Article

Conjunctival mast cell as a mediator of eosinophilic response in ocular allergy.

Division of Ophthalmology and Visual Science, Faculty of Medicine, Tottori University, Yonago, Japan.
Molecular vision (Impact Factor: 1.99). 02/2008; 14:1525-32.
Source: PubMed

ABSTRACT To determine the contribution of conjunctival mast cells to the allergen-specific inflammatory responses in eyes with allergic conjunctivitis and to test the hypothesis that mast cells act as mediators of the early phase response.
The participation of mast cells in allergen-induced inflammatory cell recruitment was studied in an experimental murine model of allergic conjunctivitis. Experimental allergic conjunctivitis was induced by a single or multiple sensitizing injections of an allergen. The conjunctiva of allergen-sensitized, mast cell-deficient (Kit(w)/Kit(w-v)) mice were reconstituted with conjunctival mast cells isolated from naïve wild type mice by subconjunctival transfer. Kit(w)/Kit(w-v) mice and conjunctival mast cell reconstituted Kit(w)/Kit(w-v) mice were evaluated for early phase reactions and late phase inflammatory responses.
The early phase response was minimal in Kit(w)/Kit(w-v) mice after both a single injection and multiple sensitization injections of the allergen. The early phase responses were fully restored following adoptive transfer of isolated conjunctival mast cells from naïve wild type mice. Eosinophilic inflammatory responses were significantly depressed in Kit(w)/Kit(w-v) mice without the impairment of allergen-specific priming. Reconstitution of the conjunctiva of Kit(w)/Kit(w-v) mice with mast cells from wild type mice fully restored the allergen-specific eosinophilic responses but not the neutrophilic responses.
Our data indicate that conjunctival mast cells are essential for eosinophilic inflammation but not for neutrophilia in allergic conjunctivitis that is mediated by mast cell activation.

0 Bookmarks
 · 
102 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Introduction: Allergic conjunctivitis (AC) is a very common disease, especially in association with allergic rhinitis but may also occur in isolated presentation. The treatment of AC has long been based on antihistamines, cromones and topical corticosteroids, but none of these drugs completely abolishes the clinical expression of AC. Areas covered: The development of new drugs for AC is analyzed highlighting the recent insights into the pathophysiological mechanisms of the disease. The major aim of development of drugs for AC is to have agents able to prevent the inflammatory effects of the interaction between the allergen and the specific IgE antibodies on mast cell surface. This may be obtained by blocking the effects of histamine (the main mediator of early allergic response) by H1-receptor antagonists, inhibiting the release of soluble factors able to recruit inflammatory cells (that sustain prolonged inflammation) by mast-cell stabilizers, inhibiting the effects of single mediators, inducing tolerance to the allergen by specific immunotherapy or even acting on factors related to activation and differentiation of T lymphocytes such as the toll-like receptors. Expert opinion: AC is an underestimated disease for which there is a search of more effective treatments. The availability of the drugs under current evaluation will allow more refined therapeutic strategies to apply according to the characteristics and the clinical severity of AC.
    Expert Opinion on Emerging Drugs 03/2014; · 2.48 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Allergy is defined as an immediate hypersensitivity type I immunological disease, which can be IgE or non-IgE driven, and in the latter case may be antibody or cell mediated. Atopy is a term used to describe individuals with a genetic predisposition for developing IgE-mediated allergic disease. But more recently, it has become evident that IgE-mediated disease can occur in non-atopic subjects. While it is now generally accepted that mucosal local IgE has a role in the expression of atopic allergic disease, the concept of 'local allergy' in non-atopic subjects has been proposed, with the term 'entopy' given to this condition. Although there is increasing evidence supporting this paradigm, entopy is only applicable to a proportion of non-atopic patients, suggesting that other disease mechanisms exist to explain non-atopic disease. This review considers the evidence for local mucosal allergy in atopic and non-atopic individuals with an emphasis on diseases affecting the upper airways and eye. Furthermore, the diagnosis, treatment and relationship between local allergy and conventional (systemic) allergy are discussed, and alternative disease mechanisms predominantly involving antibodies or their sub-components (free light chain Igs) are postulated to explain the 'entopy' paradigm. This review is intended to provide an improved understanding of the mechanisms and causes of local mucosal hypersensitivity.
    Clinical & Experimental Allergy 07/2010; 40(7):987-97. · 4.79 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: This study examines the histology of conjunctival biopsy samples from patients with persistent allergic eosinophilic conjunctivitis (AEC) or non-allergic eosinophilic conjunctivitis (NAEC). Fourteen patients with conjunctivitis and eosinophilia in cytology samples were included in the study. Seven had positive skin-prick tests (the AEC group) and seven had negative skin-prick tests (the NAEC group). Eight asymptomatic subjects with negative skin-prick tests served as a control group. In conjunctival biopsies eosinophils were identified with monoclonal antibodies. Mast cells were identified by specific immunostaining and tryptase-positive granules were counted around them. The percentage of degranulated mast cells was used as a measure of cell activation. Eosinophil and goblet cell numbers were counted, epithelial thickness was measured, and the symptoms were characterized and graded. The numbers of eosinophils in biopsies were higher in patients with AEC than in healthy controls (p = 0.010). The proportion of activated mast cells tended to be higher in AEC patients (65%) than in NAEC patients (48%) or control subjects (40%). Patients with AEC had more goblet cells than control subjects (p = 0.049) and their epithelial layer was thicker (p = 0.054). Patients with AEC had more severe symptoms than control subjects (p = 0.0005), whereas the symptoms of NAEC patients did not differ statistically from those of controls (p = 0.065). Patients with NAEC were characterized by mild eosinophilic inflammation and only minor structural conjunctival changes. The condition seems to run a relatively mild but persistent clinical course.
    Acta ophthalmologica 11/2009; 88(2):245-50. · 2.44 Impact Factor

Full-text (2 Sources)

View
25 Downloads
Available from
May 21, 2014