Role of interleukin-8 in onset of the immune response in intravesical BCG General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Abstract In intravesical therapy for superficial bladder carcinoma urothelial cells may, through the production of cytokines, contribute to the bacillus Calmette-Gu~rin (BCG)-induced local immunological reaction and associated antitumor efficacy. The aim of this study was to investigate such a role for the neutrophil-attracting cytokine interleukin-8 (IL-8). The appearance of IL-8 in patients' urine after BCG therapy was compared with BCG-induced IL-6 and IL-2 and the stability of IL-8 in urine was tested. Compared to IL-6 and IL-2, a rapid induction of IL-8 was observed, occurring after the first BCG instillation. Urinary IL-8 was highly stable, even after 24 h incubation at 37°C. The IL-8 concentration after the first instillation seemed to be associated with subsequent development of an immune response. Consequently, IL-8 seems an attractive candidate for investigation of its prognostic value for a clinical response to BCG therapy.
1 The cardiovascular e ects by g 2 -melanocyte-stimulating hormone (g 2 -MSH) are probably not due to any of the well-known melanocortin subtype receptors. We hypothesize that the receptor for PheMet-Arg-Phe-amide (FMRFa) or Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-amide (neuropeptide FF; NPFFa), other Arg-Phe containing peptides, is the candidate receptor. Therefore, we studied various Arg-Phe containing peptides to compare their haemodynamic pro®le with that of g 2 -MSH(6 ± 12), the most potent fragment of g 2 -MSH. 2 Mean arterial pressure (MAP) and heart rate (HR) changes were measured in conscious rats after intravenous administration of g 2 -MSH related peptides. 3 Phe-Arg-Trp-Asp-Arg-Phe-Gly (g 2 -MSH(6 ± 12)), FMRFa, NPFFa, Met-enkephalin-Arg-Pheamide (MERFa), Arg-Phe-amide (RFa), acetyl-Phe-norLeu-Arg-Phe-amide (acFnLRFa) and desamino-Tyr-Phe-norLeu-Arg-Phe-amide (daYFnLRFa) caused a dose-dependent increase in MAP and HR. g 2 -MSH(6 ± 12) showed the most potent cardiovascular e ects (ED 50 =12 nmol kg 71 for DMAP; 7 nmol kg 71 for DHR), as compared to the other Arg-Phe containing peptides (ED 50 =177 ± 292 nmol kg 71 for DMAP; 130 ± 260 nmol kg 71 for DHR). 4 Peptides, which lack the C-terminal Arg-Phe sequence (Lys-Tyr-Val-Met-Gly-His-Phe-Arg-TrpAsp-Arg-Pro-Gly (g 2 -pro 11 -MSH), desamino-Tyr-Phe-norLeu-Arg-[L-1,2,3,4 tetrahydroisoquinoline-3-carboxylic acid]-amide (daYFnLR[TIC]a) and Met-enkephalin (ME)), were devoid of cardiovascular actions. 5 The results indicate that the baroreceptor re¯ex-mediated reduction of tonic sympathetic activity due to pressor e ects is inhibited by g 2 -MSH(6 ± 12) and that its cardiovascular e ects are dependent on the presence of a C-terminal Arg-Phe sequence. 6 It is suggested that the FMRFa/NPFFa receptor is the likely candidate receptor, involved in these cardiovascular e ects.
Autonomic neuropathy is a common and severe complication of diabetes mellitus that leads to dysfunction of the cardiovascular system. The reduced ability to finely regulate heart rate is attributed to an impairment of cardiac parasympathetic regulation, but it is not known whether this is due to parasympathetic neuropathy and/or direct cardiac impairments. Therefore, we recorded the electrocardiogram of streptozotocin-induced diabetic rats under basal conditions and during electrical stimulation of the vagus nerve. We used the neurotrophic agent Org 2766, an adrenocorticotropic hormone [ACTH]-(4-9) analogue, to investigate the involvement of a neurogenic component in the altered vagal control of heart rate. The R-R interval was increased and atrioventricular transmission time unchanged 1 week after diabetes induction and remained so until 20 weeks. Treatment with Org 2766 could not prevent the bradycardia. After bilateral vagotomy, both diabetic and non-diabetic rats had the same R-R and P-R interval. The response of the R-R interval to electrical stimulation of the right vagus nerve was impaired, and this impairment was not reversed by Org 2766 in diabetic rats. These results suggest that neurogenic factors are of little or no importance in the impaired parasympathetic control of heart rate seen in experimental diabetes.
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