1,212 research outputs found
Human leukocyte antigen associations in occupational asthma induced by isocyanates.
No full textExposure to diisocyanates is recognized as a leading cause of occupational asthma. Occupational asthma induced by isocyanates shares many characteristics with immunoglobulin E (IgE)-mediated asthma: in both, the responsible agent is known, and the clinical presentation, response to inhalation challenge in the laboratory, and response to antiasthma drugs are similar. Although asthma mediated by an IgE mechanism occurs in atopic subjects, occupational asthma induced by isocyanates occurs mostly in nonatopic asthmatics, and an IgE-mediated mechanism has not been consistently demonstrated. However, activated T lymphocytes, methacromatic cells, and eosinophils are increased in the bronchial mucosa of allergic and nonallergic asthmatics and subjects with occupational asthma induced by isocyanates, suggesting similar, probably immunologically mediated mechanisms for both nonoccupational and occupational asthma. Occupational asthma occurs in up to 5-10% of the exposed subjects. Evaluation of major histocompatibility complex (MHC) class II genes in exposed subjects who develop toluene diisocyanate (TDI) asthma has shown a negative association with HLA-DQB1*0501 and a positive association with HLA-DQB1*0503 alleles. In addition, a high proportion of TDI asthmatics express the HLA-DQB1*0503-associated aspartic acid at residue 57, suggesting that HLA-DQ may have a key role in conferring susceptibility. Thus, asthma induced by the low-molecular-weight agent TDI may result from an immunologic reaction due to the interaction of genetic susceptibility with exposure in the workplace. Mapp CE, Balboni A, Baricordi R, Fabbri LM. Human leukocyte antigen associations in occupational asthma induced by isocyanates
The role of genetic factors in occupational asthma
No full textThis article explores the influence of genetic factors on the development of sensitisation and occupational asthma (OA). First, several types of studies aimed at examining the role of genes, as well as the role of gene-environment interactions in asthma, including the available data for OA specifically, were reviewed. Genetic approaches include linkage and allele-sharing analysis and segregation analysis. Secondly, deoxyribonucleic acid banking for epidemiological studies was focused upon, highlighting the factors to be considered in choosing the appropriate specimens for genotyping. OA, like asthma, is a multifactorial condition and, to date, no ideal genetic study has been described to examine complex gene-environment interactions. Most studies in OA have examined human leukocyte antigen-associated polymorphisms with some nonreproducible results. The search for genes in occupational asthma is still in progress, and much of the information obtained has been based on small sample sizes, using different strategies for the recruitment of subjects. The best methodological approach still needs to be determined and the results of genetic identification need to be confirmed in different samples
Late asthmatic reactions, airway inflammation and chronic asthma in TDI sensitized subjects.
No full textSensitized subjects may develop symptoms of asthma after exposure to isocyanates in their place of work. After challenge with isocyanates in the laboratory, sensitized subjects develop immediate, late and dual asthmatic reactions. We speculated that toluene diisocyanate (TDI) might cause late asthmatic reactions and increase bronchial responsiveness by causing an acute inflammatory reaction in the airways, and that airway inflammation may be responsible for persistence of occupational asthma induced by isocyanates. To test these hypotheses, we examined sensitized subjects during asthmatic reactions induced by exposure to toluene diisocyanate in the laboratory. We observed that late and dual, but not early, asthmatic reactions are associated with a transient increase of bronchial responsiveness which is associated with an acute inflammatory reaction of the airways characterized by an increase of neutrophils followed by eosinophils, by an increase of leukotriene B4 and albumin in bronchoalveolar lavage fluid, and that all these effects are inhibited by steroids. Longitudinal studies suggest that the majority of subjects with occupational asthma continue to have persistent asthma months and years after the cessation of exposure, and the results of our studies combined with the results of studies performed by others suggest that the persistence of asthma may be related to the persistence of airway inflammation
Prostacyclin activates tachykinin release from capsaicin-sensitive afferents in guinea-pig bronchi through a ruthenium red-sensitive pathway.
No full text1. We have investigated the ability of prostacyclin (PGI2) to contract guinea-pig isolated bronchi and the possible involvement of capsaicin-sensitive primary afferents in the response to PGI2. 2. PGI2 (0.1-100 microM) produced concentration-dependent contractions of the guinea-pig isolated bronchi. In vitro capsaicin desensitization (10 microM for 30 min followed by washing) significantly reduced the PGI2-induced contraction at all concentrations tested. A capsaicin-resistant component of contraction (40-60% of the overall response) was also evident. 3. Ruthenium red (3 microM), an inorganic dye which acts as a selective functional antagonist of capsaicin, significantly decreased PGI2-induced contractions, without affecting the response to substance P, neurokinin A or acetylcholine. 4. MEN 10, 207, (Tyr5, D-Trp6,8,9, Arg10)-neurokinin A (4-10) (3 microM), a selective antagonist of NK2-tachykinin receptors, significantly decreased PGI2-induced contractions and neurokinin A-induced contractions, without affecting the response to acetylcholine. 5. The effect of ruthenium red and MEN 10,207 on the one hand, and that of ruthenium red and capsaicin on the other was non additive. 6. These results indicate that PGI2-induced contraction of the guinea-pig isolated bronchi involves two distinct mechanisms, one of which involves transmitter (tachykinins) release from peripheral endings of capsaicin-sensitive primary afferents. In as much as PGI2-activation of primary afferents is sensitive to ruthenium red, we suggest that PGI2 shares a common mechanism of tachykinin release with that activated by capsaicin
Epidemiologia della bissinosi: problemi inerenti l'uso del questionario e delle prove funzionali respiratorie
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