AIRWAY-LIKE INFLAMMATION OF MINOR SALIVARY-GLAND IN BRONCHIAL-ASTHMA

T-lymphocytes are important components of the inflammatory cell infilt rate in bronchial mucosa in asthma. Because activated lymphocytes migr ate through the thoracic duct and the general circulation to remote gl andular and mucosal sites, we initiated this study to evaluate the his tologic abnormalities of a minor salivary gland (MSG) associated with bronchial asthma. Fifty-eight asthmatic patients were prospectively st udied (37 women, 21 men; mean age, 54 +/- 6 yr). Twenty-nine patients had allergic asthma (AA) and 29 had nonallergic asthma (NAA). Results were compared with those obtained from 15 healthy control subjects and 15 nonasthmatic patients with chronic obstructive pulmonary disease ( COPD). MSG was normal in 14 of 15 patients with CORD and in 14 of 15 c ontrol subjects. Forty-three of 58 (74%) asthmatic patients presented MSG abnormalities. These were significantly more frequent in asthmatic s (74%) than in patients with COPD and healthy control subjects (6%, p < 0.001 versus asthmatics) and in NAA (97%) than in AA (52%, p < 0.01 ). The main pathologic features of MSG in asthma were T-lymphocyte inf iltration (57%: AA nine of 29; NAA 24 of 29), partly degranulated mast cells (64%: AA, 11 of 29; NAA, 26 of 29), basement membrane thickenin g (64%: AA, 11 of 29; NAA, 26 of 29), and endothelial cell changes (26 %: AA, one of 29; NAA, 14 of 29). Eosinophils were found only in two c ases. Expression of ICAM-1 was demonstrated in nine of 16 patients wit h NAA, whereas VCAM-1 and E-selectin were negative in all of them. ICA M-1, VCAM-1, and E-selectin were not expressed in AA, CORD, and contro ls. We did not find any significant association between MSG changes an d the severity of the disease. Our results demonstrate that except for eosinophil infiltration, which was not found in MSG, the glandular ti ssue of MSG in bronchial asthma might express an airway-like inflammat ion that might be due to the homing of specific lymphocytes.