Allergic Mucosa Research Articles

Human Rhinovirus Infection Enhances the Th2 Environment in Allergic and Non-allergic Patients with Chronic Rhinosinusitis.

Objectives. This study was conducted to determine whether patients with allergic rhinitis might be more susceptible to human rhinovirus (HRV) infection and whether the effects of infection on the elicited immune responses are different in allergic and non-allergic patients with chronic rhinosinusitis (CRS).Methods. Uncinate process tissues were obtained from 61 CRS patients (of whom 39 had allergies and 22 did not) and were infected with HRV-16 using an air-liquid interface organ culture system. The expression levels of programmed cell death-ligand (PD-L)1, PD-L2, intracellular adhesion molecule 1, interferon-gamma (IFN-γ), interleukin (IL)-4, IL-5, and IL-10 were evaluated in the infected nasal mucosa.Results. The HRV infection rates were not significantly different between the allergy (74.4%) and non-allergy (72.7%) groups. In the allergy group, the expression of PD-L1 (P=0.013) and IL-10 (P=0.040) was significantly elevated in the HRV-infected tissues, and there was a strong correlation between PD-L1 and IL-10 (r=0.868, P<0.001). In contrast, infected tissues from the non-allergy group displayed increased levels of IL-4 (P=0.039), IL-5 (P=0.023), and IFN-γ (P=0.031), as well as an increased IL-4/IFN-γ ratio, after HRV infection (P=0.043).Conclusion. This study showed that HRV infection rates were similar in the nasal mucosa of patients with CRS regardless of the presence of allergic rhinitis. HRV infection enhanced the Th2 environment by modulating PD-L1 and PD-L2 expression levels in allergic mucosa and by increasing the IL-4/IFN-γ ratio in non-allergic mucosa.

Expression of Trefoil factor family peptides in the nasal allergic mucosa

Trefoil factor family peptides (TFFs) are the secretory products of mucous cells and are closely associated with mucins. TFFs appear to be important in mucosal healing processes. Although TFF1/3 are expressed in the human respiratory tract, their role in the nasal mucosa is not thoroughly understood. We investigated the association between TFFs and mucins and the role TFFs in the human nasal mucosa. Patients undergoing turbinectomy were included and it was determined whether patients had nasal allergies or not. The localization of TFF1/3, MUC5AC/5B expression was investigated using immunohistochemistry. The levels of the mRNA transcripts were examined using quantitative real-time PCR. TFF1/3 had a similar pattern of localization in epithelial goblet cells and submucosal glandular cells. TFF1/3 co-localized with MUC5AC in the epithelium, and co-localized with MUC5B in the epithelium and the submucosal glandular cells. The levels of TFF1/3 and MUC5B mRNA in allergic patients were significantly increased. Our results suggest that TFF1/3 may associate with MUC5AC and MUC5B in the nasal mucosa, and that up-regulation of TFF1/3 and MUC5B may play an important role in the clinical condition of the nasal allergic mucosa.

Expression of Trefoil factor family peptides in the nasal allergic mucosa

Expression of Trefoil factor family peptides in the nasal allergic mucosa

Mucosal thickening in allergic and idiopathic rhinitis mucosa and its probable mechanism

Rhinitis is a prevalent condition characterized by nasal mucosal irritation. Conflicting studies suggest that the mucosa of patients with allergic and nonallergic rhinitis undergoes thickening. To investigate mucosal epithelial thickening in allergic and idiopathic rhinitis and to determine if the mechanism is a consequence of altered proliferation or apoptosis. Interactive image analysis was performed on histologic sections of inferior nasal turbinate tissue to measure epithelial thickness in 3 patient groups. Patients with allergic rhinitis (n = 15), patients with idiopathic rhinitis (n = 15), and a healthy control group (n = 10) were compared. Immunohistochemical and morphometric analyses were used to quantify cell proliferation (Mib-1), apoptosis (terminal uridine nick end labeling technique), and the antiapoptotic factor Bcl-2. Idiopathic epithelium was found to be significantly thickened compared with healthy epithelium (P = .04). Epithelial thickening occurred in some allergic patients, but the findings did not reach statistical significance (P = .22). No statistically significant difference in proliferation as evidenced by Mib-1 staining was seen among the 3 patient groups. Allergic mucosa differed statistically significantly to that of patients with idiopathic rhinitis (P = .01) and healthy controls (P = .005) in showing increased Bcl-2 staining, suggesting reduced apoptosis. Allergic epithelium shows significantly decreased apoptosis, which might explain the increased epithelial thickening seen in some study participants. This mechanism does not, however, appear to explain the significantly increased thickening seen in the idiopathic epithelium. Furthermore, both allergic and nonallergic epithelium showed regional thinning and thickening possibly involving an inflammatory infiltrate.

Overexpression of the anaphylatoxin receptors, complement anaphylatoxin 3a receptor and complement anaphylatoxin 5a receptor, in the nasal mucosa of patients with mild and severe persistent allergic rhinitis

Although the complement anaphylatoxin peptides, complement anaphylatoxin 3a (C3a) and complement anaphylatoxin 5a (C5a), are implicated in the inflammatory process in allergic rhinitis, a direct interaction between allergic mucosa and complement receptors has not been demonstrated. We investigated the expressional levels and distributional patterns of the C3a receptor (C3aR) and C5a receptor (C5aR) in normal, mild, and severe persistent allergic nasal mucosa. Immunohistochemistry and Western blotting using C3aR and C5aR antibodies were applied to normal nasal, mild, and severe persistent allergic nasal mucosa. Complement anaphylatoxin 5a receptor was detected in the inflammatory cells of normal and allergic nasal mucosa, and its expression level was significantly higher in allergic nasal mucosa than normal nasal mucosa. C3aR in normal and allergic nasal mucosa was commonly expressed in nonmyeloid cells such as epithelial cells, submucosal glands, and nerve fibers. In addition, C3aR was expressed in the endothelium of cavernous sinuses and the surrounding perivascular muscle layer in severe persistent allergic nasal mucosa, but not in normal and mild allergic nasal mucosa. Western blotting demonstrated that the expression level of C3aR was significantly increased in severe persistent allergic nasal mucosa compared with normal and mild nasal mucosa. On the basis of the location of C3aR and C5aR, C5aR may play a role in activation of inflammatory cells, whereas C3aR may mediate mucus secretion and mucosal swelling in allergic nasal mucosa, especially severe persistent allergic nasal mucosa.

Nasal mucosal expression of nitric oxide synthases in patients with allergic rhinitis and its relation to asthma

Nitric oxide (NO) has contradictory roles in the pathophysiology of allergic inflammation in both allergic rhinitis (AR) and asthma. Small amounts of NO produced by constitutive NO synthase (NOS) is anti-inflammatory, whereas large amounts produced by inducible NOS (iNOS) are proinflammatory. To investigate the difference in constitutive endothelial NOS (eNOS) and iNOS expression in nonallergic and allergic mucosa and the possible relation of this to the coexistence of asthma in seasonal AR. Seventeen patients (10 women and 7 men) with seasonal AR and 9 nonallergic patients (5 women and 4 men) with nasal septum deviation were enrolled. Inferior turbinate nasal biopsy specimens were obtained in all. Levels of eNOS and iNOS expressed as immunohistochemical scores (HSCOREs) were determined immunohistochemically from the specimens. The mean +/- SD HSCOREs for eNOS in patients with seasonal AR were not significantly different from those of the nonallergic controls (1.85 +/- 0.78 vs 1.63 +/- 0.54; P = .12). On the other hand, the mean +/- SD HSCOREs for iNOS were significantly higher in patients with seasonal AR (1.75 +/- 0.75 vs 0.71 +/- 0.6; P = .004). Furthermore, although eNOS expression was not different between seasonal AR patients with and without asthma, the mean +/- SD HSCOREs for iNOS were significantly higher in the patients with asthma (1.93 +/- 0.78 vs 1.65 +/- 0.55; P = .01). Increased expression of iNOS might have a role in the development of allergic inflammation in upper and lower airways and in comorbidity of AR and asthma.

Reduced TLR2 gene expression is a feature of chronic rhinitic mucosa supporting the hygiene hypothesis

Objective. Pathogenic induction of the immunomodulators toll like receptors (TLRs) and beta-defensins (HBD) can steer the developing immune system toward a Th1 nonallergic pathway and might explain why farmer's children show reduced frequency of allergy. We hypothesised that chronic allergic and nonallergic rhinitis might be associated with reduced mucosal levels of TLRs and HBDs. Method. The gene expression levels of TLR2 & 4 and HBD1-4 was determined by real-time polymerase chain reaction in sections of nasal turbinate tissue from adults with persistent allergic and idiopathic rhinitis, healthy nasal mucosa and tonsil tissue. Immunohistochemistry was used to study the localisation and distribution of proteins for TLR2, HBD2, α-defensins (1-3) and neutrophil elastase Results. A significant reduction in TLR2 mRNA expression was identified in allergic mucosa compared to control mucosa, with generally reduced expression for TLR4 and HBDs. While not significant, the nonallergic group also showed reduced expression for TLRs and HBDs. With the exception of HBD4, increased gene levels were seen in tonsil tissue. HBD2 and TLR2 protein expression was localised in lining and submucosal glandular epithelium but insignificant differences were seen for HBDs, TLRs, neutrophils and α-defensin between the rhinitic and control patient groups. Conclusion. Chronic rhinitic mucosa shows reduced levels of TLR and HBD gene expression. The significant reduction in TLR2 gene expression in adult allergics support the concept that increased TLR2 is protective against the development of allergy.

Reduction of TLR2 gene expression in allergic and nonallergic rhinitis

Immunomodulators, including toll-like receptors (TLRs) and defensins, produced in response to pathogenic stimuli, can direct the developing immune system toward a T(H)1 nonallergic phenotype. Increased human beta-defensin (HBD) 4 expression is associated with infection. To determine whether reduced mucosal levels of TLRs and defensins contribute to the inflammation seen in chronic allergic and nonallergic rhinitis. Real-time polymerase chain reaction was used to determine gene expression levels of HBDs 1 through 4 and TLRs 2 and 4. Immunohistochemical analysis was used to study the localization and distribution of protein for alpha-defensins 1 through 3, HBD2, neutrophil elastase, and TLR2 in sections of nasal turbinate tissue from adults with persistent allergic and idiopathic rhinitis, healthy nasal mucosa, and tonsil tissue. Allergic mucosa showed a significant (P = .02) reduction in TLR2 messenger RNA expression compared with control mucosa and generally reduced expression for TLR4 and HBDs. Although not significant, the nonallergic group also showed reduced expression for TLRs and HBDs. With the exception of HBD4, increased target gene levels were seen in tonsil tissue. Protein expression of HBD2 and TLR2 was localized in lining and submucosal glandular epithelium but insignificant differences were seen for HBDs, TLRs, neutrophils, and a-defensin between the rhinitic and control patient groups. Subjects with allergic and nonallergic rhinitis show reduced TLR and HBD gene expression. The significant reduction in TLR2 gene expression in allergic adults supports the concept that increased TLR2 protects against the development of allergy. The low levels of HBD4 detected in both rhinitis groups suggest lack of an underlying infection pathophysiological feature.

Expression of Syk is associated with nasal polyp in patients with allergic rhinitis

Objective Numerous signalings are involved in allergic inflammation. The non-receptor protein tyrosine kinase, Syk, is widely expressed in immune-potentiated cells and plays critical roles in initiating signal transduction in response to the activation of cytokine, chemokine and other types of receptors. It has been hypothesized that Syk expression in allergic nasal mucosa and polyps with allergy is different from non-allergic mucosa, and that changes in Syk expression contribute to the activation of allergic reactions. Methods We examined whether the expression of Syk is found in allergic nasal mucosa and polyps. We investigated the expression of Syk in 46 nasal mucosa and polyps (14 samples from patients with allergic rhinitis and 32 samples with non-allergic chronic sinusitis) using an immunohistochemical technique. Results Allergic polyps had more Syk positive cells than non-allergic polyps. Syk positive cells were determined to mainly be eosinophils. There was no difference in Syk expression in the lamina propria and nasal gland between allergic mucosa and non-allergic mucosa. Conclusion Eosinophils in allergic polyps receive an intracellular signal, although the signal is not able to determine the function in the present state. Syk appears to be a promising target molecule for anti-allergic inflammation in allergic rhinitis.

알레르기비염 동물 모델에서 Budesonide, N-Acetyl-Aspartyl- Glutamate 및 Cyclosporin A 국소투여 후 비강내 아미노산 농도의 변화：미세투석법을 이용한 측정

Background and Objectives: This study aimed to measure the concentration (conc) of 19 amino acids (AAs) in the nasal cavity, to evaluate the difference of AAs conc among normal, allergic nasal mucosa, and allergic mucosa after intranasal application of budesonise, N-acetyl-aspartyl-glutamate (NAAGA), and cyclosporin (CsA) in guinea pigs. Materials and Method: Experimentally induced nasal allergy model was developed with ovalbumin in Dunkin-Hartely guinea pigs. Microdialysis was done in the inferior turbinate submucosa of normal control (C) , allergic group (A) , allergic group with intranasal application of budesonide (AS) , allergic group with intranasal application of NAAGA (AN) and allergic group with intranasal application of CsA (AC) . Results: All 19 AAs were validated at various conc in the nasal cavity. Glutamate and GABA conc were significantly higher in A than in C group. The conc serine, arginine, tyrosine, isoleucine, leucine, phenylalanine in AS group were significantly lower than those in A and C groups, whereas GABA conc was significantly higher in AS group than in A and C groups. The conc of glutamate, glycine, alanine, methionine, leucine, lysine, phenylalanine in A group were significantly higher than those in AN group, whereas tyrosine conc was reversed. There was no significant changes of AAs conc between A and AC groups. Conclusion: These results suggest that glutamate can be a novel amino acid neurotransmitter of parasympathetic nerve and GABA can act as an inhibitor of cholinergic parasympathetic nerve in the nasal cavity. (J Clinical Otolaryngol 2005;16:96–104)

Localisation of heme oxygenase isoforms in allergic human nasal mucosa

Carbon monoxide (CO) is an endogenously produced gas mediator produced by heme oxygenase (HO). Like nitric oxide (NO), CO is produced in the nasal mucosa. Given that induced NO synthase (iNOS) expression in nasal mucosa has been found to be up-regulated in allergic rhinitis, the current study investigated the expression of HO isoforms in allergic human nasal mucosa. Immunohistochemical staining for type 1 and 2 HO isoforms were carried out in nasal inferior turbinate mucosa from six patients with persistent allergic rhinitis, and compared with six control patients without nasal allergy. Focal and weak expression of HO-1 was observed in seromucous glands, with no difference between allergic and control specimens. Vascular endothelium, erythrocytes, smooth muscle and inflammatory cells (except macrophages) in the allergic group exhibited stronger HO-1 immunoreactivity compared to the control. Minimal expression was found in the respiratory epithelium in either group. Intravascular HO-1 expression was found in the allergic mucosa only. Intense HO-2 immunoreactivity was observed in the respiratory epithelium, vascular endothelium and seromucous glands in both allergic and control groups with no differences in intensity. In conclusion, unlike iNOS, HO-1 is minimally expressed in the nasal respiratory epithelium of either group. However, our findings suggest that it may be involved in the inflammatory process of allergic rhinitis at the submucosal level.

Inflammatory mediators in allergic rhinitis

Allergic rhinitis (AR) is part of a systemic disease complex. There is a close relationship between AR and asthma, which has led to the "one airway, one disease" concept. Both conditions share common immunopathology and pathophysiology. In patients with AR, allergen-triggered early and late responses are mediated by a series of inflammatory cells. Within minutes of contact with allergen, IgE-sensitized mast cells degranulate, releasing both preformed and newly synthesized mediators. Immunologic processes in both nasal and bronchial tissue involve T H 2 lymphocytes and eosinophils. Eosinophils are the predominant cell in the chronic inflammatory process characteristic of the late-phase allergic response. Eosinophils release an array of proinflammatory mediators, including cysteinyl leukotrienes, cationic proteins, eosinophil peroxidase, and major basic protein, and might serve as a major source of IL-3, IL-5, GM-CSF, and IL-13. Neuropeptides also appear to contribute to the pathophysiology of AR symptoms. Both AR and asthma exhibit marked day-night variation in symptom severity. Acknowledging both the chronobiology of AR and circadian rhythm-dependent attributes of antiallergy medications might enhance the beneficial effects of allergy therapies.

アレルギー性鼻炎患者鼻粘膜内有窓型毛細血管と浸潤好酸球および上皮障害の電子顕微鏡的観察

アレルギー性鼻炎患者鼻粘膜内有窓型毛細血管と浸潤好酸球および上皮障害の電子顕微鏡的観察

Asthma and sex hormones.

A chronic in ammatory state of the airways is considered the hallmark of asthma (1). However, the incidence, severity, and prognosis of asthma can be affected by a number of factors, including the patient's sex and age. The sex of the fetus seems to in uence the development of the respiratory apparatus. In fact, between weeks 28 and 40 of gestation, the lungs are in a more advanced state in females than in males (2), a fact which could explain, at least in part, the higher incidence of respiratory distress in male infants (3). Clinical observations and epidemiologic studies agree that childhood asthma is more frequent in boys than in girls (4). Moreover, in some children, usually boys, asthmatic symptoms that started in infancy disappear around puberty (5), while many girls have the disease only during adolescence (6). Age has been implicated in the severity of asthma. Asthma beginning during adulthood is generally more severe than childhood-onset asthma (7). Asthma that starts around the menopause or in old age is generally quite severe (5). According to two recent epidemiologic investigations, the patient's sex and age affect the hospitalization rate for asthma (8, 9), which is a marker of severity. In the ®rst study (a retrospective study of 33 269 patients), the admission rate of boys in the 0±10-year age group was almost twice that of girls. In the next decade, sex differences in the hospitalization rate were irrelevant, although there was a small, but signi®cant prevalence of females. At all ages above 20 years, hospital admission rates were higher in women than men, with a female/ male ratio ranging from 3:1 in subjects aged 20±50 years to 2.5:1 in those over 50 years of age (8). Similar data were reported by Elliasson (9). Both studies found a relationship between the age and sex of the patient and the severity of the asthma attack as indicated by duration of hospitalization. In fact, the duration of hospitalization increased with age in both sexes; moreover, hospital stays were longer in women over 30 years of age than in men of the same age (8, 9). Abbreviations. FSH: follicle-stimulating hormone; LH: luteinizing hormone; NK cell: natural killer cell; IL-1, -4, -5, -6: interleukin-1, -4, -5, -6; TGF-b: tumor growth factor-beta; PEFR: peak expiratory ow rate. Allergy 2001: 56: 13±20 Printed in UK. All rights reserved Copyright # Munksgaard 2001

Idiopathic and allergic rhinitis show a similar inflammatory response

HYPOTHESIS: Idiopathic and allergic rhinitics have similar mucosal mast cell and IgE+ cell distribution. INTRODUCTION: The pathophysiology of idiopathic rhinitis (IR) is unknown but patients differ from those with allergic rhinitis (AR) in that they do not express IgE. Our study is novel because we investigated: (1) three study groups chosen prospectively using strict selection criteria over a 4-year period; and (2) mast cell and IgE+ cell counts were on full-thickness, full-length inferior turbinate mucosa. METHODS: Patient groups: allergic (n = 17); idiopathic: (n = 16); and normal controls (n = 9). Immunohistochemistry: mast cell and IgE+ cell detection using anti-mast cell tryptase and anti-IgE antibodies with an avidin-biotin (peroxidase) complex on paraffin processed tissue. Morphometry: sections were divided into three strata comprising an epithelial layer and two submucosal layers. Statistics: Mann-Whitney non-parametric analysis. alpha = 0.05, beta = 0.2. RESULTS: The power of the study was 89%. Mast cells (P = 0.03) and IgE+ cells (P < 0.05) were significantly increased in the epithelium of idiopahtic and allergic rhinitis mucosa compared to the normal control. More IgE+ cells were counted in the AR and IR groups compared to the controls in all three strata. CONCLUSION: Mast cells and IgE+ cells are involved in the pahtophysiology of IR. We propose that IR may be a variant form of AR involving a localized IgE-mediated inflammatory response.

Increased expression of alpha2-6 linked sialic acids by nasal mucins in allergic rhinitis

Mucins have a polypeptide backbone, oligosaccharide side-chains and peripheral structures that include sialic acids. Several pathogens have specific receptors for sialic acids, including human strains of influenza A virus which preferentially recognise and bind α2-6 linked rather than α2-3 linked sialic acids.11 NElson J., COuceiro S.S., PAulson J.C. & BAum L. (1993) Influenza virus strains selectively recognise sialyloligosaccharides on human respiratory epithelium; the role of the host cell in selection of haemagglutinin receptor specificity. The aim of this study was to identify possible disease-related changes in the expression of sialic acids in nasal mucins. Nasal mucosal samples were placed in organ culture. Metabolically-labelled mucins were purified by gel filtration, blotted on to nitrocellulose membranes and probed with the sialic acid-binding lectins Sambucus nigra and Maackia amurensis. Ninety-five mucosal samples were collected (49 turbinates, 31 nasal polyps, 15 samples from FESS). Lectin binding, expressed as optical density, showed significantly increased binding of S. nigra to cellular (P = 0.02; Kruskal–Wallis) and secreted (P = 0.045) mucin from allergic mucosa compared to non-allergic mucosa. No significant differences were found in the binding patterns of M. amurensis. This study has demonstrated increased expression of α2-6 linked sialic acids in the mucins synthesised and secreted by allergic compared to non-allergic nasal mucosa. This may cause a change in the way mucins and pathogens interact in allergic rhinitis, leading to altered susceptibility to upper respiratory tract infection.

Cytokines and adhesion molecules in allergic rhinitis.

This review summarizes our current knowledge of nasal allergic inflammation based on studies of cytokines, chemokines, and adhesion molecules in allergic rhinitis. The article also includes some aspects of viral rhinitis. Due to artificial or natural allergen exposure, an increase in the number of eosinophils and basophils, mast cells, IgE-positive cells, macrophages, monocyte-like cells, Langerhans cells, and activated T-cells can be observed within the mucosa and on the mucosal surface. Mediators are known to be released in response to allergens, but do not seem to be adequate to initiate the cell recruitment. After antigen challenge, the release of proinflammatory and regulatory cytokines could be demonstrated, and TH2-type cytokine mRNA upregulation in allergic mucosa has been shown. Proinflammatory cytokines initiate an adhesion cascade and activate T-cells that create an "atopic" cytokine environment within the tissue, which also may be linked to the long-term selective recruitment of eosinophils. However, the acute selective migration of eosinophils after allergen challenge is not fully understood, nor is the role of chemokines in allergic and viral rhinitis. Allergic rhinitis clearly represents an inflammatory reaction.

Inflammatory Cytokine Expression on Nasal Polyps Developed in Allergic and Infectious Rhinitis

To investigate the expression of cytokine mRNAs in nasal polyps and the role of allergy in the pathogenesis of nasal polyposis, we studied the expression of 1L-4, IL-5, and IFN-γ mRNAs using the RT-PCR and Southern blot. Nasal polyp specimens were obtained from 14 patients with infectious rhinitis and 5 patients with perennial allergic rhinitis. Turbinate mucosa specimens were obtained from 10 patients with allergic rhinitis and from 10 healthy subjects as controls. IL-4, IL-5 and IFN-γ mRNA were expressed in most specimens of allergic turbinate mucosa. The expression of these cytokines was less frequent in normal healthy turbinate mucosa. The density ratios of IL-4, IL-5 and IFN-T to β-actin were individually determined in both polyp and turbinate tissues. The density ratio for each cytokine was relatively higher in polyp tissues than in healthy turbinate mucosa; however, there was no significant difference in the density ratios determined for polyps associated with allergic rhinitis as compared with polyps associated with infectious rhinitis. These findings indicate that nasal polyposis may differ from allergic rhinitis in the mechanism by which IL-4 and IL-5 are increased. It is concluded that allergy may have an insignificant role in the development of nasal polyps.

CD25+ T-lymphocytes induce CD11b on eosinophils in allergic nasal mucosa

In the allergic mucosa, there is a significant increase in numbers of CD25+ cells and activated eosinophils. To determine whether a link exists between the activated T-lymphocytes and tissue eosinophils in nasal allergy, we studied CD25+ cells in the nasal mucosa and compared the levels of soluble IL-2 receptor (sIL-2R) both in the serum and the nasal secretions, and further investigated expression of CD11b on eosinophils in the nasal lavage fluids and peripheral blood of patients with nasal allergy. We also examined the effects of the culture supernatant of Con A- and IL-2-activated T-lymphocytes on CD11b expression on eosinophils in the present study. The concentration of sIL-2R in the nasal secretions from patients with Japanese cedar pollinosis (JCP) was significantly higher than that from normal subjects (p < 0.01). The sIL-2R level was significantly higher in the nasal secretions than in the sera in patients (p < 0.01), and CD11b expression on eosinophils from nasal hvage fluid was significandy higher than that of eosinophils from peripheral blood of the same individuals (p < 0.01). The activated T-lymphocytes promoted eosinophil activation with upregulation of CD11b in vitro, and eosinophils in the nasal secretions from patients significantly expressed more CD11b in vivo. These results indicate that activation of T-lymphocytes is linked to eosinophil activation in nasal allergy.

The role of pro-inflammatory cytokines in recruiting inflammatory cells in the nose

Cytokines and cell adhesion receptors play a pivotal role in the recruitment of cells from the peripheral blood into inflamed tissue. Allergic rhinitis has previously been described as an inflammatory reaction characterised by the migration of granulocytes into the nasal mucosa. Using this model, we investigated the release of proinflammatory cytokines (interleukin IL-1 beta, IL-6, IL-8 and tumour necrosis factor-alpha TNF-alpha) and the expression of cell adhesion molecules (ELAM-1, ICAM-1 and LFA-1) in two studies involving biopsies as well as lavage and brush techniques. IL-1 beta and TNF-alpha can be found rapidly after allergen exposure and seem to initiate the cellular infiltration. The release of the chemokine IL-8 correlates with the continuously increasing number of granulocytes on the mucosal surface. Allergic rhinitis subjects showed significantly increased secretion levels of the proinflammatory cytokines IL-1 beta and IL-6 and of the chemokine IL-8. These findings correspond to a higher expression of the adhesion receptors ELAM-1, ICAM-1 and LFA-1 in allergic mucosa. We conclude that proinflammatory cytokines regulate the cell infiltration by the induction of adhesion receptor expression.