Mast cells in the airway mucosa and rapid development of occupational asthma induced by toluene diisocyanate
- PMID: 8385428
- DOI: 10.1164/ajrccm/147.4.1005
Mast cells in the airway mucosa and rapid development of occupational asthma induced by toluene diisocyanate
Abstract
We examined lobar bronchial biopsies taken from 18 subjects with occupational asthma induced by toluene diisocyanate (TDI) and from nine nonasthmatic control subjects. Two groups of asthmatics were identified on the basis of the duration of exposure to TDI before the onset of symptoms of asthma. Group A (n = 8) developed asthma after 2.4 +/- 0.4 yr of exposure to TDI, and Group B (n = 10) developed asthma after 21.6 +/- 3.1 yr of exposure to TDI. Both groups of asthmatic subjects had increased numbers of inflammatory cells in the airway mucosa compared with subjects in the nonasthmatic control group. Comparison between Groups A and B showed that subjects who developed asthma after short-term exposure had a significantly increased number of mast cells both in epithelium and in lamina propria than did subjects who developed asthma after long-term exposure to TDI (p < 0.01). Interestingly, the numbers of mast cells both in the epithelium (rs = -0.52, p < 0.05) and in the lamina propria (rs = -0.81, p < 0.001) were inversely correlated with the length of exposure to TDI before the onset of asthma. In conclusion, subjects who develop asthma after short-term exposure to TDI have an increased number of mast cells in the airway mucosa, suggesting that these cells may be associated with individual susceptibility differences to offending agents.
Similar articles
-
Effect of cessation of exposure to toluene diisocyanate (TDI) on bronchial mucosa of subjects with TDI-induced asthma.Am Rev Respir Dis. 1992 Jan;145(1):169-74. doi: 10.1164/ajrccm/145.1.169. Am Rev Respir Dis. 1992. PMID: 1309964
-
Airway mucosal inflammation in occupational asthma induced by toluene diisocyanate.Am Rev Respir Dis. 1992 Jan;145(1):160-8. doi: 10.1164/ajrccm/145.1.160. Am Rev Respir Dis. 1992. PMID: 1309963
-
Expression of interleukin (IL)-4 and IL-5 proteins in asthma induced by toluene diisocyanate (TDI).Clin Exp Allergy. 1997 Nov;27(11):1292-8. Clin Exp Allergy. 1997. PMID: 9420133
-
Pathogenesis of late asthmatic reactions induced by exposure to isocyanates.Bull Eur Physiopathol Respir. 1987 Nov-Dec;23(6):583-6. Bull Eur Physiopathol Respir. 1987. PMID: 2840139 Review.
-
Late asthmatic reactions, airway inflammation and chronic asthma in TDI sensitized subjects.Eur Respir J Suppl. 1991 Apr;13:136s-138s. Eur Respir J Suppl. 1991. PMID: 1659425 Review.
Cited by
-
Airway inflammation in aluminium potroom asthma.Occup Environ Med. 2004 Sep;61(9):779-85. doi: 10.1136/oem.2003.011627. Occup Environ Med. 2004. PMID: 15317920 Free PMC article.
-
Histamine release and inflammatory cell infiltration in airway Mucosa in methylene diphenyl diisocyanate (MDI)-induced occupational asthma.J Clin Immunol. 2008 Sep;28(5):571-80. doi: 10.1007/s10875-008-9199-y. Epub 2008 May 17. J Clin Immunol. 2008. PMID: 18484168
-
Oxidized CaMKII promotes asthma through the activation of mast cells.JCI Insight. 2017 Jan 12;2(1):e90139. doi: 10.1172/jci.insight.90139. JCI Insight. 2017. PMID: 28097237 Free PMC article.
-
Mast cells in airway diseases and interstitial lung disease.Eur J Pharmacol. 2016 May 5;778:125-38. doi: 10.1016/j.ejphar.2015.04.046. Epub 2015 May 8. Eur J Pharmacol. 2016. PMID: 25959386 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical