International journal of immunopharmacology最新文献

{"title":"Flt3 ligand enhances the immunogenicity of a gag-based HIV-1 vaccine","authors":"Vladimir M Pisarev ,&nbsp;Prahlad Parajuli ,&nbsp;R.Lee Mosley ,&nbsp;Jennifer Sublet ,&nbsp;Linda Kelsey ,&nbsp;Prem S Sarin ,&nbsp;Daniel H Zimmerman ,&nbsp;M.Douglas Winship ,&nbsp;James E Talmadge","doi":"10.1016/S0192-0561(00)00048-5","DOIUrl":"10.1016/S0192-0561(00)00048-5","url":null,"abstract":"<div><p><span>Liposomes<span><span> and Flt3 ligand (Flt3L), a ligand for the fms-like tyrosine kinase receptor Flt3/ FLK2, can augment the immune response to an HIV </span>peptide vaccine<span>. The HGP-30 peptide used in these studies is a synthetic peptide that corresponds to a highly conserved region of HIV-1 p17 </span></span></span><em>gag</em><span> (amino acids 86–115). Mice were immunized with HGP-30 or HGP-30 conjugated to keyhole limpet hemocyanin<span> (KLH) and delayed-type hypersensitivity (DTH) responses, antibody (IgG) amount and antigen-specific proliferative responses by spleen cells<span> were used to monitor the immune response. Daily injections of Flt3L prior to HGP-30 administration enhanced significantly an antigen-specific lymphocyte proliferation response when compared with Flt3L, HGP-30 alone or HGP-30 containing liposomes. Intravenous administration of HGP-30 was superior to intramuscular (i.m.) immunization for the induction of DTH responses. The HGP-30/KLH containing liposomes enhanced both DTH and antibody responses, while liposomes containing HGP-30 peptide elicited only T cell responses. In these studies, either Flt3L or liposomes increased DTH responses compared with the i.m. injection of the HGP-30 vaccine alone.</span></span></span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 865-876"},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00048-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21916538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of thymulin on avian IL-2 receptor expression","authors":"Dhammi Chandratilleke,&nbsp;James A. Marsh","doi":"10.1016/S0192-0561(00)00051-5","DOIUrl":"10.1016/S0192-0561(00)00051-5","url":null,"abstract":"<div><p><span><span>The effect of thymulin on IL-2 receptor (IL-2R) expression by avian </span>splenocytes<span> was examined in the functionally hypothyroid sex-linked dwarf (SLD) and in normal euthyroid K strain chickens. Daily thymulin injections of 0, 0.05 and 5.0 ng/100 g body weight were given from hatching until 4 weeks of age. ConA-treated and non-stimulated splenocytes from these animals were analyzed by flow cytometry for their expression of IL-2Rα, CD4 and CD8 cell surface molecules. ConA activation increased the number of IL-2R+ cells within K strain more than in the SLD. Thymulin treatment increased the number of IL-2R+ cells in the SLD but had the opposite effect in K strain chickens. </span></span>Mitogen activation or thymulin treatment had little effect on the IL-2R density within small cell populations. In contrast, mitogen activation increased the density of IL-2R on larger cell populations in both K and SLD. IL-2R densities on non-stimulated larger cells decreased in the SLD after thymulin exposure. Thymulin treatment produced no effect on the mean IL-2R densities for large activated cells. ConA stimulation increased the number of CD4+ cells in both strains. The density of CD4 expression was modulated by both mitogen activation and thymulin treatment. ConA stimulation produced an increase in the number of CD8+ cells. The SLD had fewer CD8+ cells than did the K strain and thymulin treatment had little effect on this population in either strain. Mitogen stimulation increased the density of CD8 on CD8+ cells but again thymulin treatment had little effect. These results suggest that thymulin can modulate IL-2R expression on splenocytes and that this effect may be dependent upon the thyroidal status of the animal. Further, these data suggest that thymulin has a differential effect on the CD4 and CD8 T-cell subpopulations.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 887-896"},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00051-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21916540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NPC-14686, a novel anti-inflammatory agent, increased intracellular Ca2+ concentrations in MDCK renal tubular cells","authors":"Chung-Ren Jan ,&nbsp;Jue-Long Wang ,&nbsp;Kang-Ju Chou ,&nbsp;Jin-Shiung Cheng ,&nbsp;Kam-Chung Lee ,&nbsp;Li-Ling Tseng ,&nbsp;Shiou-Ping Wang ,&nbsp;Kwong-Yui Tang ,&nbsp;Jong-Khing Huang","doi":"10.1016/S0192-0561(00)00054-0","DOIUrl":"10.1016/S0192-0561(00)00054-0","url":null,"abstract":"<div><p>The effect of NPC-14686 (Fmoc-<span>l</span>-homophenylalanine), a novel anti-inflammatory agent on intracellular free Ca²⁺ concentrations ([Ca²⁺]_i) in Madin Darby canine kidney (MDCK) renal tubular cells, was investigated, using fura-2 as a Ca²⁺ dye. At concentrations between 10 and 200 μM NPC-14686 increased [Ca²⁺]_i concentration dependently. The [Ca²⁺]_i signal comprised an initial rise and a sustained phase. Ca²⁺ removal inhibited the Ca²⁺ signals by 90%. In Ca²⁺-free medium, pretreatment with 100 μM NPC-14686 nearly abolished the [Ca²⁺]_i<span> increase induced by 1 μM thapsigargin<span> (an endoplasmic reticulum Ca</span></span>²⁺ pump inhibitor) and abolished the [Ca²⁺]_i increase induced by 2 μM carbonylcyanide <em>m</em>-chlorophenylhydrazone (CCCP) (a mitochondrial uncoupler). NPC-14686 (100 μM) induced a slight [Ca²⁺]_i increase after pretreatment with 2 μM CCCP and 1 μM thapsigargin. Addition of 3 mM Ca²⁺ elicited a [Ca²⁺]_i increase in cells pretreated with 100 μM NPC-14686 in Ca²⁺-free medium. Inhibition of inositol-1,4,5-trisphosphate (IP₃<span>) production by suppressing phospholipase C<span> with 2 μM U73122 did not alter NPC-14686-induced Ca</span></span>²⁺<span><span> release. Trypan blue exclusion revealed that incubation with 10 or 200 μM NPC-14686 for 1–30 min decreased </span>cell viability by 10–20% concentration dependently. Collectively, the results demonstrate that, in MDCK tubular cells, NPC-14686 induced Ca</span>²⁺ release followed by Ca²⁺ entry, with the latter playing a major role. NPC-14686 appears to release intracellular Ca²⁺ in an IP₃-uncoupled manner. NPC-14686 may be of mild cytotoxicity.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 915-921"},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00054-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21915285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repeated lipopolysaccharide administration produces tolerance to anorexia and fever but not to inhibition of thirst in rat","authors":"Felice Nava,&nbsp;Giovanna Carta","doi":"10.1016/S0192-0561(00)00058-8","DOIUrl":"10.1016/S0192-0561(00)00058-8","url":null,"abstract":"<div><p><span><span>In 24 h water and food deprived rats, a single lipopolysaccharide<span> treatment (0.25, 0.50 and 1 mg/kg, i.p.) induced inhibition of thirst and hunger as well as fever. Moreover, the same treatment increased serum cytokines, plasma nitrite/nitrate and corticosterone and urinary </span></span>prostaglandin levels. In another group of 24 h water and food deprived rats, a repeated lipopolysaccharide treatment (0.25, 0.50 and 1 mg/kg, i.p.), given at 0, 2, 6, 12 and 24 h, induced tolerance to inhibition of food intake and fever, but not to antidipsogenic effect. Moreover, the same repeated treatment stopped the increase in serum cytokines, plasma corticosterone and urinary prostaglandin concentrations and failed to reduce plasma nitrite/nitrate levels. This data, together with the evidence that a pretreatment with </span><em>N</em>^G-nitro-<span>l</span>-arginine methyl ester hydrochloride (<span>l</span><span>-NAME) (5 and 10 μg per rat) reverses the antidipsogenic effects in lipopolysaccharide tolerant rats, suggests that the persistent reduction of water intake after a repeated lipopolysaccharide treatment is due to the antidipsogenic action of nitric oxide in the brain.</span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 943-953"},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00058-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21915288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monoamine oxidase inhibitors in rheumatoid arthritis — anti-tumor necrosis factor?","authors":"Eric Lewin Altschuler","doi":"10.1016/S0192-0561(00)00047-3","DOIUrl":"10.1016/S0192-0561(00)00047-3","url":null,"abstract":"","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 1007-1008"},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00047-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80986837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"“Mechanism of thymocyte apoptosis induced by serum of tumor-bearing host: the molecular events involved and their inhibition by thymosin α-1”. By Rajat Roy, Sukh Mahendra Singh, Anil Shanker. International Journal of Immunopharmacology 22 (4) 309--321.","authors":"","doi":"10.1016/S0192-0561(00)00057-6","DOIUrl":"10.1016/S0192-0561(00)00057-6","url":null,"abstract":"","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 10","pages":"Page 833"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00057-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21798908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Onapristone (ZK299) blocks the suppressive effect of progesterone, but not that of dexamethasone, on inducible nitric oxide synthase gene expression and nitric oxide production in murine macrophages","authors":"Yasuhiro Kohmura ,&nbsp;Teruo Kirikae ,&nbsp;Fumiko Kirikae ,&nbsp;Masayasu Nakano ,&nbsp;Ikuo Sato","doi":"10.1016/S0192-0561(00)00038-2","DOIUrl":"10.1016/S0192-0561(00)00038-2","url":null,"abstract":"<div><p><span>Suppressive effects of progesterone on inducible </span>nitric oxide<span><span><span><span> synthase (iNOS) protein expression and nitric oxide (NO) production in murine peritoneal macrophages in response to </span>bacterial lipopolysaccharide (LPS) and the inhibition of the suppressive activity of progesterone by </span>onapristone (ZK299), a synthetic progesterone inhibitor, were studied. Progesterone suppressed dose-dependently LPS-induced NO production by macrophages, and scarcely detectable expression of iNOS was seen in the macrophages. ZK299 liberated the macrophages from the inhibitory effect of progesterone. Although </span>dexamethasone<span>, a synthetic glucocorticoid<span><span>, can potently suppress LPS-induced NO production by macrophages, ZK299 did not liberate the suppression by dexamethasone, suggesting that these two corticosteroids induce suppression through independent mechanisms. RT–PCR analysis showed that murine macrophages expressed no progesterone-receptor. These findings indicate that the inhibitory effect of progesterone occurs at least on the level of iNOS protein expression in the </span>signaling pathway after the LPS-stimulus. Furthermore, our present data may suggest the existence of a yet unknown type of progesterone-receptor in murine macrophages, the binding to which is responsible for the inhibitory effect of progesterone, or that progesterone may act non-specifically on the macrophages without involvement of any receptor.</span></span></span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 10","pages":"Pages 765-774"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00038-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21798902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stimulation of Ca2+-dependent exocytosis and release of arachidonic acid in cultured mast cells (RBL-2H3) by quercetin","authors":"Ariella Zussman,&nbsp;Ronit Sagi-Eisenberg","doi":"10.1016/S0192-0561(00)00034-5","DOIUrl":"10.1016/S0192-0561(00)00034-5","url":null,"abstract":"<div><p>Basic secretagogues, such as compound 48/80, stimulate secretion in rat peritoneal mast cells by directly activating the heterotrimeric G-protein Gi₃<span><span> (Aridor M, et al. Science 1993;262:1569–72). Cultured RBL-2H3 mast cells do not normally respond to basic secretagogues, but acquire such responsiveness upon prolonged exposure to the kinase inhibitor, </span>quercetin, which also increases the cellular level of Gi</span>₃ (Senyshyn J, Baumgartner RA, Beaven MA. J Immunol 1998;160:5136–44). Expression of a GTPase-deficient mutant of Gαi₃ in RBL-2H3 cells results in the stimulation of Ca²⁺<span>-triggered exocytosis and release of arachidonic acid (AA) (Zussman A, Hermuet S, Sagi-Eisenberg R. Eur J Biochem 1998;258:144–6). Here we show that long-term incubation with quercetin markedly stimulates Ca</span>²⁺<span>-triggered exocytosis and release of AA from the RBL-2H3 cells. We further show that membranes derived from such quercetin-treated cells display a reduced GTPase, but not ATPase, activity. Taken together with our previous observations, these results further implicate Gi</span>₃ as one of the cellular targets through which quercetin confers responsiveness towards the family of basic secretagogues.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 10","pages":"Pages 747-754"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00034-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21799673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of lipopolysaccharide-induced I-κB degradation and tumor necrosis factor-α expression by acriflavine, an antimicrobial agent","authors":"Sung Hee Choi ,&nbsp;Joo Yeun Cho ,&nbsp;Young Shin Chung ,&nbsp;Eun-Kyung Hong ,&nbsp;Young-Bok Han ,&nbsp;Sang Geon Kim","doi":"10.1016/S0192-0561(00)00039-4","DOIUrl":"10.1016/S0192-0561(00)00039-4","url":null,"abstract":"<div><p><span>Acriflavine<span> neutral (ACF) has been used for treatment of microbial infections for humans and fishes. Effects of ACF on the nuclear factor-κB (NF-κB) activation and tumor necrosis factor-α (TNF-α) production by lipopolysaccharide (LPS), an </span></span>endotoxin<span>, were examined in rat and RAW264.7 cells. Gel retardation analysis revealed that LPS (1 μg/kg) activated NF-κB in the liver, whereas pretreatment of rats with ACF (10 mg/kg) completely prevented the NF-κB activation. Selectivity of the NF-κB DNA binding<span> was confirmed by immunodepletion with anti-p65 and anti-p50 antibodies. Translocation of NF-κB to the nucleus is preceded by phosphorylation and proteolytic degradation of inhibitor-κBα (I-κBα) subunit. Whereas the level of I-κBα protein was rapidly decreased after treatment of rats with LPS (1 μg/kg), ACF treatment prior to LPS attenuated the decrease in I-κBα protein level. LPS-induced increase in the production of TNF-α, the principal inflammatory mediator, was prevented by ACF pretreatment by 80%. Stimulation of RAW264.7 cells with 1 μg/ml of LPS caused an increase in DNA binding activity of NF-κB, which was 80% inhibited by 1 μg/ml of ACF. LPS reduced I-κBα level in RAW264.7 cells by 77%. ACF attenuated LPS-induced decrease in I-κBα protein in a concentration-dependent manner. Production of TNF-α by LPS from RAW264.7 cells was decreased by 84% in the presence of ACF. Data showed that ACF inhibited LPS-induced NF-κB activation through inhibition of I-κBα degradation and TNF-α production in both rat and RAW264.7 cells. Inhibition of NF-κB activation and TNF-α production may be associated with the anti-inflammatory activity of ACF.</span></span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 10","pages":"Pages 775-787"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00039-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21798903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vaccination against nicotine during continued nicotine administration in rats: immunogenicity of the vaccine and effects on nicotine distribution to brain","authors":"Y Hieda ,&nbsp;D.E Keyler ,&nbsp;S Ennifar ,&nbsp;A Fattom ,&nbsp;P.R Pentel","doi":"10.1016/S0192-0561(00)00042-4","DOIUrl":"10.1016/S0192-0561(00)00042-4","url":null,"abstract":"<div><p><span>Vaccination against nicotine has been proposed as a potential treatment for nicotine dependence. Because vaccination may take months to elicit satisfactory antibody levels, the clinical usefulness of this approach will be enhanced if vaccination can be accomplished during continued nicotine intake (e.g., before a smoker quits). The current study examined the immunogenicity of a </span>nicotine conjugate vaccine<span> during continued nicotine dosing in rats, and its effects on nicotine distribution to brain. In the first experiment, nicotine was administered over 11 weeks as 20 intra venous (i.v.) bolus injections per day during the rat’s active cycle to simulate the usual pattern of nicotine intake from cigarette smoking. In the second experiment, rats received a continuous s.c. infusion of nicotine by osmotic pump for 11 weeks to provide serum nicotine concentrations equivalent to those of a heavy smoker and 24 h/day nicotine exposure. Nicotine-specific antibody titers<span> after the third booster dose were not compromised by either regimen of concurrent nicotine administration compared to those of rats receiving saline. A single additional i.v. nicotine dose was administered at the end of each experiment. The distribution of this single nicotine dose to brain was reduced by 40–60% in vaccinated rats compared to controls. Vaccine efficacy in reducing nicotine distribution to brain was not compromised by concurrent nicotine administration. These data suggest that vaccination during concurrent nicotine administration is feasible, and that the ability of vaccination to reduce nicotine distribution to brain is preserved even after months of nicotine dosing at rates approximating cigarette smoking.</span></span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 10","pages":"Pages 809-819"},"PeriodicalIF":0.0,"publicationDate":"2000-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(00)00042-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21798906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}