Mechanisms of allergyIncreased expression of IL-16 immunoreactivity in bronchial mucosa after segmental allergen challenge in patients with asthma☆,☆☆,★
Section snippets
Subjects
The study was approved by the Ethics Committee of The Royal Brompton and Harefield Hospitals NHS Trust, London, United Kingdom. The clinical characteristics of the study subjects are shown in Table I.
Characteristic Atopic asthmatic subjects Normal control subjects No. 18 6 Age (y)* 31.1 ± 7.5 22.4 ± 2.6 Sex (M/F) 8/10 6/0 Baseline FEV1 (L)* 3.68 ± 0.84 4.43 ± 0.51 PC20FEV1 (mg/mL)* 3.59 ± 3.61 >32 Total IgE (IU/mL)* 319.1 ± 270.1† 85.0 ± 114.5 RAST to Der p or G Positive
IL-16 immunoreactivity
At baseline, IL-16–immunoreactive cells were identified both in the epithelial and subepithelial areas. In normal subjects, the epithelial IL-16 immunoreactivity scores were low and score values did not differ in biopsy specimens obtained from the diluent-challenged and the allergen-challenged sites (Fig 1).
Discussion
The interaction of IL-16 and CD4+ cells may be of particular importance to asthma because IL-16 has the ability to selectively attract CD4+ cells in vitro through interaction with CD4. In this study, we used the technique of segmental allergen bronchoprovocation to investigate the role of IL-16 in the development of allergic inflammation. Our data show that specific allergen challenge was associated with an influx of inflammatory cells, particularly eosinophils. Increases in the numbers of both
References (32)
- et al.
Eosinophils, T-lymphocytes, mast cells, neutrophils, and macrophages in bronchial biopsy specimens from atopic subjects with asthma: comparison with biopsy specimens from atopic subjects without asthma and normal control subjects and relationship to bronchial hyperresponsiveness
J Allergy Clin Immunol
(1991) Interleukin-4: a prototypic immunoregulatory lymphokine
Blood
(1991)- et al.
Activation of CD4+ T cells, increased TH2-type cytokine mRNA expression, and eosinophil recruitment in bronchoalveolar lavage after allergen inhalation challenge in patients with atopic asthma
J Allergy Clin Immunol
(1993) - et al.
Randomised, dose-ranging, placebo-controlled study of chimeric antibody to CD4 (keliximab) in chronic severe asthma
Lancet
(1998) - et al.
Interleukin 16 and its function as a CD4 ligand
Immunol Today
(1996) - et al.
Expression of IL-16 in allergen-induced late-phase nasal responses and relation to topical glucocorticosteroid treatment
J Allergy Clin Immunol
(1997) - et al.
Association of increased CD4+ T-cell infiltration with increased IL-16 gene expression in atopic dermatitis
J Allergy Clin Immunol
(1998) - et al.
Mucosal inflammation in asthma
Am Rev Respir Dis
(1990) - et al.
Identification of activated T lymphocytes and eosinophils in bronchial biopsies in stable atopic asthma
Am Rev Respir Dis
(1990) - et al.
Expression of mRNA for interleukin-5 in mucosal bronchial biopsies from asthma
J Clin Invest
(1991)
Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma
N Engl J Med
Adoptive transfer of allergen-specific CD4+ T cells induces airway inflammation and hyperresponsiveness in brown-Norway rats
Immunology
CD4+ T cells can induce airway hyperresponsiveness to allergen challenge in the brown norway rat
Am J Resp Crit Care Med
Transfer of allergic airway responses with antigen-primed CD4+ but not CD8+ T cells in brown Norway rats
J Clin Invest
Depletion of murine CD4+ T lymphocytes prevents antigen-induced airway hyperreactivity and pulmonary eosinophilia
Am J Respir Cell Mol Biol
CD4+ T-lymphocytes and interleukin-5 mediate antigen-induced eosinophil infiltration into the mouse trachea
Am Rev Respir Dis
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Pathology of Asthma
2021, Encyclopedia of Respiratory Medicine, Second EditionInterleukin 16 and CCL17/thymus and activation-regulated chemokine in patients with aspirin-exacerbated respiratory disease
2017, Annals of Allergy, Asthma and ImmunologyCitation Excerpt :IL-16 is the ligand for CD4+ and serves as a specific chemoattractant; therefore, it can induce CD4+ T-cell, monocyte, and eosinophil-cell recruitment at inflammation sites.6 IL-16 is produced by CD8 and CD4 T cells, mast cells, eosinophils, dendritic cells, epithelial cells, and fibroblasts6 and is transcribed and translated in human airways, where allergens stimulate bronchial mucosa.6,7 TARC and monocyte-derived chemokine (MDC)/CCL22 selectively attract the CCR4 receptor expressed in TH2 lymphocytes, mast cells, dendritic cells, and natural killer T lymphocytes to the inflammation site.8
Refractory Chronic Rhinosinusitis with Nasal Polyposis
2017, Otolaryngologic Clinics of North AmericaCitation Excerpt :In addition to TLRs, cytokines and cell signaling molecules play a large role in mediating innate and adaptive immunity. Interleukins have been shown to mediate CRS—specifically, IL-3, IL-5, IL-6, IL-8, and IL-13 are involved in the activation of eosinophils in nasal polyps.96–98 Staikuniene and colleagues8 suggested that eotaxin-3, a known indicator of eosinophil chemotaxis and activation, may be a driver of CRSwNP via recruitment of eosinophils,99 IL-25 and IL-33 have also been identified in CRSwNP.99
Methodologic issues in the measurement of interleukin-16 in clinical blood samples using immunoassays
2012, CytokineCitation Excerpt :The mechanism of release or secretion of C-IL-16, however, is currently unknown. The relevance of IL-16 in the pathogenesis of allergic diseases like asthma, several autoimmune diseases and HIV infection has been well demonstrated [11–16]. Sources of IL-16 include lymphocytes, monocytes, macrophages, dendritic cells, mast cells, epithelial cells and fibroblasts [17–19].
Interleukins, from 1 to 37, and interferon-γ: Receptors, functions, and roles in diseases
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Supported by the Medical Research Council of Canada.
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Sophie Laberge is a recipient of an MRC Scholarship, Canada. Qutayba Hamid is a Research Scholar of the Fonds de la Recherche en Santé du Québec.
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Reprint requests: Sophie Laberge, MD, Ste-Justine Hospital, 3175 Cote Ste-Catherine, Montreal, Quebec, H3T 1C5, Canada.