lnterleukin-5 Upregulates Intercellular Adhesion Molecule-1 Gene Expression in the Nasal Mucosa in Nasal Allergy but Not in Nonallergic Rhinitis

Terada, Nobuhisa; Konno, Akiyoshi; Fukuda, Setsuya; Yamashita, Tetsuji; Abé, Tatsuya; Shimada, Hiroko; Yoshimura, Kazuya; Shirotori, Kohji; Ishikawa, Kazuo; Togawa, Kiyoshi

doi:10.1159/000236834

Cited by 13 publications

(3 citation statements)

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“…The main function of IL–5 is defined as a maturation and growth factor for eosinophils and basophils and as a chemotactic factor for eosinophil infiltration from blood vessels to the nasal airway [39]. IL–5 also functions as an inducer of intracellular adhesion molecule–1 (ICAM–1) gene expression in human nasal mucosa during nasal allergic reactions [40]. A high level of IL–5 secretion by TCCs might participate as one of the factors in the immunopathology of Japanese cedar pollinosis.…”

Section: Discussionmentioning

confidence: 99%

Peptide Specificity, HLA Class II Restriction, and T–Cell Subsets of the T–Cell Clones Specific to Either Cry j 1 or Cry j 2, the Major Allergens of Japanese Cedar (Cryptomeria japonica) Pollen

Sone¹,

Morikubo²,

Shimizu³

et al. 1999

Int Arch Allergy Immunol

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Background: Cry j 1 and Cry j 2 are thought to be the major allergens of Japanese cedar pollen. HLA class II types capable of presenting T–cell epitopes in both allergens and their role in induction of T–cell subsets are not well known. Methods: CD4+ T (Th)–cell clones (TCCs) specific to either Cry j 1 or Cry j 2 were generated. HLA class II restrictions were determined by their reactivity to the T–cell epitope in the presence of antigen presenting cells sharing matched types. Interleukin (IL)–2, interferon–γ, IL–4, and IL–5 contents in the supernatants of TCCs were estimated using enzyme immunoassay. Results: Peripheral blood mononuclear cells (PBMC) from patients induced proliferation with 100 μg/ml Cry j 1 or 3–10 μg/ml rCry j 2 stimulation. T–cell epitopes in Cry j 1 were presented to Th cells by the gene products of DRA1*01/DRB1*0901, DRA1*01/DRB5*0101, DQA1* 0102/DQB1*0602, and DPA1*01/DPB1*0501; those in Cry j 2 were restricted by DRA1*01/DRB1*0901, DRA1* 01/DRB1*1501, DRA1*01/DRB4*01, DRA1*01/DRB5* 0101, DQA1*0102/DQB1*0602, DPA1*01/DPB1*0201, and DPA1*01 and *0202/DPB1*0501. Type 2–like cells were preferentially induced in Cry j 1 stimulation, while an almost equal number of type 2– and type 1–like cells was induced in rCry j 2. Conclusions: No clear correlation existed between peptide specificity, HLA class II restriction and induction of Th–cell subsets, suggesting that the requirement of different dose of Cry j 1 or Cry j 2 to induce proliferation in PBMC may lead to distinguishable difference in induction of Th subsets between TCCs specific to Cry j 1 and Cry j 2.

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Section: Discussionmentioning

confidence: 99%

Peptide Specificity, HLA Class II Restriction, and T–Cell Subsets of the T–Cell Clones Specific to Either Cry j 1 or Cry j 2, the Major Allergens of Japanese Cedar (Cryptomeria japonica) Pollen

Sone¹,

Morikubo²,

Shimizu³

et al. 1999

Int Arch Allergy Immunol

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“…5,[30][31][32][33] The present study also found low-level expression of ICAM-1 on nasal epithelial cells under baseline conditions but increased expression during the early phase of HRV infection. Expression of ICAM-1 in airway epithelium and endothelial cells in mice is up-regulated in response to various stimuli including ozone exposure, 34 interleukin 5, 35 tumor necrosis factor ␣, interleukin 1, 36 and activated CD8 + T cells. 37 Christensen et al 38 demonstrated a correlation between elevated circulating ICAM-1 levels in serum and virusinduced T-cell activation during lymphocytic choriomeningitis virus infection, which suggested release of ICAM-1 into the bloodstream.…”

Section: Commentmentioning

confidence: 99%

Expression of ICAM-1 in Nasal Epithelium and Levels of Soluble ICAM-1 in Nasal Lavage Fluid During Human Experimental Rhinovirus Infection

Winther¹,

Arruda²,

Witek³

et al. 2002

Arch Otolaryngol Head Neck Surg

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Most rhinovirus serotypes use intercellular adhesion molecule-1 (ICAM-1) as the receptor to enter cells, but ICAM-1 expression has not been detected on normal nasal epithelial cells. During experimental rhinovirus infection, expression of ICAM-1 on nasal epithelial cells was examined with immunohistochemical staining of nasal scrape biopsy specimens, and levels of soluble ICAM-1 in nasal lavage fluid were measured by sandwich enzyme-linked immunosorbent assay technique. Expression of ICAM-1 on nasal epithelial cells increased following inoculation in 20 of 23 infected subjects. The median number of ICAM-1-positive cells per 6.25-mm(2) area of stained biopsy specimen was 0 in control samples (day 20 or 33 after inoculation), and in those without infection, 6 on day 1 (P< or =.05), 14.5 on day 3 (P< or =.01), 1.5 on day 5, and 0 on day 9. In a different group of volunteers, soluble ICAM-1 in nasal lavage fluid was higher on days 1 and 3 compared with preinoculation levels (P< or =.001), but only 11 of 23 infected subjects had a 2-fold or greater increase. Up-regulation of ICAM-1 receptor expression on nasal epithelial cells occurred within 24 hours after inoculation in experimental rhinovirus infections (prior to onset of symptoms) and declined promptly by day 5.

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“…214 The inducibleIn humans, elevated serum IL-5 was noted in expression of these molecules on endothelium symptomatic asthmatics in association with actidirects the focal adherence of leukocytes to vated T-lymphocytes and eosinophilia. 226 In allerendothelium for extravasation at sites of inflamgic rhinitis patients, IL-5 levels were elevated 48 h…”

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confidence: 99%

Nasal hyperreactivity and inflammation in allergic rhinitis

Garrelds

Veld

Wijk

et al. 1996

Mediators of Inflammation

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The history of allergic disease goes back to 1819, when Bostock described his own ‘periodical affection of the eyes and chest’, which he called ‘summer catarrh’. Since they thought it was produced by the effluvium of new hay, this condition was also called hay fever. Later, in 1873, Blackley established that pollen played an important role in the causation of hay fever. Nowadays, the definition of allergy is ‘An untoward physiologic event mediated by a variety of different immunologic reactions’. In this review, the term allergy will be restricted to the IgE-dependent reactions. The most important clinical manifestations of IgE-dependent reactions are allergic conjunctivitis, allergic rhinitis, allergic asthma and atopic dermatitis. However, this review will be restricted to allergic rhinitis. The histopathological features of allergic inflammation involve an increase in blood flow and vascular permeability, leading to plasma exudation and the formation of oedema. In addition, a cascade of events occurs which involves a variety of inflammatory cells. These inflammatory cells migrate under the influence of chemotactic agents to the site of injury and induce the process of repair. Several types of inflammatory cells have been implicated in the pathogenesis of allergic rhinitis. After specific or nonspecific stimuli, inflammatory mediators are generated from cells normally found in the nose, such as mast cells, antigen-presenting cells and epithelial cells (primary effector cells) and from cells recruited into the nose, such as basophils, eosinophils, lymphocytes, platelets and neutrophils (secondary effector cells). This review describes the identification of each of the inflammatory cells and their mediators which play a role in the perennial allergic processes in the nose of rhinitis patients.

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lnterleukin-5 Upregulates Intercellular Adhesion Molecule-1 Gene Expression in the Nasal Mucosa in Nasal Allergy but Not in Nonallergic Rhinitis

Cited by 13 publications

References 0 publications

Peptide Specificity, HLA Class II Restriction, and T–Cell Subsets of the T–Cell Clones Specific to Either Cry j 1 or Cry j 2, the Major Allergens of Japanese Cedar (Cryptomeria japonica) Pollen

Peptide Specificity, HLA Class II Restriction, and T–Cell Subsets of the T–Cell Clones Specific to Either Cry j 1 or Cry j 2, the Major Allergens of Japanese Cedar (Cryptomeria japonica) Pollen

Expression of ICAM-1 in Nasal Epithelium and Levels of Soluble ICAM-1 in Nasal Lavage Fluid During Human Experimental Rhinovirus Infection

Nasal hyperreactivity and inflammation in allergic rhinitis

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