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M L Carlos

Publications and source records attributed to M L Carlos.

5 recordsLinked to original sources
PubMed1998

Cells and cytokines in pollinosis.

Pollinosis is a spontaneous model of allergic disease self limited in time. In order to evaluate immune response during pollen exposition cellular populations CD2, CD4, CD8, CD19, CD22, CD23, CD28, CD29, CD45RA, CD45RO have been studied before, during and after pollen season by flux cytometry. Simultaneous assays of soluble CD23 and cytokines IL-2, IL-4 and IL-2 soluble receptor have been done by an ELISA method. A decrease of CD23 PBC was observed during pollen season maintained afterwards without significant changes in sol CD23. The level of CD45RO memory cells decreased during pollen season with an opposed pattern for CD45RA naive cells. PBC expressing integrin chain CD29 were also decreased during the peak of pollen season. These results show that allergen exposition triggers a turnover of CD45 PBC, a decrease of low affinity IgE receptor CD23 in PBC and a consumption or binding of cells presenting the CD29 integrin chain. Cellular mechanisms are deeply implied in the immune response to pollens and cellular changes can be used as allergic inflammation markers in pollinosis.

Allergens↗
PubMed1998

Immunotherapy and mast cell activation.

Tryptase is the more specific markers for mast cell activation and mediators release and can be used as an index of mast cell activation after challenge. Nasal provocation tests have been done in patients allergic to the pollen of Parietaria (pellitory wall) before and after specific systemic immunotherapy and tryptase release evaluated in nasal lavage fluid. After specific immunotherapy the concentration of tryptase in nasal lavage was significantly decreased to all the concentrations used in challenge and the peack of tryptase release was delayed. These results confirm that assays of tryptase in nasal fluid after nasal provocation are a reliable markers of mast cell activation. Immunotherapy with specific allergen decreases mast cell reactivity to the same allergen.

Allergens↗
PubMed1997

Nasal allergen challenge and mediators release.

Nasal allergen challenges, despite not reproducing exactly natural allergen exposure, are a very useful method to understand the complex cellular kinetics and cellular interactions that occur in allergic rhinitis. Cell-specific soluble mediator measurements can give useful diagnostic information. In this paper we present data concerning eosinophil cationic protein (ECP) and tryptase measurements after nasal allergen challenge.

Allergens↗
PubMedDate not supplied

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↗