Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using an under agarose migration (UAM) assay, we studied lymphokine-activated killer (LAK)-attractant activity in cultured conditioned medium of tumour tissues after chemotherapy as a possible mechanism of enhanced LAK cell accumulation into tumour tissues after chemotherapy. BMT-11 is a fibrosarcoma developed in C57BL/6 mice. The conditioned medium of BMT-11 tumour tissues obtained from mice treated with various anti-cancer drugs had chemotactic activity for LAK cells (LAK-attractant activity). mRNA expression of interleukin (IL)-1 alpha, IL-6, IL-8, interferon (IFN)-gamma, and tumour necrosis factor (TNF)-alpha was observed in untreated tumour tissues, which were not enhanced by cyclophosphamide treatment. mRNA expression of TGF-beta 1 was not detected in untreated tumour tissues by reverse transcription-polymerase chain reaction (RT-PCR), but was detected in tumour tissues treated with cyclophosphamide. Recombinant human TGF-beta 1 showed LAK-attractant activity at a concentration of 0.1 ng ml-1 and 1 ng ml-1, whereas fresh splenocytes were not attracted by TGF-beta 1. Anti-TGF-beta 1 antibody inhibited LAK-attractant activity in the conditioned medium of tumour tissues treated with cyclophosphamide to approximately 35% that of control at 100 micrograms ml-1. These findings indicate that TGF-beta 1 produced in the tumour tissues of mice treated with anti-cancer drugs could be a LAK attractant. By a 4 h 51Cr release assay of natural killer cell-resistant BMT-11 tumour cells, we observed that TGF-beta 1 at a concentration from 0.01 ng ml-1 to 10 ng ml-1 did not inhibit LAK activity in an effector phase. Taken together, we suggest that TGF-beta 1 produced in tumour tissues after chemotherapy participates in gathering transferred LAK cells and contributes to the therapeutic effects of transferred LAK cells.
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PMID:Transforming growth factor beta 1 (TGF-beta 1) produced in tumour tissue after chemotherapy acts as a lymphokine-activated killer attractant. 868 35

Acute GVHD (aGVHD) is one of the major problems after allogeneic BMT. The diagnosis of aGVHD is difficult to establish, relying mainly on clinical evaluations and symptoms of aGVHD, often resembling those of organ toxicity, infection or drug rash. In 21 patients after BMT several serum cytokine levels (soluble interleukin-2 receptor (sIL-2R), sTNF-R, SCF, IL-6, IL-8, G-SCF and ICAM-1) were determined in order to evaluate their value as an indicator for aGVHD. The maximum levels of sIL-2R (and none of the other evaluated cytokines) correlated significantly (r = 0.8, P = 0.008) with the severity of aGVHD. We also found a significant correlation between the day of engraftment (neutrophil count >0.5 x 10(9)/l) and the severity of aGVHD (r = 0.5, P = 0.03): engraftment was earlier in patients without aGVHD (median of day 11) than in those with aGVHD (median of day 18). No correlation between sIL-2R and fever or organ toxicity could be found. Our data suggest that the sIL-2R level might be an indicator for aGVHD, reflecting the severity of the disease. In patients with late engraftment the risk of aGVHD seems to be increased, therefore these patients especially should be monitored closely, possibly using sIL-2R levels.
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PMID:Soluble interleukin-2 receptor serum levels after allogeneic bone marrow transplantations as a marker for GVHD. 948 91

Patients who receive a donor lymphocyte infusion (DLI) for the treatment of relapsed leukemia after allogeneic BMT (alloBMT) often developed GVHD. To determine whether cytokines might have a role in GVHD, an intensive kinetic analysis of in vivo cytokine gene expression was performed on PBMC from three such patients. Expression of IL-1beta, IL-2, IFN-gamma, IL-4, IL-5, IL-8, IL-10, IL-12, TNF-alpha, and IL-2Ralpha was examined using a sensitive semi-quantitative reverse transcription (RT)-PCR assay system. Six normal controls were also analyzed for comparison. Expression of type 1 T helper (Th1) cytokines, IL-2 and IFN-gamma was greatly increased in all three patients. In particular, the changes in IL-2 gene expression correlated well with disease progression, suggesting that IL-2 has a critical role in the development of GVHD. Although the pattern of type 2 T helper (Th2) cytokine gene expression differed in each patient, the expression of IL-4 was inversely related to expression of Th1 cytokines. These results suggest that Th1 dominates in the development of human clinical GVHD.
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PMID:Kinetic analysis of cytokine gene expression in patients with GVHD after donor lymphocyte infusion. 1131 66