International journal of immunopharmacology最新文献

{"title":"Evidence for immunotoxic effects of crude Ginkgo biloba L. leaf extracts using the popliteal lymph node assay in the mouse","authors":"E Koch,&nbsp;H Jaggy,&nbsp;S.S Chatterjee","doi":"10.1016/S0192-0561(99)00080-6","DOIUrl":"10.1016/S0192-0561(99)00080-6","url":null,"abstract":"<div><p>Allergic reactions due to contact with different parts of the ancient tree <span><em>Ginkgo</em><em> biloba</em></span><span><span><span> L. have repeatedly been reported. Provocation tests<span> in patients and animal experiments have identified alkylphenols such as ginkgolic acids as causative constituents. Leaf extracts from Ginkgo are widely used to treat peripheral or </span></span>cerebral circulatory disorders and Alzheimer’s disease. Since alkylphenols are also present in leaves, potential allergic and other immunological hazards of such preparations have to be carefully controlled. Thus, we have evaluated if the </span>popliteal lymph node<span><span> assay (PLNA) in the mouse may represent a suitable model for the detection of constituents with immunotoxic properties in a complex mixture of biologically active agents such as plant extracts. Subplantar injection (2 mg) of a crude aqueous-ethanolic extract from Ginkgo leaves caused a significant lymphoproliferative reaction (LPR) in the ipsilateral popliteal lymph node. PLNA-active compounds in this extract could be enriched in the lipophilic phase by liquid–liquid partition between heptane and water. Chemical analysis of the heptane extract revealed the presence of a high concentration of alkylphenols (approx. 30%) and further subfractionation indicated that the enlargement of the popliteal lymph node was mainly due to the content of ginkgolic acids. This presumption was corroborated by observing a similar LPR following injection of a purified mixture of ginkgolic or hydroginkgolic acids. Thus, our experiments confirm that Ginkgo leaf extracts may contain constituents with immunotoxic properties, underlining the need to apply adequate production procedures to guarantee the completest possible removal of these compounds. The PLNA appears to represent a simple test model for the detection, characterisation and control of ingredients with potential immunotoxic side effects in complex </span>herbal drugs.</span></span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 3","pages":"Pages 229-236"},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00080-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21538831","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":"Nitrite inhalants spontaneously liberate nitric oxide, which is not responsible for the immunotoxicity in C57BL/6 mice","authors":"Lee S.F Soderberg ,&nbsp;Avijit Roy ,&nbsp;James T Flick ,&nbsp;John B Barnett","doi":"10.1016/S0192-0561(99)00073-9","DOIUrl":"10.1016/S0192-0561(99)00073-9","url":null,"abstract":"<div><p>Nitrite inhalant abuse has been correlated epidemiologically with HIV seropositivity and with Kaposi’s sarcoma. Using a mouse model, we have shown that inhaled isobutyl nitrite caused anemia and severely depressed immunity. In the present study, we showed that both isobutyl and cyclohexyl nitrites in air liberated nitric oxide (NO). An immunotoxic dose of 900 ppm isobutyl nitrite liberated 115 ppm NO. Mice were exposed in an inhalation chamber to 115 ppm NO, 900 ppm isobutyl nitrite, or 900 ppm cyclohexyl nitrite for 45 min/day. Following a single exposure, NO did not affect peripheral blood cell counts, while isobutyl and cyclohexyl nitrites reduced cell numbers. After 14 daily exposures, isobutyl nitrite, but not cyclohexyl nitrite or NO, reduced peritoneal macrophage tumoricidal activity. The nitrite esters likely caused immunotoxicity by mechanisms other than NO release.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 2","pages":"Pages 151-157"},"PeriodicalIF":0.0,"publicationDate":"2000-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00073-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21539481","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 influenza virus replication by cocaine","authors":"K Grattendick ,&nbsp;D.L Lefkowitz ,&nbsp;S.S Lefkowitz","doi":"10.1016/S0192-0561(99)00058-2","DOIUrl":"10.1016/S0192-0561(99)00058-2","url":null,"abstract":"<div><p><span><span><span><span>Cocaine has been shown to have a number of diverse effects on the immune system. The current investigators have previously demonstrated an inhibitory effect of cocaine on murine hepatitis virus replication in peritoneal macrophages in vitro. The present study was undertaken to examine the effects of cocaine on influenza virus replication and to further characterize that effect in an animal model. Cocaine was capable of inducing a dose-dependent reduction in influenza PR-8 replication using </span>MDCK cells in vitro. Concentrations of 100 μg/ml caused a 50% reduction of virus. To further characterize the effect in vivo, C57Bl/6 mice infected with influenza PR-8 by intranasal instillation were given daily ip injections of 10 mg/kg cocaine just prior to and for 4 days after exposure to influenza. Lungs from mice exposed to cocaine had </span>viral titers that were reduced approximately 50% compared to controls as demonstrated by </span>hemagglutination titers. Additional studies suggest that this reduction appears to be caused by an increase of cocaine-induced </span>interferon.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 2","pages":"Pages 105-111"},"PeriodicalIF":0.0,"publicationDate":"2000-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00058-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21538379","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":"In vitro IgE inhibition in B cells by anti-CD23 monoclonal antibodies is functionally dependent on the immunoglobulin Fc domain","authors":"Takehiko Nakamura ,&nbsp;William S Kloetzer ,&nbsp;Peter Brams ,&nbsp;Kandasamy Hariharan ,&nbsp;Soulaima Chamat ,&nbsp;Xianjun Cao ,&nbsp;Michael J LaBarre ,&nbsp;Paul C Chinn ,&nbsp;Ron A Morena ,&nbsp;William S Shestowsky ,&nbsp;Yan-Ping Li ,&nbsp;Agnes Chen ,&nbsp;Mitchell E Reff","doi":"10.1016/S0192-0561(99)00068-5","DOIUrl":"10.1016/S0192-0561(99)00068-5","url":null,"abstract":"<div><p><span><span>CD23, the low </span>affinity receptor<span> for IgE (FcεRII), is involved in regulation of IgE synthesis by B-lymphocytes. Five monoclonal antibodies<span><span> to human CD23 were generated from cynomolgus macaques immunized with purified soluble CD23 (sCD23). Four of the five primate antibodies blocked the binding of IgE complexes to CD23 positive cells and also inhibited the production of IgE in vitro by IL-4 induced human </span>peripheral blood mononuclear cells (PBMC). The variable domains of several primate antibodies were utilized to construct chimeric macaque/human (PRIMATIZED</span></span></span>^®) monoclonal antibodies. PRIMATIZED^® p5E8G1, containing human gamma 1 constant region, inhibited IgE production in vitro as efficiently as the parent primate antibody, but the human gamma 4 constant version, PRIMATIZED^® p5E8G4, was not as effective in IgE inhibition. An F(ab′)₂ of p5E8G1 did not inhibit IgE production but did interfere with IgE inhibition by the intact anti-CD23 antibody in a dose dependent fashion. The murine monoclonal antibody MHM6 recognizes human CD23 at a different epitope than primate antibody 5E8, and inhibits IgE production by IL-4 induced PBMC. As with the F(ab′)₂ of p5E8G1, the F(ab′)₂ of MHM6 also failed to inhibit IgE production. These data imply that the mechanism by which anti-CD23 antibodies inhibit IgE production requires cross-linking of CD23 to an IgG receptor. These data also imply that neither bivalent cross-linking of CD23 alone or inhibition of CD23 binding to its natural ligands is sufficient to inhibit IgE production.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 2","pages":"Pages 131-141"},"PeriodicalIF":0.0,"publicationDate":"2000-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00068-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21539479","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":"B cell stimulating activity of metallothionein in vitro","authors":"T Sugiura,&nbsp;U Yamashita","doi":"10.1016/S0192-0561(99)00065-X","DOIUrl":"10.1016/S0192-0561(99)00065-X","url":null,"abstract":"<div><p>The effect of metallothionein (MT) on lymphocytes was studied in vitro. Rabbit MT induced the proliferative responses of mouse splenocytes at concentrations of 1–25 μg/ml. MT synergistically enhanced Con A- or LPS-induced proliferative response of splenocytes. A similar effect was also observed for rabbit splenocytes at a similar concentration. Free heavy metals such as Cd and Zn only weakly stimulated splenocytes. 2-mercaptoethanol (2-Me) abrogated the effect of MT, suggesting that thiols in MT play an important role for splenocyte response. MT stimulated splenocytes from MT-knockout mice as well as those from normal control mouse. The responder cells for MT stimulation were B cells and MT also induced B cell differentiation to produce Ig. MT induced the calcium influx of B cells, but not T cells. These results indicate that MT has a potent immunomodulating activity, especially on B cells.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 2","pages":"Pages 113-122"},"PeriodicalIF":0.0,"publicationDate":"2000-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00065-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21539477","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":"Gestational nicotine exposure alone or in combination with ethanol down-modulates offspring immune function","authors":"P.V Basta,&nbsp;K.B Basham,&nbsp;W.P Ross,&nbsp;M.E Brust,&nbsp;H.A Navarro","doi":"10.1016/S0192-0561(99)00074-0","DOIUrl":"10.1016/S0192-0561(99)00074-0","url":null,"abstract":"<div><p>Prenatal nicotine exposure has been shown to disrupt the development of a number of peripheral organs. In the current study, we examined the effects of gestational nicotine exposure, alone or in combination with ethanol exposure, on offspring immune function. Timed pregnant rats were treated with either nicotine (6 mg/kg/day) from gestation day 4–20 using subcutaneously implanted osmotic mini-pumps or ethanol administered in the drinking water (15% w/v) from gestation day 10–20. The combined exposure group received both treatments. The ability of offspring T and B cells to proliferate in response to nonspecific stimulation by Concanavalin A or lipopolysaccharide, respectively, was determined on postnatal days 9, 15, 22, 29, 64, and 86. Offspring splenocyte β₂-adrenoceptor binding was also measured.</p><p>Nicotine or nicotine+ethanol suppressed splenocyte responsiveness to Concanavalin A or lipopolysaccharide which was similar in timing and magnitude to that seen with ethanol alone. Splenocytes from these groups remained subresponsive to stimulation well into adulthood. The combined drug treatment caused an overall reduction in spleen β-adrenergic receptor binding whereas the individual drug treatments did not alter the development of spleen β-adrenergic receptors.</p><p>Our results indicate that prenatal nicotine exposure can cause long-term suppression of the proliferative response of offspring immune cells. Moreover, the effects of nicotine+ethanol may cause more severe deficits in adulthood.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 2","pages":"Pages 159-169"},"PeriodicalIF":0.0,"publicationDate":"2000-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00074-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21539482","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":"Phenytoin and electric shock-induced apoptosis in rat peripheral blood lymphocytes","authors":"M.M Villaseñor-Garcı́a ,&nbsp;A.M Puebla-Pérez ,&nbsp;L Sandoval-Ramı́rez ,&nbsp;X Lozoya","doi":"10.1016/S0192-0561(99)00069-7","DOIUrl":"10.1016/S0192-0561(99)00069-7","url":null,"abstract":"<div><p><span><span>The apoptotic index (AI) of peripheral blood lymphocytes<span> (PBL) and plasma corticosterone<span> (CS) levels were determined in Wistar rats treated with </span></span></span>phenytoin (PHT) at therapeutic and toxic doses (100 or 200 mg/kg/day, respectively, over a period of 7 days) and stressed by bifrontal electric shock (60 Hz/40 mA/0.2 seg). The values of CS and AI were found to be significantly higher in rats submitted to electric shock (ES) and in rats treated with therapeutic and toxic doses of PHT plus ES, than in rats treated only with PHT (</span><em>P</em>&lt;0.001). The plasma concentrations of PHT were found to be significantly higher in rats treated with toxic doses than in those treated with therapeutic doses (<em>P</em><span>&lt;0.001), while the control group (without treatment) and vehicle group (propilenglycol–ethanol–water, 40:10:50), showed low levels of CS, and less than 1% of AI. The DNA analysis by electrophoresis<span> in agarose in all the groups was positive, displaying the ladder pattern characteristic of apoptotic process (200 bp), except in the control groups (no treatment and vehicle treated). Our results demonstrate that chronic stress, caused by ES, produces an elevation of CS. The values of apoptosis were correlated with the CS levels, suggesting that the apoptotic inductor process is a consequence of an increase in the concentration of corticosterone in plasma, in response to the hypothalamic–pituitary–adrenals (HPA) axis activation, while phenytoin at therapeutic doses is only a moderate apoptosis inductor.</span></span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 2","pages":"Pages 143-150"},"PeriodicalIF":0.0,"publicationDate":"2000-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00069-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21539480","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":"Inhibitory effect of TMK-688 on late asthmatic responses as well as T-cell and eosinophilic infiltration in guinea pigs with asthmatic reactions","authors":"Yuji Tohda,&nbsp;Masato Muraki,&nbsp;Akinobu Kawai,&nbsp;Takashi Iwanaga,&nbsp;Hirokazu Kubo,&nbsp;Masahiro Fukuoka,&nbsp;Sigenori Nakajima","doi":"10.1016/S0192-0561(99)00066-1","DOIUrl":"10.1016/S0192-0561(99)00066-1","url":null,"abstract":"<div><p>The effects of an oral anti-allergic agent, TMK-688, which inhibits 5-lipoxygenase, at doses of 3.2 and 10 mg/kg were studied in guinea pigs with dual-phase asthmatic response. We previously observed that pretreatment with TMK-688 inhibited the late asthmatic response (LAR) induced by ovalbumin<span> inhalation exposure. The present study focused on the effect of TMK-688 on infiltration by T-cells and eosinophils. TMK-688 inhibited both T-cell and eosinophilic infiltration. These findings suggest that TMK-688 is effective in inhibiting infiltration of T-cells and eosinophilic chemotaxis, and thereby suppresses LAR.</span></p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 2","pages":"Pages 123-130"},"PeriodicalIF":0.0,"publicationDate":"2000-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00066-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21539478","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":"Cytokines potentiate human eosinophil superoxide generation in the presence of Nω-nitro-l-arginine methyl ester","authors":"Ann S. Heiman,&nbsp;Diane Allen-Gipson","doi":"10.1016/S0192-0561(99)00075-2","DOIUrl":"10.1016/S0192-0561(99)00075-2","url":null,"abstract":"<div><p>The eosinophilic (EOS) leukocyte has been implicated as a primary effector cell in inflammatory and allergic diseases. Cytokines are among the mediators of inflammatory and allergic diseases which modulate the effector functions of EOS. Certain cytokines, elevated in patients with various allergies, are thought to modulate EOS reactive oxygen species superoxide anion and nitric oxide (NO) responses. Though EOS transcribe and translate mRNA for inducible NO synthase, the effects of cytokines on NO generation remain largely unknown. Thus, we have investigated effects of IL-3, IL-5, GM-CSF, IL-8, RANTES and the proinflammatory cytokines TNF-α and IFN-γ, on superoxide anion and NO generation by clone 15 HL-60 human eosinophilic cells. Cytokine treatments (3 and 18 h) resulted in production of small amounts of superoxide anion which were enhanced by the NO inhibitor <span>l</span>-NAME. In the presence of <span>l</span>-NAME, PMA (1 nM) stimulation significantly increased superoxide anion generation following 3 h treatments with IL-3, TNF-α or IFN-γ. Eighteen hour cytokine treatments with GM-CSF, IL-8, RANTES, IFN-γ or TNF-α primed the cells for enhanced reactive oxygen species following exposure to an EOS stimulant. Inhibition of NO synthesis resulted in increased levels of superoxide anion. Collectively, these results suggest that an environment of proinflammatory cytokines may potentiate the generation of reactive oxygen species by EOS. These results further suggest that at an inflammatory site or during an allergic response, EOS may concomitantly synthesize NO and generate superoxide anion, fractions of which may rapidly react to form the potent oxidant peroxynitrite.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 2","pages":"Pages 171-181"},"PeriodicalIF":0.0,"publicationDate":"2000-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00075-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21539483","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":"Immunogenicity of an E. coli extract after oral or intraperitoneal administration: induction of antibodies against pathogenic bacterial strains","authors":"M Huber ,&nbsp;W Baier ,&nbsp;A Serr ,&nbsp;W.G Bessler","doi":"10.1016/S0192-0561(99)00064-8","DOIUrl":"10.1016/S0192-0561(99)00064-8","url":null,"abstract":"<div><p><span><span>For the treatment of recurrent infections of the urinary tract, a </span>bacterial extract (OM-89) consisting of immunostimulating components derived from 18 </span><em>Escherichia coli</em><span> strains is orally applied to patients. We investigated in a mouse model the immunogenicity<span> of the bacterial extract after intraperitoneal or oral administration. After repeated administration of the extract, serum IgG and IgA responses against the </span></span><em>E. coli</em><span> strains used for the preparation of OM-89 were obtained. This antisera also recognized a number of bacterial strains isolated from patients with urinary tract and enterohemorrhagic </span><em>E. coli</em> infections, and bound to a variety of other pathogenic strains. Moreover, the supernatants of cell cultures prepared from the urogenital tract of mice immunized with OM-89 contained increased levels of strain specific and of total IgG and IgA. Our findings may contribute to explain the therapeutic effect of OM-89 demonstrated in clinical studies.</p></div>","PeriodicalId":14002,"journal":{"name":"International journal of immunopharmacology","volume":"22 1","pages":"Pages 57-68"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0192-0561(99)00064-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21538374","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}