykinin-induced increase in the albumin content of nasal fluids. We conclude that, in allergic rhinitis, high-dose capsaicin induces plasma extravasation in the human nose and that this effect is neuronally mediated. This provides more definitive evidence that neurogenic inflammation can occur in vivo in the human upper airway.
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PMID:Plasma extravasation through neuronal stimulation in human nasal mucosa in the setting of allergic rhinitis. 947 63

A 23-year-old woman developed allergic rhinitis in 1993. Her doctor prescribed for her Solfa (amlexanox 25 mg) and Lysozymen 90 (lysozyme chloride 90 mg) tablets. She took the tablets occasionally, whenever she developed allergic rhinitis. She noticed a macular erythema of about 3.5 cm wide on her buttocks in 1994, about 1 year after the initial prescription. We conducted a series of tests with the tablets. On patch testing, the patient had a positive reaction to Solfa 50% pet. on the eruptive area, but no such reaction on the non-eruptive area. Furthermore, on patch testing, she had no reaction to Lysozymen 90, 50% pet. on either the eruptive or the non-eruptive area. We also used open application test with Solfa 50% pet. to confirm the cause of her erythema.
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PMID:Fixed drug eruption due to amlexanox. 950 16

Rhinorrhea is a prominent symptom of the common cold. Although increases in vascular permeability and serous cell secretion have been demonstrated in human nasal mucus during active rhinovirus infections, changes in mucin constituents have not been quantified. Nonallergic (n = 48) and asymptomatic allergic rhinitis (n = 32) subjects were inoculated with rhinovirus type hanks before the spring allergy season. Nasal lavages were performed before inoculation (day 0), then daily for 5 days afterward. The subjects were divided into infected and noninfected groups on the basis of evidence of successful rhinovirus infection (nasal shedding of virus or fourfold increases in specific serum antibodies). Concentrations of interleukin (IL)-8, markers of vascular leak (IgG), seromucous cells (lysozyme), and mucoglycoprotein exocytosis [7F10-immunoreactive mucin (7F10-irm) and Alcian blue staining of acidic mucoglycoproteins] were measured in lavage fluids. The infected subgroup had maximal increases in nasal lavage fluid concentrations of IL-8 (sevenfold), IgG (fourfold), total protein (twofold), and gel-phase 7F10-irm (twofold) on day 3. There were no differences between infected allergic and nonallergic subjects. IL-8 and gel-phase 7F10-irm were significantly higher in infected than in noninfected subjects. In addition to promoting plasma exudation, rhinovirus hanks infection increases IL-8 and gel-phase mucin secretion. These processes may contribute to a progression from watery rhinorrhea to mucoid discharge, with mild neutrophilic infiltration during the common cold.
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PMID:Rhinovirus infection induces mucus hypersecretion. 960 41

Nasal allergy is the most common type I allergic disease. During allergic reaction, chemical mediators may be released from residual cell, and thus, attract additional inflammatory cells. One mediator implicated in this response is bradykinin (BK), a potent proinflammatory nonapeptide. This study was designed to investigate the effects of BK on nasal mucosa, and to determine the role of angiotensin-converting enzyme (ACE) in BK-induced nasal responses. BK nasal provocation (100 micrograms) was studied in 7 normal volunteers and 7 patients with perennial allergic rhinitis. After provoking of BK response, nasal secretions and saline lavage fluids were collected for analysis of total protein (a protein secretion marker), albumin (a vascular permeability marker), and lysozyme (a serous cell marker). In addition, after administering of Captopril 50 mg, a specific ACE inhibitor, the same protocol was performed. In both groups, BK induced plasma exudation and serous gland secretion. Premedication with captopril did not alter BK-induced responses in normal individuals. In allergic patients, captopril enhanced BK-induced vascular permeability, but not glandular secretion. These results indicate that allergic subjects have nasal hyperresponsiveness to BK, and that ACE predominantly modulates the vascular permeability of allergic nasal mucosa. It seems likely that BK may contribute to the expression of nasal allergic symptoms, and that inhibition of ACE may lead to increased nasal responsiveness.
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PMID:[Role of angiotensin-converting enzyme on bradykinin nasal provocation: comparison of normal volunteers and allergic subjects]. 1019 23

Pathophysiologic differences in neural responses to hypertonic saline (HTS) were investigated in subjects with acute sinusitis (n = 25), subjects with chronic fatigue syndrome (CFS) with nonallergic rhinitis (n = 14), subjects with active allergic rhinitis (AR; n = 17), and normal (n = 20) subjects. Increasing strengths of HTS were sprayed into their nostrils at 5-minute intervals. Sensations of nasal pain, blockage, and drip increased with concentration and were significantly elevated above normal. These parallels suggested activation of similar subsets of afferent neurons. Urea and lysozyme secretion were dose dependent in all groups, suggesting that serous cell exocytosis was one source of urea after neural stimulation. Only AR and normal groups had mucin dose responses and correlations between symptoms and lysozyme secretion (R(2) = 0.12-0.23). The lysozyme dose responses may represent axon responses in these groups. The neurogenic stimulus did not alter albumin (vascular) exudation in any group. Albumin and mucin concentrations were correlated in sinusitis, suggesting that nonneurogenic factors predominated in sinusitis mucous hypersecretion. CFS had neural hypersensitivity (pain) but reduced serous cell secretion. HTS nasal provocations identified significant, unique patterns of neural and mucosal dysregulation in each rhinosinusitis syndrome.
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PMID:Neuropathology in rhinosinusitis. 1547 96


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