{"title":"Amelioration of established Sendai viral pneumonia in the nude mouse using a monoclonal antibody to the virus fusion protein.","authors":"P Carthew, J Riley, D Dinsdale","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The pathological effect of parainfluenza type I (Sendai virus) is known to be a bronchopneumonia, which becomes a chronic pneumonia in the immunodeficient athymic (nude) mouse. The severity of this established chronic pneumonia can be dramatically altered by providing the nude mouse with humoral monoclonal antibodies which are neutralizing, and are directed against the fusion protein, of the virus. The alveolitis, which is a significant part of the pathology, is suppressed due to a reduction (greater than 90%) in the number of virus-infected alveolar macrophages present in the alveoli. This clearly identifies the infected alveolar macrophage as the primary effector cell in the pathogenesis of alveolitis caused by parainfluenza virus type I. The implications of using virus-neutralizing monoclonal antibodies, which have little immunomodulatory toxicity, in the treatment of viral pneumonias are discussed.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 6","pages":"727-35"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040719/pdf/brjexppathol00150-0126.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13700852","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":"Enhancement of inflammatory reactions in a non-immunological air pouch model in rats.","authors":"M Isaji, Y Momose, J Naito","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In a carboxymethyl cellulose (CMC) air pouch inflammation model, accumulation of exudate decreased at a relatively rapid rate and almost disappeared 3 days after a 2% CMC injection into the preformed air pouch. After a second injection of 2% CMC solution into the 1-day-old CMC pouch on the day following the first CMC injection, the decrease in rate of exudate was similar to the change seen after the first CMC injection. In another group of rats, 3 days after the first CMC injection when inflammation had subsided, a second injection of 2% CMC solution into the 3-day-old CMC pouch resulted in a marked increase of exudate accumulation, inflammatory cell infiltration and vascular permeability. Histologically, large numbers of macrophages accumulated in the 3-day-old CMC pouch and fibroblast proliferation and newly formed blood vessels were also visible. The enhanced exudative reaction was significantly inhibited by dexamethasone but not by indomethacin. These results indicate that the enhanced inflammatory reactions appear to be closely correlated with the increase of reactivity at the site of inflammation and the exudative reaction was not mediated by cyclo-oxygenase products.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 6","pages":"705-16"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040720/pdf/brjexppathol00150-0105.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13746820","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":"Biosynthesis of interleukin-I beta at inflammatory site in rabbits: kinetics and producing cells.","authors":"F Goto, K Goto, S Mori, S Ohkawara, M Yoshinaga","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Biosynthesis of interleukin-I beta (IL-I beta) by inflammatory peritoneal exudate cells (PEC) was studied in terms of biological activity (thymocyte co-mitogenic assay), IL-I beta mRNA expression (cytoplasmic slot blot analysis) and detection of immunoreactive IL-I beta molecule (immunocytochemistry). Our findings were taken to conclude that IL-I beta expression was observed only in PEC harvested from early inflammatory site and the kinetic profile of the IL-I activity during the course of the inflammation was explained by IL-I beta mRNA expression, namely de-novo synthesis by inflammatory exudate cells. With respect to a single cell level, it was definitely proved that polymorphonuclear leucocytes were the major producer of IL-I beta during the casein-induced acute inflammation in rabbits.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 6","pages":"597-606"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040718/pdf/brjexppathol00150-0005.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13832125","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":"Quantitative evaluation of myocardial injury induced by acute cerebral ischaemia and its prevention by beta 1-adrenergic blockade. An ultrastructural morphometry study.","authors":"A Kolin, A Brezina, A J Lewis, J W Norris","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The protective effects of beta 1-adrenergic blockade with metoprolol (Betaloc Astra) were demonstrated in the gerbil model of myocardial injury provoked by acute ischaemic brain lesions. The myocardial injury was reversible and lipid droplet accumulation was its most striking morphological feature. These droplets were easy to measure in EM photographs and their size was expressed as percentage of sarcoplasmic volume. The EM data of fat accumulation were compared in hearts of carotid-ligated animals with and without metoprolol pretreatment, and in animals with the carotid isolated only, at standard intervals 3-48 h after operation. While in carotid-ligated-only animals the average myocardial fat contents rose to a peak of 1.9% at 10 h, in metoprolol pretreated animals the amount of fat was always significantly lower and started to return earlier to basal values (peak at 6 h, 1.1%). In carotid-isolated-only animals, fat accumulation peaked at 6-10 h (1.1%) and returned quickly to normal levels (0.34 +/- 0.18%). This effective pharmacological blockade with metoprolol strongly supports the concept of catecholamine mediation between acute intracranial lesions and myocardial injury. The background and significance of myocardial fat accumulation is discussed. The EM morphometry of fat droplets appears to be a suitable tool for quantification of reversible myocardial damage most useful for experimental evaluation of cardioprotective measures. As changes in succinic dehydrogenase histochemistry (from 'myofibrillar' to 'granular' pattern) correlated with EM measured fat accumulation, the simplicity and speed of the SDH method recommends itself for fast orientation about presence of myocardial damage.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 6","pages":"659-67"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040714/pdf/brjexppathol00150-0063.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13746816","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":"Heterogeneity of hepatocyte antigen expression in rat liver carcinogenesis: concordance between neoplastic nodules and tumours.","authors":"M J Embleton, H S James, A J Haynes, P C Butler","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Fischer F344 rats were given a cyclical diet of 0.06% 2-acetylaminofluorene (AAF), which progressively induced oval cell proliferation, cirrhosis and hyperplastic (or neoplastic) nodules. Primary liver tumours developed from 7 months after ceasing the diet. Liver samples taken during and after AAF administration and specimens of primary tumours were processed into frozen sections and examined microscopically for morphological changes in cell populations, stained histochemically for gamma-glutamyl transpeptidase (GGTase) and four phosphatases, and stained by the immunoperoxidase technique for the presence of antigens detected by seven anti-liver cell monoclonal antibodies and monoclonal antibodies to six oncoproteins. During and after AAF treatment several of the anti-liver antibodies revealed foci of aberrantly or heterogeneously-stained cells, although anti-oncoprotein antibodies showed no consistent changes. Foci of cells positive for GGTase and heterogeneous for adenosine triphosphatase (ATPase) were also seen. Nodules invariably showed heterogeneous antigenicity, raised GGTase and abnormal ATPase expression. Primary tumours exhibited varying degrees of positivity, negativity and heterogeneity with the anti-liver monoclonal antibodies, and all were positive for GGTase. Comparison between various parameters and different lesions showed the greatest concordance between nodules and tumours, suggesting that nodules are probably the precursors of malignant tumours in this system.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 6","pages":"647-57"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040721/pdf/brjexppathol00150-0052.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13676361","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":"Immunoregulation in Heymann nephritis. II. Functional studies.","authors":"J Cornish, A Z Barabas, R Lannigan, J Rozing","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In this study, the functional properties of the cells involved in the immunoregulation of Heymann nephritis (HN) have been investigated. HN is a disease model in the rat where the pathology closely resembles membranous glomerulonephropathy (MGN) in man. This autoimmune model is induced by injection of renal tubular antigen (RTA) incorporated in Freund's complete adjuvant (FCA). The strong B cell and plasma cell response in the chronic phase of HN, as determined by cell marker analyses, is predominantly antigen-non-specific. The secondary response pattern found was not only to RTA upon repeated immunization, but also to non-related antigen (SRBC). Although cell marker studies have indicated no major quantitative changes in the T cell population throughout the development of HN, a severe deregulation of the cellular immune response is observed especially during the induction period of HN. This was shown by a strong decrease of the mitogen-induced proliferative response and IL-2 production. This phenomenon is caused by both defective cellular components and inhibitory serological factors. Finally, in the chronic phase, these aberrations gradually return to normal.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"505-13"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040602/pdf/brjexppathol00149-0015.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13956227","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":"Immunoregulation in Heymann nephritis. I. Cell marker studies.","authors":"J Cornish, A Z Barabas, R Lannigan, J Rozing","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Immunoregulation was examined in rats with Heymann nephritis (HN), an established model of membranous glomerulonephropathy (MGN). There is little known of the cellular immune events for the induction and maintenance of the autoimmune response in HN. The cell marker studies utilized fluorescein (FITC)-labelled monoclonal antibodies directed to B cells (Mark-I), and T cell subsets: pan T (ER-I), helper/inducer T (ER-2) and suppressor/cytotoxic T (ER-3). Lymphoid subsets were compared in spleen, lymph nodes, peripheral blood and bone marrow, of normal and diseased rats. Animals were investigated during the induction and chronic phases of disease. The induction of HN was associated with an early, significant, but transient increase of the non-specific myeloid component of the defence system. Subsequently, a significant increase was seen in the number of cells of the B lymphocyte lineage in HN animals, which coincided well with the overall increased humoral immune responsiveness. No alterations in the T lymphocyte subsets were noted during the development of this experimental autoimmune disease.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"495-504"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040593/pdf/brjexppathol00149-0005.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13824911","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}
N S Fernando, N W Boyce, S R Holdsworth, T J Neale
{"title":"Localization of antiglomerular basement membrane-binding polyclonal antibodies in rat lung and kidney using post-embedding immunogold electron microscopy.","authors":"N S Fernando, N W Boyce, S R Holdsworth, T J Neale","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Post-embedding immunogold electron microscopy (IAuEM) techniques utilizing low-temperature embedding in Lowicryl K4m and LR White resin were used to localize the binding sites of two sheep anti-rat glomerular basement membrane polyclonal antibodies (P1 and P2) and a sheep anti-rat lung antigen antibody. P1 localization was bilaminar in a linear pattern along the subepithelial and particularly the subendothelial aspect of the glomerular basement membrane. P2 was bound diffusely throughout the lamina densa, even at supramaximal doses. The anti-lung antibody bound in an interrupted linear pattern throughout the lung basement membrane (alveolar and capillary), and showed an intense, diffuse binding to the glomerular basement membrane. IAuEM allowed definition of the precise basement membrane binding sites of these polyclonal reagents.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"557-65"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040599/pdf/brjexppathol00149-0063.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13957461","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":"Membrane N-acetylglucosamine: expression by cells in rheumatoid synovial fluid, and by pre-cultured monocytes.","authors":"M Sharif, L S Wilkinson, J Edwards, G A Rook","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>After 21-48 h in culture, 2-8% of human peripheral blood monocytes strongly express terminal N-acetylglucosamine (GlcNAc) on their membranes. This can be detected with a monoclonal antibody selected for binding to asialo-agalacto-fetuin, and is eliminated by incubating the cells in pure N-acetylglucosaminidase. Expression of GlcNAc is transient, and can no longer be detected by day 4. These cells are a subset of macrophages since they are positive for non-specific esterase and stained by the monoclonal antibody EBM 11. GlcNAc-positive cells showing double staining with monoclonal antibodies UCHM1 and RFD7 were detected. Their numbers were not influenced by the addition of GM-CSF, IFN-gamma, 1,25-(OH)2 cholecalciferol or indomethacin. Macrophages which give membrane staining for terminal GlcNAc were also found in rheumatoid synovial fluid, and in synovial tissue, though in the peripheral blood their frequency was the same in samples from normal donors and from patients with rheumatoid arthritis. Immunoblots of 24-48-h monocyte cultures or of fresh synovial fluid cells using the anti-GlcNAc monoclonal, show the anticipated agalactosyl IgG heavy chains, and an additional band of 70-80kDa.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"567-77"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040600/pdf/brjexppathol00149-0072.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13824912","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":"Prostanoid release by macrophages at a distance from an inflammatory site.","authors":"M Tissot, S Strzalko, A Thuret, J P Giroud","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>During the development of an acute inflammatory reaction induced in the rat pleural cavity by dextran, calcium pyrophosphate, saline or phosphate buffered saline, macrophages present at a distant site (peritoneal cavity) display an increased capacity to release prostanoids: prostaglandins, prostacyclin and thromboxane. Enhanced levels of 6-keto-PGF1 alpha were observed both in peritoneal lavages (experiments in vivo) and in macrophage supernatants after 24-h culture (experiments in vitro). TXB2 levels were mainly increased in peritoneal lavages and PGE2 in culture supernatants. In vivo, levels of prostanoids in the peritoneal cavity reached a maximum 24 h after the induction of pleurisy whatever the injected substance. In vitro, amounts of arachidonic acid metabolites were highest in supernatants of cultured peritoneal macrophages harvested 72 h after the pleural injection of dextran or CaPP. These results show that the regulation of macrophage functions is closely related to prostanoid production, especially the release of PGE2 and PGI2.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"525-31"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040592/pdf/brjexppathol00149-0033.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13956229","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}