International journal of immunopharmacology最新文献

{"title":"Evidence for pleomorphism of estrogen receptor capacity and affinity in liver and thymus of immature BALB/c and (NZB×NZW) F1 mice, a model of systemic lupus erythematosus","authors":"Ryan Roa,&nbsp;Ben D. Greenstein","doi":"10.1016/S0192-0561(00)00052-7","DOIUrl":"10.1016/S0192-0561(00)00052-7","url":null,"abstract":"<div><p><span><span>Binding properties of estrogen receptors<span> in liver, thymus<span> and uterus of BALB/c and (NZB×NZW) F1 mice were compared. (NZB×NZW) F1 mice spontaneously develop an autoimmune disease resembling human systemic lupus erythematosus (SLE). It is hypothesized that </span></span></span>estradiol<span>, through its receptors, mediates the progression of murine SLE. High-speed cytosols were prepared from liver, thymus and uterus and incubated with the synthetic estrogen </span></span>³H-moxestrol (NEN). Scatchard plots were derived from binding isotherms obtained. Rectilinear Scatchard plots were obtained from all tissues, which is consistent with the presence of only one class of binding sites, or of more than one class but with the same affinity. There were, however, strain differences in that the affinity of the binding reaction was significantly higher in cytosols from BALB/c liver in males and females. In thymus, the situation was reversed in that the affinity was significantly higher in cytosols from (NZB×NZW) F1 mice. Thymic cytosols from BALB/c mice contained significantly more estrogen receptors per mg cytosol protein than did those from (NZB×NZW) F1 mice. The exacerbation of murine SLE may be due, at least in part, to these properties of estrogen receptors in liver and thymus.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 897-903"},"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)00052-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21915283","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":"Nitric oxide induces chemotaxis of neutrophil-like HL-60 cells and translocation of cofilin to plasma membranes","authors":"Reiko Adachi ,&nbsp;Sachiko Matsui ,&nbsp;Masumi Kinoshita ,&nbsp;Keiko Nagaishi ,&nbsp;Haruyo Sasaki ,&nbsp;Tadashi Kasahara ,&nbsp;Kazuhiro Suzuki","doi":"10.1016/S0192-0561(00)00045-X","DOIUrl":"10.1016/S0192-0561(00)00045-X","url":null,"abstract":"<div><p><span>Nitric oxide<span><span><span> (NO) plays various important roles in the physiological system. With regard to chemotaxis of neutrophils<span>, there are reports that endogenous NO is a mediator of chemotaxis, and others that exogenous NO inhibits chemotaxis. It is also reported that NO itself expressed chemotactic activity. On the other hand, we have recently proposed the importance of cofilin, an actin-binding </span></span>phosphoprotein, in </span>phagocyte<span><span> functions through dephosphorylation and translocation to the plasma membrane regions. Because chemotaxis is a phenomenon of dynamic cell movement, cofilin, a regulator of the cytoskeletal system, may be involved in its mechanisms. To clarify further the effect of NO on functions of leukocytes and to examine the effect of NO on cofilin, we investigated the chemotaxis of neutrophil-like HL-60 cells induced by NO, as well as the influence of NO on the phosphorylation and intracellular distribution of cofilin. Two </span>NO donors, 3-[2-hydroxy-1-(1-methylethyl)-2-nitrosohydrazino]-1-propanamine (NOC5) and </span></span></span><em>S</em>-nitroso-<em>N</em><span><span>-acetylpenicillamine (SNAP), were shown to cause chemotaxis, and, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazole-1-oxyl 3-oxide (carboxy-PTIO), a NO-specific scavenger, inhibited the chemotaxis induced by NO-donors, suggesting that NO itself released from the NO donors has chemotactic activity. LY-83583 and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one (ODQ), inhibitors of soluble guanylate cyclase, inhibited the chemotaxis to NO donors, which implies that soluble guanylate cyclase is involved in the </span>signaling pathway of this NO action. We also found that NO caused translocation of cofilin to the cell periphery, though dephosphorylation of cofilin was not detected. These results demonstrate that NO has chemotactic activity for neutrophils and caused the translocation of cofilin to the plasma membrane regions without its dephosphorylation.</span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 855-864"},"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)00045-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21916537","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":"Progesterone inhibits glucocorticoid-induced murine thymocyte apoptosis","authors":"Robert W. McMurray ,&nbsp;James G. Wilson ,&nbsp;Lenora Bigler ,&nbsp;Lianbin Xiang ,&nbsp;Anand Lagoo","doi":"10.1016/S0192-0561(00)00059-X","DOIUrl":"10.1016/S0192-0561(00)00059-X","url":null,"abstract":"<div><p><span><span>Sex and sex hormones modulate immune development and responses. A primary target of their effects is the structure and cellularity of the thymus; therefore, we examined the effects of sex and sex steroids on </span>thymocyte<span> apoptosis. We demonstrate initially that male DBA mice have a significantly higher percentage of glucocorticoid-induced apoptotic thymocytes (46.1±3.8%) than their female counterparts (31.6±3.1%; </span></span><em>P</em><span><span>=0.012). We postulated that this gender difference was due to differential modulation of glucocorticoid-induced apoptosis by sex hormones such as estrogen, testosterone or </span>progesterone<span>. Both estrogen and testosterone increased in vitro thymocyte apoptosis. In contrast, progesterone not only inhibited spontaneous in vitro thymocyte apoptosis, but also prevented in vitro glucocorticoid-induced apoptosis. Progesterone administration also suppressed glucocorticoid-induced in vivo thymocyte apoptosis. These results suggest that anti-apoptotic effects of progesterone may influence T cell development and subsequent immune responses.</span></span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 955-965"},"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)00059-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21915289","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":"Report of the second annual walker's cay colloqium on cancer vaccines and immunotherapy, March 8-11, 2000.","authors":"R. Reisfeld, J. Schlom","doi":"10.1016/S0192-0561(00)00050-3","DOIUrl":"https://doi.org/10.1016/S0192-0561(00)00050-3","url":null,"abstract":"","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"13 1","pages":"1009-14"},"PeriodicalIF":0.0,"publicationDate":"2000-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87579803","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":"Nitric oxide production by high molecular weight water-soluble chitosan via nuclear factor-κB activation","authors":"Hyun-Ja Jeong ,&nbsp;Hyun-Na Koo ,&nbsp;Eun-Young Oh ,&nbsp;Han-Jung Chae ,&nbsp;Hyung-Ryong Kim ,&nbsp;Sang-Bong Suh ,&nbsp;Cheorl-Ho Kim ,&nbsp;Kwang-Ho Cho ,&nbsp;Byung-Rim Park ,&nbsp;Seung-Taeck Park ,&nbsp;Young-Mi Lee ,&nbsp;Hyung-Min Kim","doi":"10.1016/S0192-0561(00)00055-2","DOIUrl":"https://doi.org/10.1016/S0192-0561(00)00055-2","url":null,"abstract":"<div><p><span>High molecular weight water-soluble chitosan (WSC), having an average molecular weight of 300 000 Da and a degree of deacethylation over 90%, can be produced using a simple multi-step membrane separation process. In this study, the effect of WSC on the production of nitric oxide (NO) in RAW 264.7 macrophages was evaluated. Water-insoluble chitosan alone has been previously shown to exhibit in vitro stimulatory effect on macrophages NO production. However, WSC had no effect on NO production by itself. When WSC was used in combination with recombinant interferon-γ (rIFN-γ), there was a marked cooperative induction of NO synthesis in a dose-dependent manner. The optimal effect of WSC on NO synthesis was shown 24 h after treatment with rIFN-γ. The increased production of NO from rIFN-γ plus WSC-stimulated RAW 264.7 macrophages was decreased by the treatment with </span><em>N</em>^<em>G</em>-monomethyl-<span>l</span>-arginine (<em>N</em>^G<span>MMA). The increase in NO synthesis was reflected, as an increased amounts of inducible NO synthase<span> protein. In addition, synergy between rIFN-γ and WSC was mainly dependent on WSC-induced tumor necrosis factor-α (TNF-α) and nuclear factor-κB (NF-κB) activation. The present results indicate that the capacity of WSC to increase NO production from rIFN-γ-primed RAW 264.7 macrophages is the result of WSC-induced TNF-α secretion via the signal transduction pathway of NF-κB activation.</span></span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 923-933"},"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)00055-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92018566","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":"Radioprotection of haemopoietic stem cells by a single injection of bacterial lysate — IRS-19 administered to mice before or after irradiation","authors":"Peter Fedoročko,&nbsp;Nadežda O. Macková","doi":"10.1016/S0192-0561(00)00063-1","DOIUrl":"10.1016/S0192-0561(00)00063-1","url":null,"abstract":"<div><p><span><span>Data in this report describes the effect of a single injection of bacterial lysate IRS-19 prior to irradiation of C57Bl/6 mice on recovery of colony-forming cells (CFC) after sublethal and lethal doses of radiation. The injection of IRS-19 promoted an earlier recovery of colony-forming cells in the bone marrow and spleen. For example, 5 and 9 days after 7.5 Gy irradiation, the number of CFU-S per femur was approximately 1.7–2.3-fold higher in IRS-19-injected mice than in saline-injected mice. Also, pretreatment of mice with IRS-19 induced an increase in the number of endogenous </span>haemopoietic stem cells (endoCFU-S). In the postradiation period (5–21 days) significantly increased bone marrow and spleen cellularity and accelerated myelopoietic regeneration (committed progenitor granulocyte-macrophage–colony-forming cells, GM–CFC) in the bone marrow and spleen compared with saline-treated controls. At the time of presumed irradiation, (i.e. 24 h after administration of the drug to the non-irradiated mice), there was no significant difference between the control mice and mice treated with IRS-19 in numbers of femoral and spleen GM–CFC. In contrast, the number of nucleated femoral cells decreased significantly in the group treated with IRS-19. Moreover, treatment with IRS-19 caused a sustained increase in serum colony-stimulating activity which was followed by an enhanced repopulation of GM–CFC in the femoral marrow and spleen. Administration of the agent 24 h prior to irradiation rather than postirradiation appeared most effective with respect to radioprotection. Intravenous rather than i.p. and p.o. was the most effective </span>route of administration in the mouse. Furthermore, single, high-dose injection appeared to be more effective than repeated, lower dose injections. Results suggest that the radioprotective properties associated with the administration of IRS-19 are largely a consequence of the induction of haemopoietic colony-stimulating activities and potentially the activation and/or enhancement of cytokine cascades in the recipient animals. These changes may ultimately impact the cell cycle profile of the haemopoietic cells and therefore their ability to withstand and/or recover from radiation insult.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 989-999"},"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)00063-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21915170","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":"Chlorella vulgaris culture supernatant (CVS) reduces psychological stress-induced apoptosis in thymocytes of mice","authors":"Takashi Hasegawa ,&nbsp;Kiyoshi Noda ,&nbsp;Shoichiro Kumamoto ,&nbsp;Yotaro Ando ,&nbsp;Akira Yamada ,&nbsp;Yasunobu Yoshikai","doi":"10.1016/S0192-0561(00)00049-7","DOIUrl":"10.1016/S0192-0561(00)00049-7","url":null,"abstract":"<div><p>A glycoprotein prepared from <span><em>Chlorella vulgaris</em></span><span><span> culture supernatant (CVS) is a biological response modifier (BRM) which exhibits protective activities against tumor metastasis and 5-fluorouracil-induced immunosuppression. We here show that oral administration of CVS prevented significantly the apoptosis of </span>thymocytes in mice undergoing psychological stress in a communication box. Mice were exposed to the emotional stress for 14 days by witnessing other mice being exposed to foot-shock. The numbers in thymocytes, especially CD4</span>⁺CD8⁺<span> population, were decreased significantly and apoptotic cells, as assessed by Annexin V expression, were reciprocally increased after the exposure to the psychological stress. </span><em>C</em>. <em>vulgaris</em><span><span> culture supernatant (CVS) administration significantly suppressed the increase in serum corticosterone level in the psychologically stressed mice. These results suggest that CVS prevents psychological stress and maintain </span>homeostasis in the face of external environmental changes.</span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 877-885"},"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)00049-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21916539","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":"Effect of biphenyl dimethyl dicarboxylate on the humoral immunosuppression by ethanol","authors":"Joung-Hoon Kim ,&nbsp;Yeun-Ja Mun ,&nbsp;Hyun-Ja Chun ,&nbsp;Kyung-Soo Jeon ,&nbsp;Young-Ok Kim ,&nbsp;Won-Hong Woo","doi":"10.1016/S0192-0561(00)00053-9","DOIUrl":"10.1016/S0192-0561(00)00053-9","url":null,"abstract":"<div><p>The present study was undertaken to investigate the effect of biphenyl<span><span> dimethyl dicarboxylate (PMC) on the humoral immunosuppression by ethanol (EtOH) in </span>ICR mice<span><span><span>. PMC at a dose of 6 mg/kg was orally administered to mice daily for 28 consecutive days, and the control mice were given vehicle. Mice treated with EtOH were given freely with 20% EtOH instead of water. The results of this study are summarized as follows; a gain of body weight and the relative weights of spleen and liver were significantly increased by combination of PMC and EtOH, as compared with those in mice treated with EtOH alone. Splenic plaque forming cells (PFC) and </span>hemagglutination<span> (HA) titers to sheep red blood cells<span> (SRBC), and the secondary IgG antibody response to bovine </span></span></span>serum albumin (BSA) were decreased by the treatment of EtOH alone, then restored to normal level by PMC treatment. The elevations of serum glutamic-pyruvic transaminase (S-GPT) and total protein levels caused by EtOH were reduced to normal level by the combination of PMC and EtOH. In addition, lower serum albumin and A/G ratio were also increased to normal level. These findings indicate that PMC has a protective effect against EtOH-induced humoral immunosuppression.</span></span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 905-913"},"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)00053-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21915284","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":"Modification of tumor necrosis factor-induced acute toxicity d-galactosamine challenge by polymyxin B, an anti-endotoxin","authors":"Shuhei Sakaguchi ,&nbsp;Shinobu Furusawa ,&nbsp;Katsushi Yokota ,&nbsp;Motoaki Takayanagi ,&nbsp;Yoshio Takayanagi","doi":"10.1016/S0192-0561(00)00056-4","DOIUrl":"10.1016/S0192-0561(00)00056-4","url":null,"abstract":"<div><p><span><span>Polymyxin B (PMB), an antibiotic with anti-endotoxin activity, was used to examine the participation of endogenously produced </span>endotoxin<span> in the enhancement of recombinant human tumor necrosis factor (rhTNF)-induced toxicity in </span></span><span>d</span>-galactosamine (GalN)-sensitized mice. GalN-sensitized mice (700 mg/kg, intraperitoneally (i.p.)) injected together with rhTNF (1×10⁴<span><span> U/mouse, intravenously (i.v.)) exhibited severe symptoms, with 100% mortality at 18 h. However, mice pretreated with PMB (20 mg/kg, i.p.) showed protection against the rhTNF-induced lethality<span> following GalN sensitization. Little or no effects were observed on alanine aminotransferase (ALT) activity or lactate dehydrogenase (LDH) isozyme leakage in serum in mice 7 h after administration of rhTNF alone. Administration of rhTNF to GalN-sensitized mice resulted in marked increases in ALT activity and LDH isozyme leakage relative to those in mice treated with rhTNF alone. In mice pretreated with PMB, the levels of ALT and LDH isozyme leakage 7 h after rhTNF/GalN injection were significant decreased as compared with those in mice treated with rhTNF/GalN. Similarly, injection of PMB markedly decreased </span></span>lipid peroxide formation in the liver of the GalN-sensitized mice treated with rhTNF. The injection of a low endotoxin dose (0.1 mg/kg, i.p.) markedly increased the lethality in mice treated with rhTNF (5×10</span>³ U/mouse, i.v.) and GalN, and these animals showed 100% mortality at 8 h. These findings suggested that the extent of TNF-induced toxicity caused by GalN administration may be a result of synergism between TNF and gut-derived endotoxin. It is likely that endogenously produced endotoxin play a significant role in rhTNF/GalN-hypersensitized mice.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 935-942"},"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)00056-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21915287","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":"Report of the second annual walker's cay colloquium on cancer vaccines and immunotherapy, March 8–11, 2000","authors":"Ralph A. Reisfeld,&nbsp;Jeffrey Schlom","doi":"10.1016/S0192-0561(00)00050-3","DOIUrl":"https://doi.org/10.1016/S0192-0561(00)00050-3","url":null,"abstract":"","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 11","pages":"Pages 1009-1014"},"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)00050-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91994424","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}