1. High-dose systemic or intralesional steroids are the first-line pharmacological treatments for haemangioma. However, the mechanism of action of steroids is unknown. Using the in vitro model developed by us, the present study examined some of the effects of five commonly used glucocorticoids on haemangioma biopsies taken from two patients. 2. At 12 micro mol/L, triamcinolone and dexamethasone consistently exhibited capillary growth inhibition, whereas methylprednisolone displayed an inhibitory effect during the first 7 days of culture. At this concentration, inhibition of capillary growth was observed in betamethasone-treated cultures derived from one patient but not in those derived from the other. However, hydrocortisone had a negligible effect on capillary growth. 3. Transcription of various factors considered important for haemangioma development were studied by reverse transcription-polymerase chain reaction. Neither vascular endothelial growth factor nor fibroblast growth factor-2 played a vital role in steroid-induced inhibition of capillary growth. All glucocorticoids induced a marked decrease of interleukin (IL)-6 transcripts. 4. Capillary growth inhibition in cultures treated with all glucocorticoids, except triamcinolone, was associated with an increased transcription of clusterin/apolipoprotein J (clust/apoJ), an apoptotic gene. There was increased transcription of mitochondrial cytochrome (cyt) b in the inhibited cultures resulting from triamcinolone, dexamethasone or methylprednisolone treatment that was associated with capillary growth inhibition, suggesting an important role of mitochondria in glucocorticoid-induced regression of haemangioma. 5. Our results indicate that glucocorticoids may modulate haemangiogenesis via an upregulation of cyt b, clust/apoJ and/or IL-6. The variable effects of different glucocorticoids on one or more of these factors may explain the interindividual variation in the in vivo response of haemangioma to the steroids.
Heberden Society 203 products' in ankylosing spondylitis denotes complement consumption and may represent an altered immune response to a persistent antigen in this disease.
Background Mice with constitutive transgenic (tg) expression of interleukin‐4 (IL‐4) develop autoimmune‐type disorders resembling lupus nephritis. The kidneys show progressive glomerulosclerosis with immunoglobulin (Ig) and complement deposition. Methods This study investigated the role of renal IL‐4 expression and the relevance of glomerular Ig deposition in the pathogenesis of glomerulosclerosis in IL‐4tg mice. The mice were treated with either IL‐4 neutralizing antibody or the glucocorticoid methylprednisolone (MP). To further clarify whether the renal lesions were exclusively immune‐mediated, IL‐4tg mice were cross‐bred with δ chain deficient mice (δ MT‐/‐), which are unable to produce Igs. Results Glomeruli of anti‐IL‐4‐treated tg mice showed a normal structure with negligible Ig deposits. Similarly, in MP‐treated tg mice only trace amounts of glomerular Ig deposits could be detected, although in comparison with wt mice, increased mesangial collagen deposition was evident. Despite complete absence of renal Ig deposits, IL‐4tg/δMT‐/‐ mice developed progressive glomerulosclerosis with mesangial accumulation of collagen types I, IV and V. Renal IL‐4 expression was observed in both anti‐IL‐4‐ and MP‐treated IL‐4 tg mice, as well as in IL‐4tg/δMT‐/‐ mice. There was no statistically significant difference in the number of glomerular T cells and macrophages between the groups. Conclusions Our data demonstrate that in this model glomerulosclerosis developed independently of and prior to Ig deposition, and imply that the initial accumulation of glomerular extracellular matrix was due to renal IL‐4 expression.
The development of primary abdominal lymphoma is a recognized complication of gluten-sensiti ve enteropachy (GSE). ln five patients with GSE plus lympho ma, the distribution and function of peripheral blood lymphocytes were determined and compared with 13 patients with GSE witho ut lymphoma and with 28 normal control subjects. The percentage ofT cells was lower in patients with GSE and GSE wirh lymphoma than in controls, whereas patients with GSE plus lymphoma had a significantly increased number of peripheral blood B lymphocytes when compared with GSE patients o r controls. There was no difference in K cell accivicy or lymphocyte responses co micogens and antige ns between controls, GSE or GSE plus lymphoma patients. Prospective studies are needed in patients with GSE co investigate whether this fall in peripheral blood T cells and rise in B lymphocytes is a marker of concurrent lymphoma. Can J Gastroenterol 1988; 2(1):12,14
Background Mice with constitutive transgenic (tg) expression of interleukin‐4 (IL‐4) develop autoimmune‐type disorders resembling lupus nephritis. The kidneys show progressive glomerulosclerosis with immunoglobulin (Ig) and complement deposition. Methods This study investigated the role of renal IL‐4 expression and the relevance of glomerular Ig deposition in the pathogenesis of glomerulosclerosis in IL‐4tg mice. The mice were treated with either IL‐4 neutralizing antibody or the glucocorticoid methylprednisolone (MP). To further clarify whether the renal lesions were exclusively immune‐mediated, IL‐4tg mice were cross‐bred with δ chain deficient mice (δ MT‐/‐), which are unable to produce Igs. Results Glomeruli of anti‐IL‐4‐treated tg mice showed a normal structure with negligible Ig deposits. Similarly, in MP‐treated tg mice only trace amounts of glomerular Ig deposits could be detected, although in comparison with wt mice, increased mesangial collagen deposition was evident. Despite complete absence of renal Ig deposits, IL‐4tg/δMT‐/‐ mice developed progressive glomerulosclerosis with mesangial accumulation of collagen types I, IV and V. Renal IL‐4 expression was observed in both anti‐IL‐4‐ and MP‐treated IL‐4 tg mice, as well as in IL‐4tg/δMT‐/‐ mice. There was no statistically significant difference in the number of glomerular T cells and macrophages between the groups. Conclusions Our data demonstrate that in this model glomerulosclerosis developed independently of and prior to Ig deposition, and imply that the initial accumulation of glomerular extracellular matrix was due to renal IL‐4 expression.
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