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The galactose-inhibitable surface lectin of Entamoeba histolytica, a possible candidate for a subunit vaccine to prevent amoebiasis. 溶组织内阿米巴的半乳糖抑制表面凝集素，可能是预防阿米巴病的亚单位疫苗的候选物。
Behring Institute Mitteilungen Pub Date : 1997-03-01
H Lotter, E Tannich
{"title":"The galactose-inhibitable surface lectin of Entamoeba histolytica, a possible candidate for a subunit vaccine to prevent amoebiasis.","authors":"H Lotter,&nbsp;E Tannich","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Invasive amoebiasis, a spectrum of diseases caused by the enteric protozoan parasite Entamoeba histolytica, constitutes a major health problem mainly in tropical and subtropical countries with poor sanitary conditions. The different forms of the disease are characterized by massive tissue lesions. Amoeba-induced tissue destruction requires an intimate contact between E. histolytica trophozoites and host cells. This contact is predominantly mediated by a galactose-inhibitable lectin located on the surface of the amoebae. Therefore, the lectin is considered a prime candidate for the development of a vaccine to prevent amoebiasis. This communication reports on recent developments in characterizing the structure and function of the E. histolytica surface lectin and its use as a subunit vaccine.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"112-6"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20242596","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}
引用次数: 0
Developmentally regulated changes in the cell surface architecture of Leishmania parasites. 利什曼原虫细胞表面结构发育调控的变化。
Behring Institute Mitteilungen Pub Date : 1997-03-01
M J McConville, J E Ralton
{"title":"Developmentally regulated changes in the cell surface architecture of Leishmania parasites.","authors":"M J McConville,&nbsp;J E Ralton","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The cell surface of Leishmania parasites is coated by a highly unusual glycocalyx which varies markedly during the parasite life cycle. The predominant molecule on the extracellular promastigote (sandfly) stage is a complex lipophosphoglycan (LPG), which together with a number of GPI-anchored proteins and a family of low molecular weight glycoinositolphospholipids (GIPLs), forms a morphologically distinct protective coat over the plasma membrane. The structure of the LPG has been shown to vary in different species and during promastigote development in the sandfly. This polymorphism is thought to be important in allowing Leishmania parasites to colonize a range of insect hosts, and in facilitating the regulated migration of promastigotes along the sandfly alimentary canal. Stage-specific changes in LPG are also involved in preadapting promastigotes to life in the mammalian host. This complex glycocalyx coat is absent from the amastigote stage that proliferates in the phagolysosomes of mammalian macrophages, as the expression of both the LPG and GPI-anchored proteins is massively down-regulated. Instead, the plasma membrane of amastigotes is coated by a densely packed layer of parasite-derived GIPLs and host-derived glycosphingolipids. We propose that the down-regulation of the promastigote macromolecules and the acquisition of host glycolipids by amastigotes represents an important strategy to avoid detection by specific and non-specific components of the immune system.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"34-43"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20244729","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}
引用次数: 0
A method to measure the cytoplasmic pH of single, living Plasmodium falciparum parasites. 一种测定单个活恶性疟原虫细胞质pH值的方法。
Behring Institute Mitteilungen Pub Date : 1997-03-01
S Wünsch, C Sanchez, M Gekle, U Kersting, K Fischer, P Horrocks, M Lanzer
{"title":"A method to measure the cytoplasmic pH of single, living Plasmodium falciparum parasites.","authors":"S Wünsch,&nbsp;C Sanchez,&nbsp;M Gekle,&nbsp;U Kersting,&nbsp;K Fischer,&nbsp;P Horrocks,&nbsp;M Lanzer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Here we describe a novel methodology for the investigation of the intracellular pH of P. falciparum. This method is based on a fluorescent dye with pH-dependent spectral properties, which can be monitored using a digital imaging system. This non-invasive method allows the cytoplasmic pH of single, living P. falciparum parasites to be measured while still within the host erythrocyte. It was found that schizonts from the P. falciparum clone D10 have a cytoplasmic pH of 7.18 to 7.23, differing slightly on the buffering system used. The pH of uninfected erythrocytes is 7.10 +/- 0.05. This method offers an opportunity to study the parasite's physiology and define transport mechanisms essential for parasite growth.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"44-50"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20244730","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}
引用次数: 0
Schistosoma mansoni infection induces a type 1 CD8+ cell response. 曼氏血吸虫感染诱导1型CD8+细胞应答。
Behring Institute Mitteilungen Pub Date : 1997-03-01
E J Pearce, J Pedras-Vasconcelos
{"title":"Schistosoma mansoni infection induces a type 1 CD8+ cell response.","authors":"E J Pearce,&nbsp;J Pedras-Vasconcelos","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We have found that infection with the large extracellular parasite S. mansoni leads to the development of a type 1 CD8+ T cell response. While there are many poorly understood aspects of this immune response, our working hypothesis is that it functions primarily to regulate the parasite egg-antigen induced Th2 response, which itself is responsible for circumoval granunuloma formation. This view of the activity of CD8+ cells mirrors Bloom and colleagues' postulate that type 2 CD8+ cells function to regulate Th1 responses. Since it is well recognized that Th1 and Th2 cells can cross regulate each other, why should a type 1 CD8+ rather than a Th1 response be used for the regulation of the Th2 response during schistosomiasis? The answer to this may in part lie in the apparent dependence of the type 1 CD8+ cells on IL-4. Because of this, there is little likelihood for the over-production of IFN-gamma (a potentially dangerous proinflammatory cytokine) and \"suppression\" is provided only when needed. Th1 cells have no such dependence on IL-4 for IFN-gamma production. Current work in the laboratory is directed towards testing the various hypotheses put forward here.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"79-84"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20242591","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}
引用次数: 0
In control of its fate: gene regulation in Toxoplasma gondii. 控制其命运:刚地弓形虫的基因调控。
Behring Institute Mitteilungen Pub Date : 1997-03-01
J G Mattsson, H Erhardt, D Soldati
{"title":"In control of its fate: gene regulation in Toxoplasma gondii.","authors":"J G Mattsson,&nbsp;H Erhardt,&nbsp;D Soldati","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The intracellular protozoan parasite Toxoplasma gondii is an important opportunistic pathogen in animals and man. In parallel to its clinical significance, T. gondii is also receiving considerable attention as an attractive model organism for intracellular parasitism. Regulation of gene expression at various levels underlies the intricate interplay between the parasite and its host cell, as well as the interconversions between different life-stages. In this article we will discuss some of what is currently known about gene organization and gene regulation in T. gondii as well as some of the tools available to dissect the parasite at a molecular level.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"25-33"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20244728","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}
引用次数: 0
Nonspecific resistance to Mycobacteria: the role of the Nramp1 gene. 分枝杆菌非特异性耐药:Nramp1基因的作用。
Behring Institute Mitteilungen Pub Date : 1997-03-01
E Buschman, S Vidal, E Skamene
{"title":"Nonspecific resistance to Mycobacteria: the role of the Nramp1 gene.","authors":"E Buschman,&nbsp;S Vidal,&nbsp;E Skamene","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The genus Mycobacteria consists of over 50 species that include two of the best-known human pathogens, M. tuberculosis and M. leprae, the causes of tuberculosis (TB) and leprosy, respectively. Whereas the spread of leprosy currently appears to be under control, there are presently about 30 million active cases of TB worldwide, with an alarming increase in the number of multidrug resistant case of M. tuberculosis. As strategies for antibiotic intervention against TB become more limited, it is imperative to develop new therapeutic approaches against this oppressive disease. One promising avenue is to characterize the host genes and gene products which regulate resistance to mycobacterial infections. In the mouse, resistance and susceptibility to intracellular growth of Mycobacteria in macrophages is controlled by the Bcg (Nramp1) gene, which has now been cloned and shown to encode a macrophage transmembrane protein with a putative transporter function. Sequencing of Nramp1 revealed that susceptibility to infection is associates with a single, nonconservative glycine to aspartic acid substitution at position 169 (G169D). Although the intracellular location of the Nramp1 protein in macrophages has not yet been determined, a phagosomal site has been postulated. Consistent with the proposed role of Nramp1 in macrophage activation, recent studies of the Nramp1 promoter region have revealed consensus sequences associated with responsiveness to IFN-gamma and LPS. Finally, a total of 11 polymorphisms have been identified within the human NRAMP1 gene which are being used to test for linkage of NRAMP1 alleles with human susceptibility to TB and leprosy.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"51-7"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20244731","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}
引用次数: 0
Of microbes, macrophages and nitric oxide. 微生物，巨噬细胞和一氧化氮。
Behring Institute Mitteilungen Pub Date : 1997-03-01
C Bogdan
{"title":"Of microbes, macrophages and nitric oxide.","authors":"C Bogdan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>One of the most prominent functions of nitric oxide (NO) is its participation in antimicrobial and antiviral defense. This paper summarizes the evidence for this function and compiles the infectious agents which are currently thought to be controlled via high out-put generation of NO as it occurs in activated macrophages and other cells expressing the inducible isoform of NO-synthase (iNOS, NOS-2). Several less appreciated forms of interaction between NO and microbes will also be reviewed, including the role of NO as an immunosuppressive or tissue-destructive molecule during the course of infections, the regulation of microbial antioxidant systems by host cell-derived NO, the contribution of NO to parasite stage conversion, the induction or suppression of macrophage iNOS by microbial products, and the existence of endogenous NO synthase pathways in certain bacteria and parasites.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"58-72"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20244732","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}
引用次数: 0
The role of chemokines and accessory cells in the immunoregulation of cutaneous leishmaniasis. 趋化因子和辅助细胞在皮肤利什曼病免疫调节中的作用。
Behring Institute Mitteilungen Pub Date : 1997-03-01
H Moll
{"title":"The role of chemokines and accessory cells in the immunoregulation of cutaneous leishmaniasis.","authors":"H Moll","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The course of infection with Leishmania parasites is determined by the type of the developing CD4+ T cell immune response. Macrophages and Langerhans cells/dendritic cells play a decisive role in the interaction between the parasites and the host's immune system because they serve as host cells, as accessory cells that present parasite antigen, deliver costimulatory signals and secrete cytokines modulating the T cell activity and as effector cells eliminating the microorganisms. Therefore, we put particular emphasis on characterizing the role of these cells in cutaneous leishmaniasis and the factors regulating their activities. Our results show that (1) expression of the chemokine monocyte chemoattractant protein 1 (MCP-1) is associated with macrophage infiltration into the lesion and stimulation of leishmanicidal activity, (2) Langerhans cells are required for the transport of Leishmania from the infected skin to the draining lymph node and initiation of the specific T cell immune response in the early phase of infection, (3) lymph node dendritic cells containing persistent parasites may be involved in the maintenance of specific immunity, (4) Langerhans cells are able to present L. major LPG to T cells and (5) treatment of mice with antigen-pulsed Langerhans cells induces protective immunity against cutaneous leishmaniasis.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"73-8"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20242590","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}
引用次数: 0
Malaria sporozoites and chylomicron remnants compete for binding sites in the liver. 疟疾孢子子和乳糜微粒残余物在肝脏中竞争结合位点。
Behring Institute Mitteilungen Pub Date : 1997-03-01
V Nussenzweig
{"title":"Malaria sporozoites and chylomicron remnants compete for binding sites in the liver.","authors":"V Nussenzweig","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Like Malaria sporozoites and the circumsporozoite protein, remnants of lipoproteins are rapidly cleared from the circulation and enter hepatocytes. Here we review the evidence that the same set of liver heparan sulfate proteoglycans are the initial binding sites of malaria sporozoites and the lipoprotein remnants.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"85-9"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20242592","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}
引用次数: 0
The role of the cytoskeleton in host cell invasion by Toxoplasma gondii. 细胞骨架在刚地弓形虫侵袭宿主细胞中的作用。
Behring Institute Mitteilungen Pub Date : 1997-03-01
J Dobrowolski, L D Sibley
{"title":"The role of the cytoskeleton in host cell invasion by Toxoplasma gondii.","authors":"J Dobrowolski,&nbsp;L D Sibley","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The protozoan parasite Toxoplasma gondii provides a model system for studying invasion by intracellular parasites belonging to the phylum Apicomplexa. Taking advantage of the versatility of T. gondii for genetic and cell biological studies, we have shown that parasite motility and cell invasion are powered by an actin-myosin based motor in the parasite. Unlike bacterial cell uptake, parasite invasion does not involve significant alterations in the host cell cytoskeleton. Instead, invasion is an active process of penetration into the host cell by the parasite. The force for cell penetration is provided by a unique form of substrate-dependent motility termed gliding. Gliding motility is characterized by the rearward capping of surface membrane proteins that propels the parasite forward in a helical spiral. Both actin and myosin are localized beneath the plasma membrane in the parasite where they presumably combine to produce the force necessary for motility. During cell invasion, the rearward capping of cell surface receptors envelopes the parasite in a unique vacuole derived from the host cell plasma membrane. This system offers insights into force generation and motility in a simple organism that is also an important human pathogen.</p>","PeriodicalId":8816,"journal":{"name":"Behring Institute Mitteilungen","volume":" 99","pages":"90-6"},"PeriodicalIF":0.0,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20242593","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}
引用次数: 0
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