The Journal of allergy and clinical immunology
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J. Allergy Clin. Immunol. · Jun 2001
Anaphylaxis caused by the new ant, Pachycondyla chinensis: demonstration of specific IgE and IgE-binding components.
There have been no reports dealing with the pathogenic mechanism and IgE-binding components in patients with anaphylaxis caused by a sting from Pachycondyla chinensis. ⋯ IgE-mediated reactions contributed to the development of P chinensis -induced anaphylaxis. Eight IgE-binding components and one major allergen (12 kd) were identified. Further studies will be needed to clarify the role of sIgG4 and to identify allergenic relationships with major bee and wasp allergens.
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J. Allergy Clin. Immunol. · Jun 2001
Natural rubber pharmaceutical vial closures release latex allergens that produce skin reactions.
The release of allergenic proteins from natural rubber vial closures (stoppers) into aqueous pharmaceuticals may induce allergic reactions in individuals with latex allergy (LA) receiving medications from such vials. ⋯ Natural rubber vial closures released allergenic latex proteins into the tested solutions in direct contact during storage in sufficient quantities to elicit positive intradermal skin reactions in some individuals with LA. These data support a recommendation to eliminate natural rubber from closures of pharmaceutical vials.
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J. Allergy Clin. Immunol. · Jun 2001
Changes in sputum cell counts after exposure to occupational agents: what do they mean?
Exposure to occupational agents can induce eosinophilic inflammation in subjects with occupational asthma (OA). It might also induce nonspecific changes in airway inflammation in subjects without OA. ⋯ Exposure to occupational agents per se does not induce airway inflammation. Changes in both sputum eosinophil counts and methacholine responsiveness are satisfactory predictors of a significant bronchial responsiveness to occupational agents.
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J. Allergy Clin. Immunol. · Jun 2001
L-Selectin is required for the development of airway hyperresponsiveness but not airway inflammation in a murine model of asthma.
Airway inflammation and airway hyperresponsiveness (AHR) are fundamental features of asthma. Migration of inflammatory cells from the circulation into the lungs is dependent on adhesion molecule interactions. The cell surface adhesion molecule L-selectin has been demonstrated to mediate leukocyte rolling on inflamed and noninflamed pulmonary endothelium. However, its role in the development of airway inflammation and AHR in asthma has not been examined. ⋯ L-selectin plays a crucial role in the development of AHR but not allergic inflammation in an animal model of asthma. L-selectin represents a potential target for novel asthma therapies specifically aimed at controlling AHR.