Changes in interleukin-1 and tumor necrosis factor production by peripheral blood monocytes after specific bronchoprovocation test in occupational asthma.

The pathogenetic mechanisms of occupational asthma (OA) due to low-molecular-weight compounds have been poorly defined, and further studies are required to clarify the role of immunologic mechanisms in OA. Until now cellular mechanisms have been less investigated than humoral ones. We have evaluated interleukin-1 (IL-1) and tumor necrosis factor (TNF) production by peripheral blood monocytes (PBM), and peripheral T-cell subpopulations in 22 subjects with possible OA before and after specific bronchoprovocation test (SBPT). After SBPT, three subjects had an immediate reaction, seven a late reaction, and two a dual reaction. Ten subjects had no asthmatic reaction to SBPT. Spontaneous release of IL-1 from PBM did not change significantly after SBPT. TNF activity was increased 48 h after SBPT in immediate reactions and 72 h after SBPT in late-dual reactions. These results suggest that exposure to occupational agents may induce activation of PBM with increased spontaneous release of cytokines, such as TNF.

[Asthma caused by Lucilia Caesar larvae: clinical and immunologic study]. / L'asma da bigattini (larve della mosca carnaria): studio clinico e immunologico.

Lucilia Caesar larvae (LCL) are used as live fish bait by anglers. Five cases of asthma and rhinoconjunctivitis following exposure to LCL are reported. Three had work-related asthma as they were working on a fish bait farm or shop and two had asthma when they went fishing. In one subject exposure to LCL caused asthma, rhinoconjunctivitis and contact urticaria. In four subjects peak expiratory flow rate (PEFR) was monitored during exposure to LCL. In three out of four subjects there was evidence of LCL-related asthma. In one subject it was not possible to record PEFR during exposure to LCL, as he had not gone fishing since 1985. Two extracts of LCL were prepared: one was the PBS (phosphate-buffered saline) washing fluid of LCL, the other was the PBS extract of homogenized LCL. Positive cutaneous prick tests to both LCL extracts were detected in three out of four symptomatic subjects. Specific IgE against both LCL extract antigens were found by the RAST method in four out of five subjects with LCL-related asthma. One subject had both negative skin tests and RAST. Specificity and potency of LCL-IgE binding was shown by RAST inhibition method performed on the serum pool of four patients with positive RAST results. Significant inhibition of more than 50% by LCL washing fluid at a dilution extract was found at a dilution of 1:10 and by homogenized LCL extract at a dilution of 1:100. No significant inhibition of LCL-IgE binding by dermatophagoides, parietaria and milk antigens was found. This study demonstrated that LCL emanations are potent sensitizers and elicit IgE-mediated asthma.