Pavlovian Conditioning of Allergic Rhinitis in Humans
Alan J. Husband in Psychoimmunology CNS-Immune Interactions, 2019
The role of Pavlovian conditioning in humans with perennial allergic rhinitis was investigated using release of tryptase from sensitised mast cells as an indicator of allergic responsiveness. Two important animal studies have supported a role for the central nervous system in the expression of allergic reactions via classical Pavlovian conditioning procedures. In the first study, histamine was released in guinea pigs following a classical conditioning procedure where an odour in a contingent manner. In the second study, mast cell protease II was produced in rats after an audiovisual cue (CS) was paired with an immunological challenge. The implications of behavioural conditioning for both the understanding and treatment of human diseases involving mast cell degranulation are far-reaching. If conditioning of allergic rhinitis had been effected, it would be expected that re-exposure to the CS would result in elevated levels of tryptase and allergic symptoms in Group 1 relative to the control groups.
Percutaneous and Intracutaneous Diagnostic Tests of IgE- Mediated Diseases (Immediate Hypersensitivity)
Stephen F. Kemp, Richard F. Lockey in Diagnostic Testing of Allergic Disease, 2000
The fundamental application of skin testing is to detect mast cell-bound immunoglobulin (IgE) speci c for the allergen introduced in the skin (i.e., detection of sensitization). The allergy skin test in this context can be viewed as a human bioassay to detect cell-bound allergen-speci c IgE analogous to in vitro tests that detect circulating allergen-speci c IgE. In contrast to in vitro tests, cutaneous allergen-induced in ammation also re ects allergic disease in miniature. The immediate cutaneous in ammatory response occurs due to the release of mast cell in ammatory mediators triggered by binding of the allergen to mast cell-bound allergen-speci c IgE, thus mimicking the natural disease. Skin testing also can help to determine the clinical relevance of an allergen. It can indicate the likelihood that other organs, or the organism as a whole, will exhibit an allergic in ammatory response to the same or a cross-reacting allergen after a systemic, local, natural, or iatrogenic exposure.
Mast Cells, NGF and Neurobehavioural Regulations in Developing and Adult Mice
Alan J. Husband in Psychoimmunology CNS-Immune Interactions, 2019
Administration of Nerve growth factor (NGF) antibodies or sialoadenectomy before fighting session strongly inhibited Mast cell (MC) degranulation. MCs are elusive elements, up to mainly considered as specific releasers of histamine in the course of inflammation. The lack of MCs is found in brain tissues, where large numbers of MCs within central nervous system and MCs placed along blood vessels modulate the access of several mediators to the nervous system, thus regulating permeability of the neuromusculature. Morphological analysis of peritoneal MCs from fighting mice showed that they undergo a higher level of membrane disruption and loss of granule content than MCs from the peritoneal fluid of non-fighting controls. NGF antibodies administered to isolated mice before experiencing fighting blocked MC degranulation, thus suggesting that degranulation is specifically caused by a rise in the level of circulating NGF, and is not due to the action of other growth factors similarly stored and released from the salivary glands.
Mast Cell Alterations in Chronic Psoriasis Vulgaris: Response to Low-Strength Anthralin Treatment
Published in Upsala Journal of Medical Sciences, 1986
Mast cell degranulation (MCD) was studied in lesions of chronic psoriasis vulgaris before and during topical treatment with low-strength anthralin. Before the treatment, two forms (A and B) of mast cells with Type I MCD were distinguished in the lesions, in addition to mast cells showing Type II MCD. In Type I MCD, electron-dense mast cell granules in form A mast cells, and electron-dense mast cell granules and vacuoles containing granule matrix in form B mast cells, were released as intact structures by the mechanism of diacytosis. Distinct gaps of the mast cell plasma membranes were observed. Around blood vessels, beneath the epidermal-dermal junction and in the intercellular space of strata basale and spinosum, the mast cell granules appeared partly as intact structures and partly in more or less disintegrated form. In Type II MCD the granule matrix was released into the extracellular compartment by the mechanism of exocytosis. During treatment with low-strength anthralin, the mast cell changes underwent regression. In macular psoriasis only form A mast cells of Type I MCD were demonstrated, and the released intact mast cell granules were restricted to the immediate neighbourhood of the mast cells. There were no mast cell granules in the epidermis. At the sites with clinically complete clearance of psoriatic lesions, the mast cells displayed no degranulation but distinct gaps were still found in the mast cell plasma membranes. Low-strength anthralin's mode of action in psoriasis is suggested to involve regression of a series of systems, including prevention of mast cell degranulation, thereby inhibiting release of histamine, proteinase and other mast cell mediators sustaining the psoriatic process.
Direct Effects of Conjugated Linoleic Acid Isomers on P815 Mast Cells in vitro
Published in Immunological Investigations, 2012
Siddharth Krishnan, Joshua Russell, MaryLou Bodziak, Stephen Koury, Patricia Masso-Welch
Conjugated linoleic acid (CLA) is a dietary fatty acid which causes extensive remodeling and mast cell recruitment in the mouse mammary gland. Two CLA isomers, 9,11- and 10,12-CLA, have differing effects in vivo, with only 10,12-CLA increasing mast cell number. The purpose of this project is to test the hypothesis that CLA acts directly on the mast cell. The P815 mastocytoma cell line was assayed for the effects of CLA on mast cell number, proliferation, apoptosis, and differentiation. Both CLA isomers decreased viable mast cell number, with no effect on membrane integrity, or cell cycle distribution. 10,12-CLA induced an increase in apoptosis, assessed by Annexin-FITC binding. Both isomers increased mast cell granularity, and secretion of MMP-9. The complex effects of CLA isomers on mast cells in the mammary gland are distinct from direct effects on mast cells in vitro, and may require interactions between multiple cell types present in vivo.
Ionizing radiation induces degranulation of human mast cells and release of tryptase
Published in International Journal of Radiation Biology, 2007
Martin Albrecht, Kerstin Müller, Frank M. Köhn, Viktor Meineke, Artur Mayerhofer
Purpose: Skin fibrosis is a hallmark of ionizing radiation-induced tissue injury and we hypothesized that mast cells via their products (especially tryptase) are involved in this event. We therefore investigated whether: (i) irradiation with 5 Gray (Gy) is able to induce the release of the typical mast cell mediator tryptase from human mast cells (HMC-1) in vitro, (ii) this effect can be influenced by application of clinically relevant mast cell blockers, and (iii) irradiation leads to mast cell degranulation in ex vivo skin culture models. Materials and methods: The human mast cell line (HMC)-1, as well as ex vivo skin tissue served as experimental models. Fluorescence activated cell sorting (FACS), Enzyme linked immunosorbent assays (ELISA), mast cell degranulation assays and immunohistochemistry were applied. Results: Ionizing radiation induces a time-dependent, statistically significant increase in the release of tryptase by HMC-1 cultured in vitro. Mast cell degranulation and secretion of tryptase was partially, but not significantly, inhibited by pre-incubation with the histamine-1 receptor (H1) blocker cetirizine. Mast cell degranulation was also clearly evident after irradiation using an ex vivo skin culture model of mastocytoma tissue. Conclusions: We propose that ionizing radiation leads to a degranulation of dermal mast cells, an event which is accompanied by the release of tryptase.
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