Background. This study was undertaken to investigate the qualitative and quantitative changes that interstitial dendritic cells (IDC) of the heart undergo during the time course of experimental myocardial infarction.Methods and Results. Left coronary arterial ligations were performed in 43 rats that were killed 2, 4, 7, 14, and 21 days after surgery. Thirteen unoperated and 39 sham-operated rats were used as controls.

We measured levels of cytokines and type III procollagen aminopeptides (procollagen III peptides) in bronchoalveolar lavage fluid obtained from 20 patients with stable pulmonary fibrosis (PF) and seven patients with progressive PF, and nine control subjects to determine the role of cytokines in the development of PF. Procollagen III peptide levels were markedly increased in progressive PF patients. Tumour necrosis factor-alpha, interleukin-6, transforming growth factor-beta and interferon-gamma (IFN-gamma) levels were elevated in both PF patients as compared with controls, with a tendency of higher levels in progressive patients, whereas interleukin-1 beta (IL-1 beta) level was decreased in both PF patients. When the correlation between procollagen III peptide and various cytokine levels was analysed the only significant correlation was inversely between procollagen III peptide and IFN-gamma in progressive PF patients. These results indicated that although multiple cytokines may be involved in the development of PF, the negative role of IFN-gamma in active collagen synthesis could be also important.

Although we cannot exclude the possibility of a direct toxic effect of IL-2 on myocytes, our observations suggest that the myocardial damage produced by this agent is triggered by IL-2-activated lymphocytes that exert cytolytic effects, first on endothelial cells and then on cardiac myocytes, thus producing lesions that involve both the cardiac microcirculation and the muscle cells.

) caused an increased number of neutrophils in liver and lung; VLS and parenchymal cell and endothelial damage were not found. The VLS and the cellular damage caused by the combination of IL-2 and IFN were much more severe than those produced by IL-2 alone. In animals treated with IL-2, IFN-α, and IL-1α, VLS was minimal and parenchymal and endothelial cell damage were less severe than after IL-2 alone or IL-2 plus IFN-α. Taken together, these observations show that IL-1α reduces ultrastructural changes produced by IL-2 and IFN-α. This reduction may be clinically useful in the treatment of neoplasms.