Expression of Interleukin-16 in Allergic Rhinitis

Abstract

Background: Interleukin-16 (IL-16) has been characterized as a chemoattractant for a variety of CD4+ T cells. Several inflammatory diseases, including allergic disorders, have been reported to correlate with IL-16. We first examined the IL-16 expression of serum and mucosal tissue in patients with allergic rhinitis. Methods: Forty-eight patients with a clinical history of house dust mite (HDM) or pollen-sensitive allergic rhinitis were included in this study. Serum IL-16 was analyzed by enzyme-linked immunosorbent assay (ELISA). IL-16 expression of nasal mucosa was detected by immunohistochemistry. Results: IL-16 levels were elevated in the serum of patients with allergic rhinitis compared with normal controls. In particular, serum IL-16 levels in HDM-sensitive patients were higher than those in pollen-sensitive patients. IL-16 was significantly correlated with eosinophils in the peripheral blood of allergic rhinitis patients. Histologically, IL-16 was expressed in infiltrated lymphocytes and nasal gland cells. Conclusions: Our data indicate that one of the sources of elevated serum IL-16 in allergic patients may be gland cells and lymphocytes in allergic nasal mucosa. This IL-16 cytokine may be strongly associated with the developmental mechanism of allergic rhinitis.

IL-16 Variability and Modulation by Antiallergic Drugs in a Murine Experimental Allergic Rhinitis Model

“…Regarding eosinophils, IL-5 has been known as a main eosinophil chemoattractant factor, whereas it was reported that IL-16 neutralization suppressed eosinophilic chemotaxis by 60% in vitro[22], which indicates that IL-16 may also have a positive correlation with this matter. Our previous report confirmed that IL-16 serum level and local expressions in patients with allergic rhinitis were significantly correlated with the blood eosinophil percentage [13]. In addition, IL-16 can indirectly activate specific responses of eosinophils; in CD4-mediated cells, IL-16 elicits the extracellular release of RANTES and eotaxin, which then act in an autocrine fashion on CCR3 receptors to stimulate both enhanced leukotriene C 4 production and the release of IL-4 from within eosinophils [26].…”

“…Eosinophils and T cells are major IL-16 production sources in allergic disease [13, 27]; therefore, inhibition of their migration and activation induced by the drugs is one possible process. In the present study, both fexofenadine and ramatroban, which have antihistamine effects and anti-PGD2 or TxA2 effects, respectively, could inhibit IL-16; this suggested that IL-16 upregulation was induced through both histamine- and PGD2 (or TxA2)-mediated allergic pathways.…”

“…IL-16 has been much reported in allergic diseases, including atopic asthma and allergic rhinitis [12, 13]. IL-16 is upregulated in the bronchial mucosa and in bronchoalveolar lavage fluid after allergen challenge in atopic asthmatic patients or OVA-sensitized asthmatic model mice [3, 14].…”

“…IL-16 increases in the nasal mucosa of patients with seasonal allergic rhinitis during the pollen season or after allergen challenge, and topical steroid treatment inhibits IL-16 mRNA and protein expression in the nasal mucosa [12, 15]. Previously, we reported that IL-16 protein expression was increased in the serum and nasal mucosa of patients with perennial and seasonal allergic rhinitis when compared to healthy controls, and that the serum IL-16 level was significantly correlated with the blood eosinophil percentage [13]. These reports suggest that IL-16 is well related to the pathology of allergic rhinitis, but the detailed mechanisms remain largely unknown.…”

Correlation between serum IL-16 and atopic dermatitis

“…This IL-16 in turn recruits more eosinophils, capable of producing IL-4, to the sites of inflammation. This is believed to be one of the mechanisms underlying exacerbation of AD (Karaki et al, 2005). In acute and chronic AD lesions, the expression of IL-16 mRNA increases in epidermal keratinocytes and skin T lymphocytes.…”