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A new simple and rapid in vitro test is proposed for identification of adherent and non-adherent leucocyte subpopulations. The test based on adherence of latex (polystyrene) particles to the cell surface utilizes latex particle suspension commercially available for routine examination of the rheumatoid factor in blood of patients with progressive rheumatoid arthritis.
The initial attachment and the accumulation of Staphylococcus epidermidis on polymer surfaces in multilayered cell clusters embedded in amorphous slime, which together lead to the plastic-adherent phenotype detected by the adherence assay used in this study, have been proposed to be major virulence factors of these bacteria. An antigen specific for plastic-adherent S. epidermidis strains was detected by an indirect immunofluorescence test using absorbed antiserum raised against the strongly plastic-adherent S. epidermidis 1457. A coagglutination assay was established, which allowed the quantitation of the antigen in bacterial extracts under different physiologic growth conditions. Expression of the antigen and of plastic adherence depended significantly on the presence of glucose in the growth medium. Parallel to increased plastic adherence, a 32- to 64-fold increase in the amount of the antigen was detected in bacterial extracts of cells grown in tryptone soya broth (TSB) compared with that in extracts of cells grown in TSB lacking glucose. A parallel time-dependent increase of plastic adherence and expression of the antigen was observed after stimulation by glucose of stationary-phase cultures of plastic-adherent S. epidermidis strains grown in TSB lacking glucose. The antigen consisted most probably of polysaccharide, because its immunologic reactivity was completely abolished by periodate oxidation but was resistant to protease digestion. A significant proportion of cells of plastic-adherent as compared with nonadherent S. epidermidis strains grown in TSB were located in large cell clusters exceeding 50 cells, which completely disintegrated after periodate oxidation of the cell preparations. Periodate oxidation of adherent bacterial films in situ led to release of the adherent cells from the plastic surface. These results strongly indicate a functional relation of the antigen to adherence of S. epidermidis to polymer surfaces, most probably by mediating intercellular adhesion of cells leading to accumulation in multilayered cell clusters.
This study examined the role of fibronectin in promoting particulate attachment to sites of urothelial injury. Variables influencing adherence of the rat transitional carcinoma cell line 4909 and "non-cellular" styrene-divinylbenzene microspheres to fibronectin were studied in an in vitro system. A soluble synthetic peptide fragment (Gly-Arg-Gly-Asp-Ser [GRGDS]) duplicating the receptor binding domain of fibronectin (RGD) was used to determine whether cell adherence could be inhibited by fibronectin receptor blockade. In vitro findings were correlated with an in vivo assay of both cellular and non-cellular particulate adherence to injured urothelium. Time, plated cell density, substrate concentration, GRGDS concentration, and cell viability, were all found to be significant independent variables influencing in vitro cellular adherence (p less than 0.0001). Receptor blockade with GRGDS significantly decreased in vitro tumor cell adherence to fibronectin. In vitro microsphere binding increased as a direct function of fibronectin concentration but was not time dependent (p less than 0.0001 and p = 0.14 for fibronectin concentration and time respectively). The in vivo adherence of both tumor cells and microspheres was significantly increased in injured bladders compared to controls (p less than 0.01). Receptor blockade with GRGDS failed to inhibit in vivo cell adherence to sites of urothelial injury. Microspheres proved to be competitive inhibitors of cellular adherence in competitive binding assays. In vitro microsphere binding demonstrated a pH dependence with maximal binding at pH 7.2. These data suggest that in vitro tumor cell adherence to fibronectin differs from in vivo tumor cell adherence to sites of urothelial injury. Manipulations which inhibit in vitro adherence, specifically fibronectin receptor blockade and cell death, fail to effect in vivo binding to the extreme that non-cellular particulate appears to bind to the same site, and with similar affinity, as cellular particles.
Formalin-fixed human small intestinal mucosa possessing villi and lymphoid follicle epithelium of Peyer's patches at the mucosal surface was used to test the adherence ability of clinically isolated strains of Vibrio cholerae O1. V. cholerae O1 grown on CFA agar for approximately 3 h at 37 degrees C had various levels of cellular hemagglutinins (HAs) and manifested adherence abilities that were roughly correlated with the cellular HA levels, irrespective of cellular HA types. V. cholerae O1 adhered better to epithelium over ileal lymphoid follicles than to epithelium of jejunal or ileal villi. Cells of different morphology which constituted lymphoid follicle epithelium were almost equal targets for adherence. In contrast, V. cholerae O1 grown on CFA agar for approximately 20 h at 37 degrees C in many cases had lower levels of cellular HAs and adherence abilities. Contrary to the above observations with cellular HAs and adherence, piliation of V. cholerae O1 was rather more extensive at approximately 20 h of incubation at 37 degrees C than at approximately 3 h of incubation at 37 degrees C. L-Fucose inhibited adherence to a varied extent depending on the cellular HA types, while D-mannose enhanced adherence in some strains. Heating of V. cholerae O1 diminished adherence ability. This adherence model system provides a tool by which various V. cholerae O1 strains can be preliminarily tested for adherence ability and site in human small intestine.
Improvement in medication adherence is often proposed as a potential advantage of pharmacogenetic-guided prescribing over a traditional one-size-fits-all approach. This paper provides a review of the published literature and presents the findings of studies that measure adherence to medication as an outcome of pharmacogenetic-informed care, or that measure the impact of pharmacogenetic-informed care on psychological factors that are associated with medication adherence. Adherence-related psychological factors are mapped to the Theoretical Domains Framework (TDF) to provide insight into how participants interact with pharmacogenetic-informed care as an intervention and to consider this in the context of medication adherence. A total of 23 studies were included, with 10 quantitative studies measuring medication adherence outcomes associated with pharmacogenetic-informed care. Five of these studies found a statistically significant improvement in adherence in the pharmacogenetic-tested group, two reported a small but non-significant trend, and three showed no difference. Additionally, 13 studies examined the impact of pharmacogenetic-informed care on psychological factors related to adherence. These factors were mapped to 10 TDF domains: knowledge (8 studies); social/professional role and identity (1); beliefs about capabilities (2); optimism (4); beliefs about consequences (10); intentions (5); goals (1); memory, attention and decision processes (7); social influences (4); and emotion (8). The findings suggest that although the evidence for pharmacogenetic-informed care improving medication adherence is mixed and limited, pharmacogenetic-informed care appears to positively influence psychological factors that may support adherence. These include improving knowledge, supporting decision-making and generally being perceived as a positive experience by patients.
F9 and PC13 embryonal carcinoma (EC) cells adhered rapidly to growth substrata coated with fibronectin or laminin. When F9 cells were induced to differentiate into visceral or parietal endoderm-like cells, their ability to adhere to laminin diminished, but their adherence to fibronectin remained unchanged. Correspondingly, permanently differentiated teratocarcinoma-derived endoderm cells (PYS-2 and PSA-5e) adhered markedly less efficiently to laminin than to fibronectin. F9 cells adhered to proteolytic fibronectin fragments containing the cell-binding site but not to fragments containing gelatin- or heparin-binding sites. They also adhered slowly to gelatin, but this adhesion was completely blocked by cycloheximide. The results show that the teratocarcinoma stem cells may have specific mechanisms mediating adhesion to fibronectin and laminin and that endodermal differentiation leads to a reduction in their capacity to adhere to laminin but not to fibronectin.
Adherence of red blood cells from SJL mice suffering of chronic relapsing experimental allergic encephalomyelitis was studied to myelin basic protein coated microtiter plates. Control animals received either bovine serum albumine or "protein-antigen free" adjuvant using the same immunization protocol. Characteristic changes in adherence were found in bovine or human myelin basic protein injected animals compared to the bovine serum albumine immunized group. After a nonspecific increase in adherence between Days 2 to 6 observed in all 3 groups, in the encephalitogen challenged animals on Days 13-14 a marked decrease in red blood cell adherence was detected which maintained at this decreased level during the clinically active stage of the disease and reappeared with the relapse of EAE. No such decreased adherence of red blood cells was observed in BSA immunized animals or in adherence of cells from myelin basic protein injected animals to other basic type protein such as histone. Thus, decreased adherence of red blood cells in animals with EAE appears to be an interestingly unique measure of the disease activity.
Administration of proteose peptone to donors of peritoneal exudate cells resulted not only in quantitative increase in the mono-histiocytic cells but also in their activation as judged by their rapid adherence to surfaces, strong acid phosphatase reaction and increased numbers of lysosomes and phagocytic vacuoles. The three-hour adherent fraction of peritoneal exudate cells (from normal as well as peptone-stimulated mice) contains a large number of activated lymphocytes and fibroblastoid cells and is not enriched in macrophages. Moreover, the adherent cells, when collected by scraping, are unsuitable for immediate biological use since they lose the enzymatic equipment. For purification of histiocytes and macrophages by adherence, the 2-day cultivation of peritoneal cells was found to be optimal, as judged by the number of acid phosphatase positive cells. Their decrease after 4-day cultivation may indicate over-growth of the fibroblast and epithelial cell lineages. The non-adherent fraction was found to be enriched in lymphocytes as well as in mast cells; numerous macrophages were observed, too.
Rat lymph node cells taken at the peak of cytolytic activity following a skin allograft were separated into adherent and nonadherent fractions by incubation on monolayers of thoracic duct lymphocytes either of the same strain as the graft donor or of an Ag-B different strain. In the face of a 3-fold enrichment of cytolytic activity in the adherent cells and a 3-fold depletion in the nonadherent cells there was no detectable partition of graft-vs-host (GVH) activity. Supplementary experiments supported the simplest interpretation of this finding, namely that the antigen receptors on GVH-reactive cells did not influence their adherence in this system. Similarly, there was no partition of the GVH activity of nonimmune lymph node cells by adherence. Labeling lymph node cells with either radioactive uridine or thymidine in vitro, suggested that about 20% of DNA-synthesizing cells in the immune population adhered because of antigen recognition.
The ability of enzyme-dissociated synovial adherent cells (SAC) obtained from patients with active rheumatoid arthritis to restore the proliferation and differention of peripheral blood mononuclear non-adherent cells (NAC) into immunoglobulin-secreting cells (ISC) was investigated. Autologous combinations of cells were used in this study to eliminate allogeneic reactions. Peripheral blood NAC, prepared by glass adherence and leucine methylester treatment to remove monocytes, almost completely lost their capacity to proliferate and differentiate into ISC in response to pokeweed mitogen. The response of NAC was restored by adding 12.5% of 'fresh SAC', which was obtained by glass-adherence after an overnight culture of non-rosette forming, enzyme-dissociated rheumatoid synovial cells. Although the response was also restorable by adding more than 25% fresh SAC, this was less satisfactory than adding 12.5% SAC. 'Old SAC', obtained by glass-adherence after 7 days culture of enzyme-dissociated synovial cells, did not restore the response of NAC. Immunohistochemical studies showed that 55% of fresh SAC and 3% of old SAC expressed HLA-DR antigens. When 100 units/ml of interferon gamma was present, 25% of old SAC remained HLA-DR-positive and some of these cells retained a dendritic morphology after 7 days culture. The results indicate that rheumatoid synovia contain macrophage-like cells that can effectively support the ultimate differentiation of lymphocytes to ISC.
EPEC adherence factor (EAF) plasmids from three strains of enteropathogenic Escherichia coli (EPEC) - E2347/69 (O127:H6), E20517 (O111:H2) and E24582 (O142:H6) - were examined. The EAF plasmids were all marked with ampicillin resistance by transposition of Tn801 to give pDEP1, pDEP2 and pDEP11, respectively. All three plasmids showed incompatibility with an FIme and an FIV plasmid and had some similarity in restriction enzyme digest patterns. Plasmid pDEP1 differed from pDEP2 and pDEP11 in being autotransferring and fertility-inhibition positive. An EAF probe consisting of a 1 kb BamHI-SalI restriction endonuclease fragment of the prototype EAF-associated plasmid pMAR2 hybridized to similar-sized SalI-BamHI fragments of pDEP1 and pDEP11 but to a different-sized fragment of plasmid pDEP2. Loss of the EAF plasmids from EPEC strains resulted in a marked reduction in the ability of these strains to adhere to HEp-2 cells. The EAF-plasmid-negative variants did not express a 94 kDa outer-membrane protein (OMP). When these EAF plasmids were reintroduced into EAF-plasmid-negative EPEC strains a high level of adherence equivalent to that of the parent EPEC strains was restored and a 94 kDa OMP was usually expressed. However, when EAF plasmids were transferred into E. coli K12 or non-EPEC E. coli the host strains either did not adhere or adhered poorly to the HEp-2 cells. These transconjugants did not express a 94 kDa OMP.
Our previous study showed the occurrence of Branhamella catarrhalis (B. catarrhalis) pulmonary infections which varies seasonally. To investigate the role of normal throat microflora in this seasonal variation of the occurrence of B. catarrhalis infection, seventy seven throat cultures were done in 45 patients with chronic pulmonary diseases from January to December in 1985. The isolation rate of Corynebacterium species as normal microflora was relatively higher in summer than in winter. Therefore in vitro competitive adherence to human epithelial cells between Corynebacterium pseudodiphtheriticum (C. pseudodiphtheriticum) and B. catarrhalis was done to examine bacterial interference. Preincubation or simultaneous incubation of C. pseudodiphtheriticum reduced the number of B. catarrhalis adherent to epithelial cells (p less than 0.02). The mean number of adherent C. pseudodiphtheriticum (average; 13.86) was higher than that (average; 1.22) of adherent B. catarrhalis. There was no antagonism in the growth on blood agar between C. pseudodiphtheriticum and B. catarrhalis. These findings suggest Corynebacterium species as normal throat microflora may interfere the adherence of B. catarrhalis to human epithelial cells and may protect against colonization and infection with B. catarrhalis. Bacterial interference of Corynebacterium species may be associated with the low occurrence of B. catarrhalis pulmonary infections in summer.
Mouse bone marrow-derived adherent cell populations promoted proliferation of haemopoietic cells in vitro in a liquid culture system for at least 4 weeks. Adherent cell layers derived from other haemopoietic organs (foetal liver, adult spleen) and fibroblasts from embryonic tissues did not maintain haemopoietic cells in this system. Medium, conditioned by adherent cells derived from foetal liver, spleen and embryonic tissues displayed a considerable colony stimulating activity (CSA). Marrow-derived adherent cells produced no detectable CSA. A possible relationship between the in vitro expression of a growth-promoting activity of an adherent cell population on haemopoietic cells, and its endogenous CSA production, is discussed.
This study examined the specific tumoricidal activity of lymphokine-activated killer (LAK) cells derived from tumor-infiltrating lymphocytes that prevent the growth of secondary tumors in animals harboring progressing primary tumors. A pre-implanted gelatin sponge was employed to capture infiltrating host effectors during the expression of concomitant tumor immunity. Additionally, this study compared the cytolytic activity of these sponge-derived cells with those of counterpart splenic lymphocytes. The cells from both sources were cultured for 4 days in IL-2 to generate LAK cells which were further expanded in IL-2-containing medium for up to 11 days. The cytotoxic activities of these cells were measured in a Chromium-51 release assay. The data revealed that the culture of splenic, or sponge-derived lymphocytes results in the emergence of non-adherent and adherent cell populations with LAK activity. The 4-day sponge-derived LAK cells (adherent and non-adherent) exhibited significant cytolysis of EMT6 cells while the spleen-derived counterparts showed minimal cytotoxicity toward these targets. Some NK activity in LAK cells derived from both sources was evident by their lysis of YAC-1 cells. LAK cells from both sources were incapable of lysing histo-compatible EL-4 (H-2b) tumor cells. The lysis of the EMT6 cells by the sponge-derived LAK cells was maintained over an 11-day period of culture in IL-2. Conversely, the spleen-derived LAK cells were unable to significantly lyse EMT6 cells during this period of in vitro culture. These results show the superior specific tumoricidal activity of LAK cells derived from lymphocytes mediating tumor rejection in vivo (sponge-derived) over that of counterpart splenic lymphocytes.
The binding of PMNs to extracellular matrix and cells is crucial to PMN host defense. Adherence mechanisms and the many families of molecules involved are major areas of study. We present here details of an enzyme-assessed microtiter plate assay for neutrophil adherence. This assay uses low numbers of cells (50,000/well) and permits analysis of several hundred wells in a short period of time, by using an ELISA reader. With this assay we observed 5- to 10-fold increases in the number of adherent human PMNs in response to nanogram amounts of LPS or as little as 5.0 micrograms/ml of aggregated IgA. Although fluoride blocked the LPS-induced adherence response, IgA-induced cell binding was largely unaffected.
Adherent enteropathogenic Escherichia coli 0119 strains had a larger lipopolysaccharide core than non-adherent strains, although the O-chains were identical. The core from the non-adherent strain 19392 contained five hexose residues in the outer region, with three L-glycero-D-manno-heptose residues and 3-deoxy-D-manno-octulosonic acid (KDO) in the inner region. The core of adherent strain JCP88 had an atypical structure consisting of six hexose residues, KDO, and equimolar amounts of L-glycero-D-manno-heptose and D-glycero-D-manno-heptose. The core of a rough JCP88 mutant resembled an incomplete 19392 core.
Recombinant human tumor necrosis factor (TNF) and recombinant human lymphotoxin (LT) were analyzed for their effects on inflammation-related functions of human polymorphonuclear neutrophilic granulocytes (PMN) in vitro, TNF at a concentration of 10 U/ml (corresponding to 10(-11) mol/l) enhanced PMN adherence to nylon fibres. It strongly inhibited the chemotactic migration of PMN in the Boyden chamber assay towards the chemotactic tripeptide formyl-methionyl-leucyl-phenylalanine (FMLP), C5a, LTB4 and a monocyte-derived chemotaxin (MOC) without affecting random migration and without being chemotactic itself. It did not stimulate superoxide anion (-O2.) production of PMN in suspension. However, it induced considerable -O2. release from PMN that had become adherent on nylon fibres. All these effects were abrogated by prior incubation of the cytokine with polyclonal and monoclonal antibodies against TNF. LT concentrations of 1,000 U/ml or higher were required to observe a moderate inhibition of chemotactic migration towards the above chemotactic factors and to elicit some -O2. production from nylon fibre-adherent PMN. LT did not increase the adherence of PMN to nylon fibres and it was not chemotactic. The results indicate that TNF is a potent modulator of PMN functions.
Cell-mediated cytotoxicity of adherent and non-adherent subpopulations of mouse lymph node cells sensitized in vitro on monolayers of syngeneic, methylcholanthrene-induced sarcoma cells was examined by inhibition of 3H-thymidine incorporation. The cell-mediated cytotoxicity of nylon wood-adherent, non-adherent and unfractionated lymph node cells was found to be equally efficient.