Reports on allergies findings from University of London, Imperial College provide new insights
2007 NOV 21 -- "Subjects with allergic asthma develop isolated late asthmatic reactions after inhalation of allergen-derived T cell peptides. Animal experiments have shown that airway hyperresponsiveness (AHR) is CD4+ cell-dependent," scientists in London, the United Kingdom report. "It is hypothesised that peptide inhalation produces increases in non-specific AHR and a T cell-dominant bronchial mucosal inflammatory response Bronchoscopy, with bronchial biopsies and bronchoalveolar lavage (BAL), was performed in 24 subjects with cat allergy 6 h after aerosol inhalation of short overlapping peptides derived from Fel d 1, the major cat allergen. Biopsy specimens and BAL fluid were studied using immunohistochemistry and ELISA Twelve of the 24 subjects developed an isolated late asthmatic reaction without a preceding early ( mast cell/histamine-dependent) reaction characteristic of whole allergen inhalation. These responders had significant between-group differences ( responders vs non-responders) in the changes ( peptide vs diluent) in AHR ( p = 0.007) and bronchial mucosal CD3+ ( p = 0.005), CD4+ ( p = 0.006) and thymus- and activation-regulated chemokine ( TARC)+ ( p = 0.003) but not CD8+ or CD25+ cells or eosinophils, basophils, mast cells and macrophages. The between- group difference for neutrophils was p = 0.05 but with a non- significant within- group value ( peptide vs diluent, responders, p = 0.11). In BAL fluid there was a significant betweengroup difference in TARC ( p = 0.02) but not in histamine, tryptase, basogranulin, C3a or C5a, leukotrienes C4/ D4/ E4, prostaglandins D2 or F2 alpha Direct activation of allergen- specific airway T cells by peptide inhalation in patients with atopic asthma leads to increased AHR with local increases in CD3+ and CD4+ cells and TARC but no significant changes in eosinophils or basophil/ mast cell products," wrote F.R. Ali and colleagues, University of London, Imperial College. The researchers concluded: "These findings support previous animal experiments which showed a CD4+ dependence for AHR." Ali and colleagues published their study in Thorax (Airway hyperresponsiveness and bronchial mucosal inflammation in T cell peptide-induced asthmatic reactions in atopic subjects. Thorax, 2007;62(9):749-756). For additional information, contact A.B. Kay, University of London Imperial College, Alexander Fleming Bldg, London SW7 2AZ, UK. The publisher's contact information for the journal Thorax is: B M J Publishing Group, British Med Association House, Tavistock Square, London WC1H 9JR, England. Keywords: United Kingdom, London, Allergen, Allergies, Allergy Medicine, University of London, Imperial College. This article was prepared by Immunotherapy Weekly editors from staff and other reports. Copyright 2007, Immunotherapy Weekly via NewsRx.com.
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