Abstract

This study aims to determine whether the combined blockade of IL-1β and TNF-α can alleviate the pathological allergic inflammatory reaction in the nasal mucosa and lung tissues in allergic rhinitis (AR) guinea pigs. Healthy guinea pigs treated with saline were used as the healthy controls. The AR guinea pigs were randomly divided into (1) the AR model group treated with intranasal saline; (2) the 0.1% nonspecific IgY treatment group; (3) the 0.1% anti-TNF-α IgY treatment group; (4) the 0.1% anti-IL-1β IgY treatment group; (5) the 0.1% combined anti-IL-1β and TNF-α IgY treatment group; and (6) the fluticasone propionate treatment group. The inflammatory cells were evaluated using Wright's staining. Histopathology was examined using hematoxylin-eosin staining. The results showed that the number of eosinophils was significantly decreased in the peripheral blood, nasal lavage fluid, and bronchoalveolar lavage fluid (P < 0.05), and eosinophil, neutrophil, and lymphocyte infiltration and edema were significantly reduced or absent in the nasal mucosa and lung tissues (P < 0.05) in the combined 0.1% anti-IL-1β- and TNF-α IgY-treated guinea pigs. The data suggest that topical blockade of IL-1β and TNF-α could reduce pathological allergic inflammation in the nasal mucosa and lung tissues in AR guinea pigs.

Highlights

  • Allergic rhinitis (AR) is an IgE-mediated type I hypersensitivity inflammatory disease of the nasal mucosa

  • Our previous study demonstrated that proinflammatory cytokines (IL-1β, TNF-α, IL-18, IL-22, and IL-33), T helper 2 (Th2) cytokines (IL-5, IL-9, and IL-13), TGF-β1, and OVA-specific IgE levels in the peripheral blood (PB) and nasal lavage fluid (NLF) were significantly decreased by an intranasal instillation of 0.1% combined anti-IL-1β and antiTNF-α IgY antibodies in ovalbumin- (OVA-) induced AR guinea pigs [1]

  • We aim to determine whether the combined blockade of IL-1β and TNF-α can alleviate pathological allergic inflammatory reactions and reduce inflammatory cell infiltration in the nasal mucosa and lung tissues in OVA-induced AR guinea pigs. These results demonstrate that combined anti-IL-1β and TNF-α IgY antibodies block IL-1β and TNF-α inflammatory cytokines and that this action is a mechanism for the treatment of allergic rhinitis

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Summary

Introduction

Allergic rhinitis (AR) is an IgE-mediated type I hypersensitivity inflammatory disease of the nasal mucosa. IgE bound to FcεRI on mast cells and eosinophils is cross-linked by allergens, resulting in the release of diverse preformed and newly synthesized mediators to promote the local recruitment and activation of leukocytes and the production of inflammatory cytokines and T helper 2 (Th2) cytokines, which contribute to the development of late-phase reactions (2 h to 24 h after exposure to an allergen). Eosinophil infiltration in the nasal mucosa was increased in AR guinea pigs [2] and mice [3]. The total number of inflammatory cells, primarily eosinophils, in the bronchoalveolar lavage fluid (BALF) and pulmonary tissues was increased in OVA-sensitized guinea pigs [4] and rats [5]. Inhibition of proinflammatory cytokines is Mediators of Inflammation effective for controlling and alleviating allergic inflammation because proinflammatory cytokines precede Th2 cytokines in the pathological response [4]

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