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Biomedical subjects

J R de Sousa

Publications and source records attributed to J R de Sousa.

7 recordsLinked to original sources

Platelet aggregation in allergic reactions.

The platelet aggregation in the presence of 4 aggregation inducers was studied in 63 allergic patients, consisting of atopic and non-atopic asthmatics and aspirin-sensitive subjects, before and after inhalation tests or in vitro incubation with allergen. Basal platelet aggregation was decreased in 43% of the atopic patients for adrenaline and also in a smaller percentage for other agonists. A decreased aggregation was also observed in 3 out of 6 nonatopic patients and in aspirin-sensitive patients. In vivo or in vitro provocation tests decreased aggregation in some additional patients. These results point out to a compromise of platelets in allergic mechanisms.

Humans

Cellular interactions in asthma.

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.

Asthma

T cells, macrophages and platelets in asthma.

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.

Asthma

Platelet reactivity to "in vitro" allergen challenge in asthmatic patients.

Platelet involvement in inflammation and allergic states is now well documented. In fact, it has been suggested that platelets can be triggered by either activated cells as monocytes and macrophages or by allergen itself. This latter possibility is still a matter of controversy. In this study we analysed platelet "in vitro" response to allergen, by optical aggregation technique, in 25 asthmatic patients, being 20 atopic and 5 non atopic patients. Platelet aggregation response to epinephrine, ADP, collagen and arachidonic acid was studied in all patients. In addition, allergen was added to platelet rich plasma and platelet reactivity was recorded both before and after stimulations with collagen. Platelet aggregation studies confirmed and abnormality of ADP induced platelet aggregation, that exhibited great variability among patients. In most cases this defect was the only one found in asthmatic patients and it should be further analysed. Results also showed a nonspecific response to allergen when dissolved in glycerol. This was due to glycerol rather than to allergen, since lyophilized allergen did not affect platelets, and glycerol added to platelet rich plasma induced the same type of curve. So, allergen by itself does not imply platelet aggregation. Experiments with IgE did not provoke either platelet agglutination or platelet aggregation. Furthermore, previous incubation with allergen immediately before collagen induced aggregation did not significantly change platelet response. This study allows the conclusion that platelet reactivity to allergen contact must be an expression of multicellular cooperation rather than a direct effect on platelet IgE receptors stimulation.

Adenosine Diphosphate

Platelets and hypersensitivity.

Platelets are anucleated blood cells not exclusively committed to hemostasis. They participate in inflammation, tissue repair, the immune response and hypersensitivity. In this review, the role of platelets in hypersensitivity is summarized. In order to understand the profound implications of these cells, the authors introduce the involvement of platelets in inflammation and immune reactions. Both the pathophysiology and the biology of the interaction of platelets with other cells are then summarized. These interactions justify the actual knowledge about the possibilities for the involvement of platelets in clinical states of hypersensitivity. Furthermore, the participation of platelets in allergy is supported by biological and clinical evidence, including in vitro studies of platelet activity in hypersensitivity states, the demonstration of platelet killing and the response to parasite contact, as well as animal studies in which the response to immune aggression is dependent on platelet reactivity. However, the need for more complete and developed clinical studies is clearly stressed, as several therapeutic approaches can already be proposed for a better control of these processes.

Blood Platelets