CYTOKINE MESSENGER-RNA EXPRESSION IN LUNG-TISSUE FROM TOXIC OIL SYNDROME PATIENTS - A TH2 IMMUNOLOGICAL MECHANISM

In 1981, an epidemic occurred in Spain, toxic oil syndrome (TOS), in p eople who consumed rapeseed oil denatured with 2% aniline, and it was one of the largest intoxication epidemics ever recorded. In 1989, a si milar disease, eosinophilia-myalgia syndrome (EMS) was reported in the USA and was associated with the ingestion of L-tryptophan. The pathol ogic findings in TOS showed primary endothelial injury, with cell prol iferation and perivascular inflammatory infiltrates. Immunologic mecha nisms have presumably been operative in the pathogenesis and perpetuat ion of TOS. Our previous findings pointed to a T-cell activation durin g acute phase of the disease. In order to analyze which T-cell subset is involved on TOS, we have developed an mRNA extraction procedure fro m paraffin-embedded lung tissues in patients with pulmonary involvemen t. We analyzed mRNA expression from different cytokines (IL-1, IL-2, I L-4, IL-5, IFN-gamma, GM-CSF) and CD25 (interleukin 2 receptor) and CD 23 (low affinity IgE receptor), using RT-PCR technique. In lung tissue s from these patients a T-cell activation was observed. We found a sig nificant increase in Th1 (P = 0.006) and Th2 (P = 0.003) cytokine prof ile in TOS patients with respect to controls. The increment in TH2 res ponse with respect to TH1 is significant (P = 0.03) in TOS lung specim ens. Non-significant differences were obtained in other cytokines and receptors studied as IL-1, CD25, CD23 and GM-CSF. Data presented in th is paper are the first clear evidence that an immunological mechanism is directly implicated in this illness. (C) 1997 Elsevier Science Irel and Ltd.