Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among the cereals, wheat, rye, barley and oats, have been reported to cause protein contact dermatitis. However, in these cases neither the involvement of an immunological mechanism nor the role of specific protein(s) has been demonstrated. We present a case of protein contact dermatitis from corn. The patient presented with a Type I sensitization to corn, as shown by the presence of specific immunoglobulin (Ig)E and positivity to prick tests with both a flour suspension and the salt-soluble protein fraction of this cereal. The same corn preparations induced a strong urticarial reaction on scratch testing. This reaction was followed several days later by the appearance of erythema and then eczema at the site of application. When boiled, these preparations became inactive on both prick and scratch testing. Patch tests were negative in all cases. Immunoblotting performed with the patient's serum showed the presence of a unique IgE-binding protein band with a molecular weight of around 14 kDa, belonging to the salt-soluble corn protein fraction. Our results give the first clear evidence that cornflour can induce protein contact dermatitis. The IgE-binding 14-kDa protein has characteristics identical to those of the trypsin/alpha-amylase inhibitors from cereals.
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PMID:Contact urticaria and protein contact dermatitis from corn in a patient with serum IgE specific for a salt-soluble corn protein of low molecular weight. 1537 49

In mouse skin, sulfur mustard (SM) is a potent vesicant, damaging both the epidermis and the dermis. The extent of wounding is dependent on the dose of SM and the duration of exposure. Initial responses include erythema, pruritus, edema, and xerosis; this is followed by an accumulation of inflammatory leukocytes in the tissue, activation of mast cells, and the release of mediators, including proinflammatory cytokines and bioactive lipids. These proinflammatory mediators contribute to damaging the epidermis, hair follicles, and sebaceous glands and to disruption of the epidermal basement membrane. This can lead to separation of the epidermis from the dermis, resulting in a blister, which ruptures, leading to the formation of an eschar. The eschar stimulates the formation of a neoepidermis and wound repair and may result in persistent epidermal hyperplasia. Epidermal damage and repair is associated with upregulation of enzymes generating proinflammatory and pro-growth/pro-wound healing mediators, including cyclooxygenase-2, which generates prostanoids, inducible nitric oxide synthase, which generates nitric oxide, fibroblast growth factor receptor 2, and galectin-3. Characterization of the mediators regulating structural changes in the skin during SM-induced tissue damage and wound healing will aid in the development of therapeutic modalities to mitigate toxicity and stimulate tissue repair processes.
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PMID:Tissue injury and repair following cutaneous exposure of mice to sulfur mustard. 2737 23