Biomedical subjects
Publications and source records attributed to M H Simoes.
Immediate phase of asthma is induced by mast cells. Late phase asthmatic response is related to other cells such as, macrophages, lymphocytes, eosinophils, and could pass to chronicity and is usually associated with bronchial hyperreactivity. Pathological or functional studies of the different cells involved, could be done in peripheral blood, broncho-alveolar lavage, bronchial biopsies or nasal lavages.
The role of T cells, macrophages and platelets in asthma is discussed. Peripheric T cell populations are normal as well in atopic as in non atopic. Macrophages can release histamine releasing factors and PAF in presence of allergens. Platelets stimulated by contact with allergens or PAF decreased the aggregation pattern induced by common inducers. These data show that different cells can play a role in the inflammatory process in asthma.
Human Basophil Degranulation Test (HBDT) has been employed for the research of Histamine Releasing Factor (HRF) from macrophages in asthma. Macrophages have been obtained from broncho-alveolar lavages, incubated with specific allergens and the products of this stimulation added to HBDT preparations. The production of an active HRF has been observed only in macrophages from atopic patients. The effect of this HRF seems to be IgE dependent, the degranulation of human basophils being in general significant only for basophils of atopic patients.
Alveolar macrophages (AM) from control (n = 12) and atopic patients (n = 19, 12 without treatment, 4 treated with theophylline and 3 with theophylline and corticosteroid) were compared for their capacity to release mediators. AM were purified by 2 h adherence and challenged with either ubiquitous allergen, specific sensitizing allergens, anti-IgG or anti-IgE serum. The release of paf-acether, lyso paf-acether and beta-glucuronidase was measured. Paf-acether and its lyso derivative were assayed on washed rabbit platelets. Enzyme and mediator releases were obtained after specific allergenic or anti-IgE serum challenge of AM from untreated atopic patients. No release of paf-acether was detected from AM, from control or treated atopic patients after in vitro immunological challenge, whereas that of lyso paf-acether was greatly reduced in both treated groups. Release was obtained by immunological challenge of AM from control patients after passive sensitization with atopic serum. The release of mediators with bronchoconstriction activity by AM could represent an alternative causal pathway in human asthma.