• Journal of Life Science
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• v.15 no.4 s.71
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• pp.641-646
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• 2005

An approximately 10-fold higher level of adherence of Salmonella typhimurium strain TML to Int-407 cells was observed with organisms grown in Luria broth or in high-iron containing medium than those grown in low-iron containing medium. Iron specifically enhanced adherence, while other cations such as calcium, cobalt, copper, potassium, magnesium and manganese did not. It was suggested that iron did not act as a passive ligand - probably it stimulated production of bacterial factors necessary for adherence. A similar pattern of iron modulation of adhesiveness was also seen in Salmonella mutants with single or different combinations of multiple mutations in genes encoding the mannose sensitive hemagglutinin (type 1 fimbriae), mannose resistant hemagglutinin and flagellum. The adhesiveness of an isogenic fur mutant was modulated by iron in a manner similar to the wild-type strain, suggesting that iron modulation of adherence is independent of the fur gene product.

• Tuberculosis and Respiratory Diseases
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• v.43 no.2
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• pp.210-220
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• 1996

Background : Neutrophils or monocytes separated in vitro by the adherence to plastic surface are known to be activated by surface adherence itself and subsequent experimental data might be altered by surface adherence. In the process of surface adherence, adhesion molecules have a clear role in intracellular signal pathway of cellular activation. Human alveolar macrophages(HAM) are frequently purified by the adherence procedure after bronchoalveolar lavage. But the experimental data of many reports about alveolar macrophages have ignored the possibility of adhesion-induced cellular activation. Method : Bronchoalveolar lavage was performed in the person whose lung of either side was confirmed to be normal by chest CT. With the measurement of hydrogen peroxide release from adherent HAM to plastic surface and non-adherent HAM with or without additional stimulation of phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine (fMLP), we observed the effect of the adherence to plastic surface. We also evaluated the effect of various biological surfaces on adhesion-induced activation of HAM. Then, to define the intracellular pathway of signal transduction, pretreatment with cycloheximide, pertussis toxin and anti-CD11/CD18 monoclonal antibody was done and we measured hydrogen peroxide in the culture supernatant of HAM. Results : 1) The adherence itself to plastic surface directly stimulated hydrogen peroxide release from human alveolar macrophages and chemical stimuli such as phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine(fMLP) colud not increase hydrogen peroxide release in these adherent macrophages which is already activated. 2) PMA activated human alveolar macrophages irrespective of the state of adhesion. However, fMLP stimulated the release of hydrogen peroxide from the adherent macrophages, but not from the non-adherent macrophages. 3) HAM adherent to A549 cell(type II alveolar epithelium-like human cell line) monolayer released more hydrogen peroxide in response to both PMA and fMLP. This adherence-dependent effect of fMLP was blocked by pretreatment of macrophages with cycloheximide, pertussis toxin and anti-CD18 monoclonal antibody, Conclusion : These results suggest that the stimulatory effect of PMA and fMLP can not be found in adherent macrophage because of the activation of human alveolar macrophage by the adherence to plastic surface and the cells adhered to biologic surface such as alveolar epithelial cells are appropriately responsive to these stimuli. It is also likely that the effect of fMLP on the adherent macrophage requires new protein synthesis via G protein pathway and is dependent on the adhesion between alveolar macrophages and alveolar epithelial cells by virtue of CD11/CD18 adhesion molecules.

• Journal of Microbiology and Biotechnology
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• v.12 no.5
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• pp.746-752
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• 2002

The purpose of the present study was to examine the antagonistic activities of Enterococcus faecalis strain PL9003 (PL9003) on Helicobacter pylori. This strain was isolated from infant feces and found to inhibit both the growth of H. pylori and its in vitro adherence to the human gastric cell line MKN-45. The binding of PL9003 to MKN-45 was observed under a light microscope after Cram staining and under a scanning electron microscope. When detected with an FITC-conjugate antibody, both viable and nonviable PL9003 were found to decrease the number of H. pylori bound to MKN-45. When detected by an enzyme-linked immunoabsorbent assay, about 70% of the H. pylori bound on MKN-45 disappeared with the four-1314 addition of viable or nonviable PL9003. The spent culture supernatant (SCS) of PL9003 also decreased the viability of H pylori even after neutralization and pepsin treatment. The above results suggest that PL9003 has a potential as a new probiotic for the stomach.

• Archives of Plastic Surgery
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• v.47 no.4
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• pp.371-371
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• 2020

• IMMUNE NETWORK
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• v.13 no.4
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• pp.148-156
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• 2013

The $PrP^C$ is expressed in many types of immune cells including monocytes and macrophages, however, its function in immune regulation remains to be elucidated. In the present study, we examined a role for $PrP^C$ in regulation of monocyte function. Specifically, the effect of a soluble form of $PrP^C$ was studied in human monocytes. A recombinant fusion protein of soluble human $PrP^C$ fused with the Fc portion of human IgG1 (designated as soluble $PrP^C$-Fc) bound to the cell surface of monocytes, induced differentiation to macrophage-like cells, and enhanced adherence and phagocytic activity. In addition, soluble $PrP^C$-Fc stimulated monocytes to produce pro-inflammatory cytokines such as $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6. Both ERK and $NF-{\kappa}B$ signaling pathways were activated in soluble $PrP^C$-treated monocytes, and inhibitors of either pathway abrogated monocyte adherence and cytokine production. Taken together, we conclude that soluble $PrP^C$-Fc enhanced adherence, phagocytosis, and cytokine production of monocytes via activation of the ERK and $NF-{\kappa}B$ signaling pathways.

• The Journal of Korean Medicine
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• v.22 no.1
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• pp.46-52
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• 2001

Objectives: This experimental study was carried out to evaluate the effects of PSM(polysaccharide of mushroom) on the immune activity. Methods: The following were performed; Immunotoxicity testing for immunopathology, IgO production & LPS mitogen response for humoral immunity, DTH, ConA mitogen response for cell-mediated immunity, and macrophage adherence & phagocytosis for nonspecific immunity in vitro or in vivo. Results: PSM showed a protective effect on cyclophosphamide-induced leukopenia, increased IgG production and lymphoproliferative responses to LPS; inhanced DTH and lymphoproliferative response Con A; and activated macrophage adherence and phagocytosis to SRBC. Conclusions: It is suggested that PSM can be used for cancer patients with immunosuppression and adapted to many other diseases.

• YAKHAK HOEJI
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• v.53 no.3
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• pp.119-124
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• 2009

Cell-cell adhesion managed by various adhesion molecules plays an important role in regulating functional activation of cells. This event mediates attachment of inflammatory cells to endothelial cells, interaction of antigen-presenting cells with T cells and metastatic adherence of cancer cells to epithelial tissue cells. Therefore, this cellular response is considered as one of therapeutic target to treat various cancers and inflammatory diseases. To develop proper model for evaluation of functional activation of adhesion molecules, the ability of U937 and Jurkat T cells responsive to various adhesion inducers such as phorbal-12-myristate-13-acetate (PMA), staurosporin and monoclonal antibodies to CD29, CD43 and CD98 was investigated using quantitative cell-cell adhesion assay. U937 cells made more cell-cell clusters by the treatment of antibodies to CD29 and CD43 than Jurkat T cells, while Jurkat T cells exhibited increased cell-cell adhesion ability in CD98 antibody treatment. In agreement, the surface levels of CD29 and CD98 were highly observed in U937 and Jurkat T cells, respectively. Therefore, our data suggest that Jurkat T and U937 cells can be used for model system to evaluate functional activation of adhesion molecules such as CD29 and CD98.

• Journal of Applied Biological Chemistry
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• v.64 no.4
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• pp.357-362
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• 2021

In this study, to investigate the anticariogenic effect of red ginseng, the antibacterial effect, cell adherence and biofilm formation inhibitory effect of n-hexane extract of red ginseng marc (HERGM) against Streptococcus mutans, the causative bacteria of caries, were measured. The growth of S. mutans was inhibited in proportion to the concentration of HERGM, and was hardly observed at a concentration above 125 ㎍/mL (MIC =125 ㎍/mL). It was found that HERGM acts on the cell membrane and the nucleic acid component of the cell was leaked. In addition, HERGM inhibited the adherence and biofilm formation of S. mutans by more than 90% at a concentration of 125 ㎍/mL. GTase activity was completely inhibited at a concentration of 50 ㎍/mL of HERGM. In conclusion, it was found that HERGM commonly inhibited the growth and biofilm formation of S. mutans.

• IMMUNE NETWORK
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• v.3 no.3
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• pp.176-181
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• 2003

Background: The molecular basis of follicular dendritic cells (FDC)-germinal center (GC) B cell interaction is largely unknown, although this cellular interaction is thought to be important for the whole process of GC B cell differentiation. Methods: Using FDC-like cells, HK, and highly purified GC B cells, we attempted to identify the molecules that play critical roles in the interactions between FDC and B cells. GC B cells were co-cultured with HK cells and soluble CD154 in the presence or absence of various function-blocking monoclonal antibodies to examine their effect on GC B cell binding to HK cells and B cell proliferation. Results: Anti-CD11a and anti-CD54 antibodies inhibited GC B cell binding to HK cells while anti-CD49d and anti-CD106 antibodies did not. GC B cell proliferation was not impaired by the disruption of GC B cell-HK cell adherence. Conclusion: Our results suggest that CD11a/CD18-CD54 interactions play an important roles in the initial binding of GC B cells to FDC and diffusible growth factors from FDC may be responsible the massive proliferation of GC B cells.

• Asian-Australasian Journal of Animal Sciences
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• v.20 no.4
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• pp.569-576
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• 2007

Four hundred and fifty tilapias ($6.77{\pm}0.23$ g) were assigned randomly to six groups to evaluate the feasibility of the tested antibacterial peptides (ABPs) and oligosaccharides as substitutes for antibiotics. The control group was fed with a commercial tilapia diet; other five groups were fed with the same commercial diet supplemented with konjac glucomannan (KGLM), cluster bean galactomannan (CBGAM), and three animal intestinal ABPs derived from chicken, pig and rabbit at 100 mg/kg respectively. After 21 days of feeding, growth, disease resistance, and in vivo anti-adherence were determined. Furthermore, the inhibitory effect of tested agents on adhesion of Aeromonas veronii biovar sobria (A.vbs) strain BJCP-5 to tilapia enteric epithelia in vitro was assessed by cell-ELISA system. As a result, the tested agents supplemented at 100 mg/kg show significant benefit to tilapia growth and disease resistance (p<0.05), and the benefit may be correlated with their interfering in the contact of bacteria with host mucosal surface. Although none of the tested agents did inhibit the growth of BJCP-5 in tryptic soy broth at $100{\mu}g/ml$, all of them did inhibit the adhesion of A.vbs to tilapia enteric epithelia in vivo and in vitro. In vitro mimic assays show that three ABPs at low concentrations of $25{\mu}g/ml$ and $2.5{\mu}g/ml$ have the reciprocal dose-dependent anti-adherence effect. The inhibition of ABPs may be correlated with a cation bridging and/or receptor-ligand binding, but not with hydrophobicity. The KGLM and CBGAM inhibited the adherence of BJCP-5 to tilapia enteric epithelia with dose-dependent manner in vitro, and this may be through altering bacterial hydrophobicity and interfering with receptor-ligand binding. Our results indicate that the anti-adherence of the tested ABPs and oligosaccharides may be one of the mechanisms in promoting tilapia growth and resistance to A.vbs.