Allergic mucosal inflammation

Allergic Mucosal Inflammation 64 7.1.4 Do Mast Cells Initiate ... 

C.H., Holgate, S.T. and Howarth, P.H. (1993). Immunolocalization of cytokines in the nasal mucosa of normal and perennial rhinitic subjects the mast cell as a source of IL-4, IL-5 and IL-6 in human allergic mucosal inflammation. J. Immunol. 151, 3853-3865. 

Plate I (a) Visualization of normai human bronchus by fibreoptic bronchoscopy, (b) Corresponding image from a patient with miid allergic asthma showing evidence of mucosal inflammation after initiation of a iocai response... 

Mucosal biopsy specimens from patients with asthma contain lymphocytes, many of which express surface markers of inflammation. There are two types of T-helper CD4-F cells. Type 1 T-helper (Thl) cells produce IL-2 and interferon-y (IFN-y), both essential for cellular defense mechanisms. Th2 cells produce cytokines (IL-4, -5, -6, -9, and -13) that mediate allergic inflammation. It is known that Thl cytokines inhibit the production of Th2 cytokines, and vice versa. It is hypothesized that allergic asthmatic inflammation results from a Th2-mediated mechanism (an imbalance between Thl and Th2 cells). ... 

Inflammatory influences. Inflammation (p. 1211), which usually accompanies infection and can also arise from allergic responses, is affected by many substances.2293-6 These include chemotactic factors that attract neutrophils and monocytes2220 2294 and the adhesion molecules that assist in the movement of lymphocytes. 229e/f Some epithelial tissues, such as the mucosal surfaces of the gastrointestinal tract, are maintained in a continuous very low level of inflammation. This reflects the balance between activation of the immune system and inhibition of the system by signals from microorganisms both pathogenic and commensal 229 h... 

Winkler B, Baier B, Wagner S, Repa A, Scheiner O, Kraft D, Wiedermann U Mucosal tolerance as therapy of type I allergy Intranasal application of recombinant Bet v 1, the major birch pollen allergen, leads to the suppression of allergic immune responses and airway inflammation in sensitized mice. Clin Exp Allergy 2002 32 30-36. 

IgE has the lowest percentage of total Ig at only 0.002 %, and the serum concentration approximates only 0.00002 mg/mL. This isotype is derived from adenoid tissue and then transported into the blood. In spite of its small quantities, IgE is very important in, and is responsible for, about 90% of allergic reactions. The impact of this immunoglobulin is to trigger the release of vasodilators for an inflammatory response, for example histamine. IgE may also protect external mucosal surfaces by promoting inflammation and enabling IgG, complement proteins and leucocytes to enter the tissue. 

Lymphocytes (T cells)—a group of white blood cells of crucial importance to the adaptive part of the organism s immune system. There are many kinds of lymphocytes (Th 0, Th c, Th 1, Th 2, Th 17). Cytokines produced by T cells probably play a major role in orchestrating allergic inflammation. TH 1 cells produce IFN-y and IL-2 but not IL-4 or IL-5 after activation. TH2 cells produce mainly IL-4, IL-13, and IL-5 but not IL-2 or IFN-y. TH2 cells characterize human allergic responses and are present at mucosal surfaces during the late but not immediate response to an allergen exposure. 

The mucosal inflammatory responses which accompany asthma, allergic inflammation and helminthic infestations are characterized by a marked and specific infiltration of eosinophils into the relevant mucosal surfeces. Of the cytokines secreted by activated T lymphocytes, IL-3, IL-5 and GM-CSF promote maturation, activation and prolonged survival of the eosinophil (Lopez etal., 1986 Rothenberg et al., 1988, 1989). 11 5 is unique in that, unlike IL-3 and GM-CSF, it acts specifically on... 

Thus, we demonstrated here in vivo that mucosal contact with SEB is capable of aggravating several features of bronchial allergic inflammation bronchial eosinophilic inflammation, IL-4, IL-5 and IFN-y levels in bronchi and systemic circulation, bronchial expression of eotaxin-1 and TGF-(3, and allergen-specific IgE titers [53], Not only bronchial but also nasal mucosal contact with SEB is capable of inducing a more severe bronchial allergic inflammation in sensitized mice. 

The infant immune system is not fnlly mature at birth it has deficits in the ability to prevent invasion of pathogens and to respond to antigens. Of particular concern in the context of ingredients new to infant formulas is the increased permeability of the gut mucosal barrier in the presence of inflammation or infection or if the integrity of the epithelial cell layer is disrupted. The increased permeability allows macromolecules to be absorbed, which stimulates allergic responses to food proteins. 

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