lactoferrin and Rhinitis--Allergic--Seasonal

Topics: Anaphylaxis; Anti-Glomerular Basement Membrane Disease; Antigen-Antibody Complex; Asthma; Complement System Proteins; Cytotoxicity, Immunologic; Humans; Immunoglobulins; Interferons; Lactoferrin; Leukocytes; Lung; Macrophages; Muramidase; Phagocytosis; Reagins; Respiratory Hypersensitivity; Rhinitis, Allergic, Seasonal; Sarcoidosis; Tuberculosis, Pulmonary

Ten subjects with asymptomatic seasonal allergy, outside of their allergy season, underwent allergen provocation following 1 hour of exposure to air at either 20 degrees C and 30% relative humidity (RH) or air at 37 degrees C and 90% RH. The ipsilateral changes following antigen challenge were compared under the two conditions. Conditioning of the nose to 37 degrees C, 90% RH reduced total histamine release (7.9 +/- 1.8 ng vs 4.2 +/- 1.3 ng; p < or = 0.05), sneezes (6 +/- 2 vs 3 +/- 1; p < or = 0.05), pruritus (score of 17.4 +/- 6.0 vs score of 2.0 +/- 1.8 out of a total score of 100, p < or = 0.01), nasal airway resistance (1.4 +/- 0.8 kPa/L/sec vs 0.2 +/- 0.1 kPa/L/sec; p < or = 0.05), human serum albumin levels (389.6 +/- 53.4 micrograms vs 242.2 +/- 37.9 micrograms; p < or = 0.05), and congestion (score of 23.8 +/- 4.8 vs score of 10.6 +/- 5.4 out of a total score of 100, p < or = 0.01). It had no effect on the volume of secretions (p = 0.8), lactoferrin levels (p = 0.3), or rhinorrhea (p = 1.0). Thus air at 37 degrees C and 90% RH partially reduces the early response to antigen. Its effects are greatest on histamine release, the vascular response, and neural responses, with no effect on the glandular response. The mechanisms underlying these effects are unknown.

Topics: Adult; Air; Airway Resistance; Allergens; Cross-Over Studies; Female; Humans; Humidity; Infant, Newborn; Lactoferrin; Nasal Cavity; Nasal Mucosa; Respiratory Therapy; Rhinitis, Allergic, Seasonal; Serum Albumin

We have found activated neutrophils (PMNs) in skin chambers overlying the site of ongoing human allergic reactions. To determine whether this activation is due to component(s) released early in these IgE-mediated reactions, we investigated the in vitro effects of skin chamber fluids (CF) on resting blood PMNs. These skin CF had been previously obtained, at different time periods, at pollen-antigen-challenged or buffer-control-challenged sites in sensitive human subjects. PMNs incubated with CF obtained during the first hour of antigen challenge (first-hour CF) generated significantly more superoxide (O2-) than spontaneous production (p less than 0.001) and more than PMNs incubated with first-hour buffer-site CF (p less than 0.002). A pattern similar to O2- generation was observed in lactoferrin secretion during the incubation of the three cell aliquots described above (p less than 0.001). After these incubations, the subsequent responsiveness of the PMNs present in the cell buttons to opsonized zymosan, a PMN activator, was assessed. PMNs previously incubated with first-hour CF generated significantly more net O2- in response to opsonized zymosan than did PMNs previously incubated with first-hour buffer-site CF (p less than 0.001) or buffered saline (p less than 0.001). Again, a similar difference in the patterns of net lactoferrin secretion was observed (p less than 0.02). These events were not associated with PMN damage. Analogous studies with CF previously obtained during the second- to first-hour of antigen or buffer challenge stimulated much less than first-hour CF. We conclude that one or more components released early in IgE-mediated skin reactions can activate PMNs. The nature of the activating component(s) is unknown, with no evidence of activation by histamine, antigen, or other components found to date in first-hour CF.

Topics: Adult; Allergens; Diffusion Chambers, Culture; Humans; Hypersensitivity, Immediate; Lactoferrin; Lymphocyte Activation; Middle Aged; Neutrophils; Pollen; Rhinitis, Allergic, Seasonal; Skin; Superoxides; Zymosan

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.

Topics: Adult; Albumins; Allergens; Female; Histamine; Histamine Release; Humans; Lactoferrin; Male; Muramidase; Nasal Cavity; Nasal Mucosa; Nasal Provocation Tests; Prostaglandin D2; Proteins; Rhinitis, Allergic, Seasonal; Therapeutic Irrigation; Time Factors

We aimed to study the participation of neurogenic mechanisms in nasal allergic inflammation by assessing the effect of neurogenic stimulation on the secretory and cellular responses of nasal mucosa in patients with allergic rhinitis.. A group of patients suffering from seasonal allergic rhinitis was challenged intranasally with incremental doses of capsaicin (0.3, 3, 12 microg) during and after the pollen season. Clinical symptoms after provocations were monitored, and unilateral nasal lavages were obtained. The nasal lavage fluid (NAL) was assayed for concentration of total protein, albumin, lactoferrin, and number of leukocytes, following by differential count.. Capsaicin challenge during the pollen season produced greater congestion (P < 0.01) and rhinorrhea (P < 0.05) than after the season. The intensity of burning sensation (pain) was similar on both occasions. Capsaicin failed to increase albumin content in NAL both during and after the season. Total protein was increased only after the highest dose of capsaicin (P < 0.03) after the season. The number of eosinophils in basal lavages was higher during the season. During the season, the total number of leukocytes at least doubled in 7/12 patients and the percentage of eosinophils increased in 6/12 patients after the capsaicin challenge.. Our study demonstrated that during the symptomatic period the nasal mucosa of allergic patients is more susceptible to neurogenic stimulation, showing enhanced secretory and inflammatory (cellular) responses.

Topics: Airway Resistance; Albumins; Capsaicin; Female; Humans; Lactoferrin; Leukocyte Count; Male; Nasal Cavity; Nasal Lavage Fluid; Nasal Mucosa; Nasal Provocation Tests; Proteins; Rhinitis, Allergic, Seasonal; Seasons

The aim of this study was to determine whether allergic inflammation induces nasal hyperreactivity to bradykinin by enhancing neuronal responsiveness.. We compared the response to localized, unilateral nasal challenge with bradykinin in patients with perennial allergic rhinitis and nonallergic subjects, and in patients with seasonal allergic rhinitis challenged in and out of season. Weights of secretions from each nostril were recorded, and levels of albumin and lactoferrin in secretions recovered from each nostril were assayed. Contralateral administration of atropine (0.32 mg) was used to evaluate the role of cholinergic reflexes in nasal hyperresponsiveness to bradykinin.. In patients with symptomatic allergy, bradykinin induced greater symptom scores than in asymptomatic atopic or nonallergic control subjects. Moreover, bradykinin caused sneezing in a majority of patients with symptomatic allergy but in none of the asymptomatic atopic or nonallergic control subjects. Only patients with symptomatic allergy showed dose-dependent bilateral increases in secretion weights and levels of the serous glandular marker, lactoferrin. In contrast, bradykinin induced similar increases in ipsilateral, but not contralateral, levels of albumin in all patient populations. Atropine inhibited contralateral secretion and lactoferrin production (p < 0.05) in patients with symptomatic allergy.. The induction of sneezing and of atropine-inhibitable contralateral glandular secretion demonstrates that allergic inflammation causes nasal hyperreactivity to bradykinin, at least in part, by enhancing neuronal responsiveness.

Topics: Adult; Albumins; Allergens; Atropine; Bradykinin; Cross-Over Studies; Double-Blind Method; Female; Humans; Hypersensitivity; Immunoglobulin E; Inflammation; Lactoferrin; Male; Muscarinic Antagonists; Nasal Mucosa; Nasal Provocation Tests; Reflex; Rhinitis, Allergic, Perennial; Rhinitis, Allergic, Seasonal