Biomedical subjects

D Proud

Publications and source records attributed to D Proud.

At least 37 records · Page 2Linked to original sources

PubMed1999

Relationship between histamine and physiological changes during the early response to nasal antigen provocation.

To investigate the temporal relationships of mediator release and physiological changes during the early response to allergen, we challenged allergic individuals intranasally with antigen and followed their responses. This was done by using small filter paper disks to challenge one nostril and collect secretions from both the challenged and the contralateral nostril, thus enabling us to evaluate the nasonasal reflex. There was a significant increase in sneezing after allergen challenge that peaked within 2 min and returned to baseline. The weights of nasal secretions as well as nasal symptoms increased immediately and remained significantly elevated for 20 min in both nostrils. Nasal airway resistance increased slowly, reaching its peak at approximately 6 min after challenge on the ipsilateral side, but it did not change on the contralateral side. Histamine levels peaked 30 s after removal of the allergen disk on the side of challenge, whereas albumin levels peaked after those of histamine. Lactoferrin paralleled the increase in secretion weights and occurred in both nostrils. Increasing doses of antigen produced dose-dependent increases in all parameters, whereas control challenges produced no response. These studies describe a human model for the evaluation of the allergic response that is capable of simultaneously measuring mediator release and the physiological response, including the nasonasal reflex. This model should prove useful in studying the mechanism of allergic rhinitis in humans.

Adult↗

PubMed1999

Airway neural responses to kinins: tachyphylaxis and role of receptor subtypes.

To further define the role of neural responses in the hyperreactivity of inflamed human upper airways to bradykinin (BK), we determined if repeated challenges with BK led to tachyphylaxis of neurally mediated responses in subjects with perennial allergic rhinitis. We also tested the hypothesis that enhanced reactivity to kinins in inflamed airways was caused by induction of B1-kinin receptors by comparing the effects of the selective B1-receptor agonist, des-Arg10-lysylbradykinin, and the B2 receptor agonist, BK, in the lower airways of asthmatics and in the upper airways of subjects with perennial allergic rhinitis. Repeated BK challenges led to tachyphylaxis of sneezing and of neurally mediated serous glandular secretion in subjects with perennial allergic rhinitis. Surprisingly, tachyphylaxis of increased local vascular permeability was also observed. By contrast, repeated challenges with BK in normal subjects led to reproducible increases in vascular permeability. Provocation with des-Arg10-lysylbradykinin did not cause bronchoconstriction in asthmatic subjects or increase glandular secretion or vascular permeability in the upper airways of subjects with rhinitis. We conclude that increased reactivity to kinins in inflamed human airways is mediated, at least in part, by neural reflexes, and is not caused by induction of B1-receptors.

Asthma↗

PubMed1999

Characterization of vagal afferent subtypes stimulated by bradykinin in guinea pig trachea.

In vitro electrophysiological techniques were used to examine the effect of bradykinin on guinea pig trachea and bronchus afferent nerve endings arising from the nodose or jugular ganglia. The data reveal that bradykinin activates nerve terminals of jugular C and Adelta fibers. Although the fibers were too few in number to study rigorously, bradykinin also stimulated nodose C fibers innervating the trachea and bronchus. In contrast, Adelta fibers arising from the nodose ganglion were unresponsive to bradykinin challenge. The responses in both jugular C and Adelta fiber types were blocked by a selective bradykinin B2 receptor antagonist and were not dependent on the efferent release of sensory neuropeptides. These data indicate that the sensitivity of guinea pig airway afferent fibers to bradykinin is dependent more on the ganglionic origin of the cell body than on the conduction velocity of its axon.

Action Potentials↗

PubMed1998

Acute respiratory response to prolonged, moderate levels of sidestream tobacco smoke.

Environmental tobacco smoke (ETS) is a significant component of indoor air pollution yet the acute upper respiratory response has not been well studied. The goal of this study was to determine the response of healthy subjects to moderate levels of sidestream tobacco smoke (SS). Twenty-three subjects were challenged on 2 separate days to clean air or SS (2 h, 15 ppm carbon monoxide, at rest). Subjects completed symptom questionnaires, posterior rhinomanometry, and body plethysmography. Average total and differential cell counts and albumin concentration were determined on nasal lavage samples. The urinary cotinine: creatinine ratio was used as a biomarker of exposure. Following SS exposure, irritant and rhinitis symptoms increased, nasal resistance rose from 4.9+/-0.4 to 6.3+/-0.6 cm H2O/L/s and specific airway conductance decreased from 0.14+/-0.01 to 0.13+/-0.01 cm H2O(-1) s(-1). Total cell counts, neutrophils, and albumin were unchanged. An increased nasal congestive response did not correlate with an increased cotinine: creatinine ratio. A history of ETS rhinitis did not predict an increased group response to smoke, but individuals with the largest physiologic and inflammatory response were historically ETS sensitive. In summary, healthy normal subjects demonstrate nasal congestion with exposure to moderate levels of SS without evidence of increased nasal vascular permeability.

Adolescent↗

PubMed1998

Influence of the cytosolic carboxyl termini of human B1 and B2 kinin receptors on receptor sequestration, ligand internalization, and signal transduction.

To determine the role of the cytoplasmic carboxyl termini of human B1 and B2 kinin receptors (B1KR and B2KR, respectively) in the internalization of their respective ligands, des-Arg10-kallidin and bradykinin (BK), both wild type receptors, as well as truncated B2KRs, a mutated B2KR, and chimeric receptors were stably expressed in Chinese hamster ovary cells. Incubation of [3H]BK at 37 degrees C with cells expressing wild type B2KR resulted in pronounced and rapid ligand internalization ( approximately 80% after 10 min). By contrast, incubation of 3H-labeled des-Arg10-kallidin with cells expressing B1KR resulted in a modest, slow internalization of the ligand (<20% after 10 min). Replacement, from Cys324, of the cytoplasmic carboxyl terminus of the B2KR with that of the B1KR from Cys330 (both Cys residues are putative palmitoylation sites) greatly reduced ligand internalization ( approximately 40% after 10 min) without significantly altering Kd or ligand-induced signal activation. By marked contrast, the corresponding replacement, of the sequence from Cys330 of the cytoplasmic carboxyl terminus of the B1KR with the segment of the B2KR, led to a striking increase of ligand internalization ( approximately 75% within 10 min) without altering Kd or ligand-induced signal activation. Truncation of the B2KR to within three amino acids of Cys324 (truncation at Gly327) led to strongly reduced ligand internalization ( approximately 40% after 10 min). Truncation of the B2KR up to Lys315 almost completely abolished internalization of [3H]BK (10% after 10 min). This additional reduction is apparently not caused by the loss of the potential palmitoylation site at Cys324, since a B2KR with a point mutation of Cys324 to Ala internalized [3H]BK as rapidly as the wild type B2KR. From these results we conclude that the cytoplasmic carboxyl terminus of the human B2KR contains sequences that are necessary and sufficient to permit rapid ligand-induced sequestration of human kinin receptors and internalization of their agonists.

Animals↗

PubMed1998

The kinin system in rhinitis and asthma.

The past decade has seen renewed interest in the potential role of kinins in airway diseases. The correlation between kinin generation and symptoms of inflammation, together with the demonstration that administration of kinins to the airway mucosa can induce relevant symptoms, provides strong circumstantial support for a role of kinins in the pathogenesis of airway diseases, such as allergic and viral rhinitis and asthma. Definitive studies of the effects of blockade of kinin actions on symptomatic responses, however, are still needed. The effects of kinins in the airways, and the mechanisms by which they exert their actions clearly vary depending on the presence of inflammation in the airways. Although a growing body of evidence implicates activation of sensory nerves as an important component of kinin effects in inflamed airways, the components of inflammation that modify the response of these sensory nerves, the mechanisms by which neuronal responsiveness alters, and the degree of selectivity of neuronal activation to bradykinin are all topics that require further delineation.

Animals↗

PubMed1998

Daily variations of serum diamine oxidase and the influence of H1 and H2 blockers: a critical approach to routine diamine oxidase assessment.

OBJECTIVE AND DESIGN: Histamine in food has been shown to induce intolerance reactions mimicking food allergy. These reactions seem to be due to impaired histamine metabolism caused by reduced diamine oxidase activity. To validate routine serum diamine oxidase assessment, daily variations of diamine oxidase were evaluated. METHODS: Blood was drawn from each of 20 healthy volunteers (10 female, 10 male; mean age 32.5 years) every 2 h from 9 a.m. to 5 p.m., and diamine oxidase activity was measured using the C14 putrescine method. To assess possible influences of H1 and H2 blockers on diamine oxidase activity, diphenhydramine, ketotifen, cimetidine, and ranitidine were incubated at pharmacologic concentrations with human placental diamine oxidase (identical to neutrophilic and eosinophilic diamine oxidase). Inhibition of diamine oxidase activity was calculated as the percentage of inhibition versus control. In addition, the known diamine oxidase inhibitors, dihydralazine and aminoguanidine, were used as positive controls. RESULTS: Serum diamine oxidase levels showed no significant daily variations (0.041 +/- 0.025; 0.037 +/- 0.022; 0.041 +/- 0.023; 0.040 +/- 0.023; 0.038 +/- 0.025 nKat/l) and no significant sex differences (female 0.040 +/- 0.028 nKat/l versus male 0.039 +/- 0.019 nKat/l). Antihistamines had no influence on diamine oxidase activity except for cimetidine, which caused 25% inhibition at the highest dose tested ( p < 0.0002) (positive control: aminoguanidine 85% inhibition (p< 0.0001), dihydralazine 68% inhibition (p<0.0001)) and diphenhydramine, which caused 19% increase (p<0.0001) of enzyme activity. CONCLUSION: Serum diamine oxidase levels do not show daily variations allowing assessment anytime during office hours. However, diagnostic interpretation of serum diamine oxidase levels may be difficult.

Adult↗

PubMed1998

Epithelia cells as regulators of airway inflammation.

The past decade has seen major advances in our understanding of the metabolic and biochemical functions of the epithelial cell. As a result, the traditional view of the epithelium as a relatively passive physical barrier to the internal environment has been superseded by the concept that the epithelial plays a key role in regulating airway inflammation. The epithelial cell experts this modulatory effect in several ways. Epithelial cells can function maintain mucosal integrity and to modulate local immune responses. They can also limit inflammatory processes by degrading, or inhibiting, proinflammatory mediators and proteins. However, the epithelium also responds to a range of stimuli by producing biologically active mediators that can influence airway inflammation. These include, but are not limited to a broad range of cytokines and chemokines that can exert profound effects on inflammatory cells, as well as lipid and peptide mediators. This review will highlight some of these aspects of the role of the epithelium in regulating airway inflammation.

Asthma↗

PubMed1998

Comparison of nasal mucosal responsiveness to neuronal stimulation in non-allergic and allergic rhinitis: effects of capsaicin nasal challenge.

BACKGROUND: Neuronal involvement has been implicated in the pathophysiology of non-allergic and allergic rhinitis, contributing to the typical exacerbation of these conditions upon exposure to non-specific environmental irritants. OBJECTIVES: To determine if non-allergic and allergic rhinitis are characterized by increased responsiveness of the nasal mucosa to sensorineural stimulation. METHODS: Nasal challenges with capsaicin and its vehicle were performed in three groups of subjects -- non-allergic rhinitics, perennial allergic rhinitics, and healthy controls -- and resultant symptom scores, glandular secretion reflected by lactoferrin levels, and plasma extravasation reflected by albumin levels in nasal lavage fluid were compared. RESULTS: Capsaicin-sensitive nerve stimulation produced increases in symptom scores and lactoferrin levels which were similar among the three groups of subjects. On the other hand, only the group of subjects with allergic rhinitis demonstrated a significant capsaicin-induced increase in albumin levels and a trend in total protein levels. CONCLUSIONS: We conclude that non-allergic rhinitis is not characterized by increased responsiveness of capsaicin-sensitive nerve fibres; while allergic rhinitis is marked by hyperresponsiveness manifested as increased albumin leakage in nasal fluids. This may reflect the activity of an axonal reflex to sensorineural stimulation.

Administration, Intranasal↗

PubMed1998

Intranasal salmeterol inhibits allergen-induced vascular permeability but not mast cell activation or cellular infiltration.

BACKGROUND: Salmeterol is a long-acting beta2-adrenergic agonist that is widely used in the treatment of asthma. It has been suggested that non-bronchodilator actions of salmeterol may contribute to its efficacy. OBJECTIVE: To further evaluate the potential non-bronchodilator actions of salmeterol in vivo, using a model of nasal challenge with allergen. METHODS: Twelve asymptomatic subjects with seasonal allergic rhinitis participated in a randomized, double-blind, placebo-controlled crossover trial of the effects of a single dose of 100 microg of salmeterol on the response to allergen challenge. Sneezing and symptom scores, and levels of histamine and albumin in nasal lavages, were measured throughout the protocol. Concentrations of tryptase, prostaglandin D2 and lysozyme were measured during the acute allergic response, while levels of IL-3, IL-5 and IL-8 were measured at later time points. Numbers of eosinophils and of total white blood cells were also recorded. RESULTS: Salmeterol did not affect sneezing or symptom scores at any point. During the immediate response to allergen challenge, mast cell activation, reflected by concentrations of histamine, tryptase and prostaglandin D2, and serous glandular secretion, assessed by measurements of lysozyme, were unaffected by salmeterol treatment but vascular permeability, reflected by concentrations of albumin in nasal lavages, was significantly reduced. At later time points, salmeterol had no effect on levels of histamine or albumin and did not affect cellular infiltration. Concentrations of IL-3, IL-5 and IL-8 were not increased by allergen challenge in these subjects, so the effects of salmeterol could not be evaluated. CONCLUSIONS: Treatment with a single dose of salmeterol had no effect on activation of mast cells or cellular infiltration but inhibited vascular permeability. The ability of salmeterol to inhibit antigen-induced vascular permeability may contribute to its therapeutic efficacy in asthma.

Administration, Intranasal↗

PubMed1998

Activation of antiviral protein kinase leads to immunoglobulin E class switching in human B cells.

An epidemiologic association between viral infections and the onset of asthma and allergy has been documented. Also, evidence from animal and human studies has suggested an increase in antigen-specific immunoglobulin E (IgE) production during viral infections, and elevated levels of IgE are characteristic of human asthma and allergy. Here, we provide molecular evidence for the roles of viral infection and of activation of the antiviral protein kinase (PKR) (double-stranded-RNA [dsRNA]-activated protein kinase) in the induction of IgE class switching. The presence of dsRNA, a known component of viral infection and an activator of PKR, induced IgE class switching as detected by the expression of germ line epsilon in the human Ramos B-cell line. Furthermore, dsRNA treatment of Ramos cells resulted in the activation of PKR and in vivo activation of the NF-kappaB complex. Interestingly, infection of Ramos cells with rhinovirus (common cold virus) serotypes 14 and 16 resulted in the induction of germ line epsilon expression. To further evaluate the role of PKR in the viral induction of IgE class switching, we infected Ramos cells with two different vaccinia virus (cowpox virus) strains. Infection with wild-type vaccinia virus failed to induce germ line epsilon expression; however, a deletion mutant of vaccinia virus (VP1080) lacking the PKR-inhibitory polypeptide E3L induced the expression of germ line epsilon. Collectively, the results of our study define a common molecular mechanism underlying the role of viral infections in IgE class switching and subsequent induction of IgE-mediated disorders such as allergy and asthma.

B-Lymphocytes↗

PubMed1998

Nitric oxide inhibits rhinovirus-induced cytokine production and viral replication in a human respiratory epithelial cell line.

To better understand the early biochemical events that occur in human rhinovirus (HRV) infections, we examined the kinetics and mechanisms of interleukin-8 (IL-8) and IL-6 production from infected epithelial cells. Several HRV strains caused IL-8 and IL-6 production, but HRV-16 induced maximal IL-8 and IL-6 mRNA expression and protein production more rapidly than did HRV-14, despite similar rates of replication of the two viral strains. Viral induction of cytokine mRNA does not require new protein synthesis, since it was unaffected by cycloheximide treatment. The potent glucocorticoid budesonide did not affect viral replication or cytokine mRNA induction but modestly inhibited cytokine protein production. Interestingly, the nitric oxide donor 3-(2-hydroxy-2-nitroso-1-propylhydrazino)-1-propanamine (NONOate) inhibited both rhinovirus replication and cytokine production in a dose-dependent fashion without reducing levels of cytokine mRNA. The NONOate effects were due to release of nitric oxide, because NONOate that had been depleted of its nitric oxide content had no effect. Thus, nitric oxide may play an important anti-inflammatory and antiviral role in colds and nitric oxide donors may represent a novel therapeutic approach.

Cell Line↗

PubMed1998

Plasma extravasation through neuronal stimulation in human nasal mucosa in the setting of allergic rhinitis.

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.

Adult↗

PubMed1997

Stable expression of the human kinin B1 receptor in Chinese hamster ovary cells. Characterization of ligand binding and effector pathways.

To delineate ligand binding and functional characteristics of the human B1 kinin receptor, a stable clone of Chinese hamster ovary cells expressing a single class of binding sites for [3H]des-Arg10-lysylbradykinin with a Kd of 0.3 nM and a Bmax of 38 fmol/mg protein ( approximately 40,000 receptors/cell) was isolated. Studies with peptide analogs showed that a lysine residue at position 1 (based on the lysylbradykinin sequence) of ligands was essential for high affinity binding to the human B1 receptor. In marked contrast to cloned Chinese hamster ovary cells expressing the human kinin B2 receptor, which internalized approximately 80% of the ligand within 5 min upon exposure to 2 nM [3H]bradykinin, exposure of cells expressing the B1 receptor to 1 nM [3H]des-Arg10-lysylbradykinin resulted in minimal ligand internalization. Stimulation of the B1 receptor led to inositol phosphate generation and transient increases in intracellular calcium, confirming coupling to phospholipase C, while immunoprecipitation of photoaffinity-labeled G-proteins from membranes indicated specific coupling of the receptor to Galphaq/11 and Galphai1,2. The B1, unlike the B2, receptor does not desensitize (as demonstrated by continuous phosphoinositide hydrolysis), enhancing the potential role of this receptor during inflammatory events.

Animals↗

PubMed1997

Nasal provocation with allergen induces a secondary serum IgE antibody response.

The study of the IgE response to seasonal antigen exposure is limited by its occurrence once a year and by the variability of patient exposure to pollens. To overcome these problems, we investigated whether nasal challenge with antigen causes an increase in serum anti-ragweed IgE levels. We challenged individuals with ragweed allergy intranasally with nanogram quantities of ragweed antigen extract and measured their serum anti-ragweed IgE levels before and at weekly intervals after challenge. In a series of studies we found that there was a reproducible rise in antigen-specific serum IgE levels beginning the first week after challenge that plateaued at about 180% of baseline levels during the fourth week and remained elevated for 8 weeks. Not all individuals showed this response. The magnitude of the allergen-specific IgE response to nasal challenge appeared to be greater than the response to seasonal exposure. Treatment with intranasal beclomethasone before challenge did not affect the response. The results demonstrate a human in vivo model for the study of the antigen-specific secondary IgE response to allergen.

Administration, Intranasal↗

PubMed1997

Dose-dependent effects of capsaicin nasal challenge: in vivo evidence of human airway neurogenic inflammation.

BACKGROUND: Nerve involvement has been implicated in the pathophysiology of chronic respiratory inflammatory diseases. Peptidergic nerve stimulation has been shown to induce leukocyte activation and plasma extravasation in the airways of various animal species. The occurrence of this phenomenon of neurogenic inflammation in the human airway, however, has not been established. OBJECTIVE: We conducted this study to determine whether neuronal stimulation can induce reproducible and dose-dependent inflammatory changes in the human upper airway. METHODS: Ten volunteers with active allergic rhinitis participated in the study. Capsaicin, the pungent component of hot pepper that specifically stimulates afferent nerve fibers, was administered by means of nasal spray in doses of 1 microg, 10 microg, and 100 microg in a double-blind, randomized, crossover manner with 1 week between doses. Symptom scores before and after capsaicin nasal challenge were recorded by using visual analog scales. Nasal lavage fluids collected before and at 30 minutes, 1 hour, and 4 hours after capsaicin challenge were analyzed for leukocyte counts; albumin and lysozyme levels were measured to evaluate effects on plasma leakage and gland secretion, respectively. RESULTS: Capsaicin nasal challenge produced symptoms of burning, congestion, and rhinorrhea. Leukocyte counts or albumin and lysozyme levels were not significantly increased after administration of 1 microg of capsaicin at any time point. On the other hand, there were significant increases in leukocyte counts 1 hour (p < 0.05) and 4 hours (p = 0.008) after 10 microg of capsaicin and 30 minutes (p = 0.009), 1 hour (p = 0.007), and 4 hours (p = 0.007) after 100 microg of capsaicin. Albumin and lysozyme levels were both significantly increased 30 minutes after 10 microg and 100 microg of capsaicin (p = 0.005 for both). Comparison of changes in symptom scores, leukocyte counts, and albumin and lysozyme levels among the three capsaicin challenges indicated generally increasing effects with higher capsaicin doses. CONCLUSION: Capsaicin-sensitive nerve stimulation in subjects with active allergic rhinitis produces reproducible and dose-dependent leukocyte influx, albumin leakage, and glandular secretion. These results provide in vivo evidence for the occurrence of neurogenic inflammation in the human upper airway with active allergic disease.

Adult↗

PubMed1997

A double-blind study of the discontinuation of ragweed immunotherapy.

BACKGROUND: Immunotherapy effectively treats the symptoms of allergic rhinitis and improves its pathophysiology. We studied whether the effects of immunotherapy on the early response to nasal challenge with antigen and seasonal symptoms persist after discontinuation. METHODS: Twenty subjects with ragweed allergy who were receiving immunotherapy and who had nasal challenges performed before initiation of treatment were selected. The patients had been receiving maintenance therapy with aqueous ragweed extract at a dose of 12 microg of Amb a 1 equivalent for a minimum of 3 years, at which point they were randomized to receive either placebo injections or to continue with the maintenance dose. Nasal challenges were performed before and 1 year after randomization. Nasal challenges were monitored by counting the number of sneezes and measuring histamine, N-alpha-tosyl-L-arginine methyl ester-esterase activity, and kinins in recovered nasal lavages. In the same year symptom diaries were collected during the ragweed season. RESULTS: The initial immunotherapy significantly reduced responses to nasal challenge in both groups. The group continuing to receive active treatment showed no significant changes from the response before randomization. In contrast, the group randomized to placebo treatment showed a partial return of histamine, kinins, and N-alpha-tosyl-L-arginine methyl ester-esterase in nasal secretions and the numbers of sneezes. IgG antibodies to ragweed declined only in the group switched to placebo treatment. Seasonal rises of IgE antibodies to ragweed did not return during the first season after treatment was stopped. Symptoms reported during the ragweed season were not different between the groups. CONCLUSIONS: One year after discontinuation of ragweed immunotherapy, nasal challenges showed partial recrudescence of mediator responses even though reports during the season appeared to indicate continued suppression of symptoms.

Adolescent↗

PubMed1997

Treatment with hot, humid air reduces the nasal response to allergen challenge.

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.

Adult↗