BACKGROUND: Gamma-delta (gammadelta) T cells regulate immune responses to foreign protein at mucosal surfaces. Whether they can modify allergen-induced early (EAR) and late airway responses (LAR) is unknown. OBJECTIVE: We have tested the hypothesis that the CD8+ subtype of gammadelta T cells decreases allergen-induced LAR and airway eosinophilia in the rat. METHODS: Brown Norway rats were administered, intraperitoneally, 3.5 x 10(4) lymph node CD8+gammadelta T cells from naive or sensitized rats. The recipients were sensitized to ovalbumin (OVA) in Al(OH)(3) 3 days after cell transfer and challenged with aerosolized OVA 14 days later. Serum IgE was measured before allergen challenge. After challenge, lung resistance was monitored for 8 hours and then bronchoalveolar lavage (BAL) was analyzed for eosinophil major basic protein (MBP), IL-4, IL-5, IL-13, and IFN-gamma messenger RNA-expressing cells. RESULTS: gammadelta T cells from naive donors significantly decreased LAR in OVA-challenged sensitized rats, whereas MBP(+) eosinophils were decreased by both gammadelta T cells from naive and sensitized donors. EAR and serum IgE levels were unchanged. The expression of IL-4, IL-5, and IL-13 by BAL cells of gammadelta T cell recipients was attenuated compared with OVA-challenged controls. This was accompanied by an increase in the expression of IFN-gamma. CONCLUSIONS: Our results are consistent with a suppressive role of CD8+gammadelta T cells on allergic airway responses. However, only gammadelta T cells from naive donors inhibit LAR.
BACKGROUND: The factors underlying recent increases in the prevalence of respiratory allergy are largely unknown. OBJECTIVE: To assess the association between allergic sensitization and several lifestyle/environmental factors. METHODS: A cross-sectional population-based study of 15-69-year-olds in Copenhagen was carried out in 1990. The participation rate was 77.5% (1112/1435). Different lifestyle/environmental factors (explanatory variables) were defined based on questionnaire data. Dependent (outcome) variables were skin prick test (SPT) positivity or specific IgE positivity to common aeroallergens. Explanatory variables associated with outcome in univariate analysis (P
Out of 16 workers in a trout processing industry, ten experienced work-related cough, dyspnoea, and nasal secretion. A clinical examination was performed including specific IgE, precipitating antibodies IgG for trout and processing water, skin prick testing and peak flow monitoring. A total of four workers showed a positive allergic reaction. Processing water contained endotoxin and bacteria in high amounts. It is concluded, that work-related respiratory symptoms should be investigated and the cause at the workplace identified, so that preventive measures can be introduced.
BACKGROUND: Skin prick tests of native spices (commercial powdered spices) are common in patients with allergy to birch or mugwort pollen. Clinical symptoms from spices are infrequent but occasionally severe. OBJECTIVE: To compare the skin prick test results with native spices and spice extracts and to determine the clinical relevance of test material. METHODS: Skin prick tests with the native spices coriander, caraway, paprika, cayenne, mustard, and white pepper were made twice at 2-month to 2.9-year intervals in 49 patients. During the latter time, tests were also made with spice extracts and spice-specific serum IgE was measured. RESULTS: The reproducibility of skin test results with native spices was 67% to 100%. Spice extracts, except white pepper, elicited positive skin test reactions in half those with positive reactions to native spices. Higher specific IgE concentrations (> or = 3.5 PRU/mL) were seen in cases where the skin tests were positive to the corresponding spices with 5% extracts of > 8 kD Mw. Three-fourths of the patients with positive skin tests to native spices were positive to birch pollen and one-half to a vegetable. Mild clinical symptoms from spices were reported by one-third. CONCLUSIONS: Spice allergens partly crossreact with those of pollens and vegetables. A minority of spice allergens may give clinical symptoms. The > 8-kD 5% extracts may be relevant skin prick test materials for identifying patients at risk of developing severe symptoms from ingested spices.
Exposure to various xenobiotics, including oxidant gases, diesel exhaust, and certain pesticides, has been reported to exacerbate pulmonary allergic hypersensitivity responses. Increased lymphocyte proliferative responses to parasite antigens or increased antibody responses to sheep erythrocyte have also been reported in rats exposed to TCDD before infection or immunization. As a result, these studies were conducted to test the hypothesis that TCDD exposure exacerbates the allergic response to house dust mite antigen. Brown Norway rats were injected, ip, with 0, 1, 10, or 30 microg TCDD/kg 7 days before intratracheal (it) sensitization to semipurified house dust mite allergen (HDM). Fourteen days later, rats were challenged with HDM and immediate bronchospasm was measured. At this time point, plus 2 and 7 days later, inflammatory cells in bronchoalveolar lavage fluid (BALF), HDM-specific IgE levels in serum, and HDM-driven cell proliferation in bronchial lymph nodes and spleen were evaluated. TCDD exposure decreased both immediate bronchoconstriction and specific IgE synthesis after the HDM challenge; 7 days later, HDM-specific IgE responses remained suppressed. Total serum IgE levels were similar in all groups. HDM challenge alone significantly increased cellular and biochemical indicators of lung injury, both of which were suppressed by TCDD exposure. The proliferative response of lymph node cells, but not of spleen cells, to HDM was also suppressed at the highest TCDD dose, although the splenic response to Concanavalin A was elevated. It appears that early events in the response to HDM are affected by TCDD exposure, since message for IL5 was dramatically reduced 2 days after sensitization, but not after challenge. We therefore conclude that TCDD exposure suppressed, rather than enhanced the development of allergic immune responses and the expression of immune-mediated lung disease.