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Katsuya Gomi - One of the best experts on this subject based on the ideXlab platform.

  • Cell Wall α 1 3 glucan prevents α amylase adsorption onto fungal Cell in submerged culture of aspergillus oryzae
    Journal of Bioscience and Bioengineering, 2017
    Co-Authors: Silai Zhang, H Sato, Takahiro Shintani, Sakurako Ichinose, Mizuki Tanaka, Ken Miyazawa, Akira Yoshimi, Katsuya Gomi
    Abstract:

    We have previously reported that α-amylase (Taka-amylase A, TAA) activity disappears in the later stage of submerged Aspergillus oryzae culture as a result of TAA adsorption onto the Cell Wall. Chitin, one of the major Components of the Cell Wall, was identified as a potential factor that facilitates TAA adsorption. However, TAA adsorption only occurred in the later stage of cultivation, although chitin was assumed to be sufficiently abundant in the Cell Wall regardless of the submerged culture period. This suggested the presence a factor that inhibits TAA adsorption to the Cell Wall in the early stage of cultivation. In the current study, we identified α-1,3-glucan as a potential inhibiting factor for TAA adsorption. We constructed single, double, and triple disruption mutants of three α-1,3-glucan synthase genes (agsA, agsB, and agsC) in A. oryzae. Growth characteristics and Cell Wall Component analysis of these disruption strains showed that AgsB plays a major role in α-1,3-glucan synthesis. In the ΔagsB mutant, TAA was adsorbed onto the mycelium in all stages of cultivation (early and later), and the ΔagsB mutant Cell Walls had a significantly high capacity for TAA adsorption. Moreover, the α-1,3-glucan content of the Cell Wall prepared from the wild-type strain in the later stage of cultivation was markedly reduced compared with that in the early stage. These results suggest that α-1,3-glucan is a potential inhibiting factor for TAA adsorption onto the Cell Wall Component, chitin, in the early stage of submerged culture in A. oryzae.

  • identification of potential Cell Wall Component that allows taka amylase a adsorption in submerged cultures of aspergillus oryzae
    Applied Microbiology and Biotechnology, 2011
    Co-Authors: H Sato, Yoshiyuki Toyoshima, Takahiro Shintani, Katsuya Gomi
    Abstract:

    We observed that α-amylase (Taka-amylase A; TAA) activity in the culture broth disappeared in the later stage of submerged cultivation of Aspergillus oryzae. This disappearance was caused by adsorption of TAA onto the Cell Wall of A. oryzae and not due to protein degradation by extraCellular proteolytic enzymes. To determine the Cell Wall Component(s) that allows TAA adsorption efficiently, the Cell Wall was fractionated by stepwise alkali treatment and enzymatic digestion. Consequently, alkali-insoluble Cell Wall fractions exhibited high levels of TAA adsorption. In addition, this adsorption capacity was significantly enhanced by treatment of the alkali-insoluble fraction with β-glucanase, which resulted in the concomitant increase in the amount of chitin in the resulting fraction. In contrast, the adsorption capacity was diminished by treating the Cell Wall fraction with chitinase. These results suggest that the major Component that allows TAA adsorption is chitin. However, both the mycelium and the Cell Wall demonstrated the inability to allow TAA adsorption in the early stage of cultivation, despite chitin content in the Cell Wall being identical in both early and late stages of cultivation. These results suggest the existence of unidentified factor(s) that could prevent the adsorption of TAA onto the Cell Wall. Such factor(s) is most likely removed or diminished from the Cell Wall following longer cultivation periods.

Susanne Eschenburg - One of the best experts on this subject based on the ideXlab platform.

Seung Hyun Han - One of the best experts on this subject based on the ideXlab platform.

  • Wall teichoic acid is an essential Component of staphylococcus aureus for the induction of human dendritic Cell maturation
    Molecular Immunology, 2017
    Co-Authors: Sung Jun Hong, Sun Kyung Kim, Cheolheui Yun, Seung Hyun Han
    Abstract:

    Staphylococcus aureus is a Gram-positive pathogen that can cause chronic skin inflammation, pneumonia, and septic shock. The immunomodulatory functions of Wall teichoic acid (WTA), a glycopolymer abundantly expressed on the Gram-positive bacterial Cell Wall, are poorly understood. Here, we investigated the role of WTA in the phenotypic and functional activation of human monocyte-derived dendritic Cells (DCs) treated with ethanol-killed S. aureus. WTA-deficient S. aureus mutant (ΔtagO) exhibited attenuated binding and internalization to DCs compared to the wild-type. ΔtagO induced lower expression of maturation markers on and cytokines in DCs than the wild-type S. aureus. Furthermore, autologous human peripheral blood mononuclear Cells cocultured with ΔtagO-treated DCs exhibited a marked reduction in T Cell proliferative activity, the expression of activation markers, and the production of cytokines compared to the wild-type S. aureus-stimulated DCs. Collectively, these results suggest that WTA is an important Cell Wall Component of S. aureus for the induction of DC maturation and activation.

Ada Elgavish - One of the best experts on this subject based on the ideXlab platform.

  • nf kappab activation mediates the response of a subpopulation of basal uroepithelial Cells to a Cell Wall Component of enterococcus faecalis
    Journal of Cellular Physiology, 2000
    Co-Authors: Ada Elgavish
    Abstract:

    Earlier in vitro studies revealed that treatment of basal urothelial Cells (UT) with lipoteichoic acid, a Cell Wall Component of Enterococcus faecalis (LT-2), stimulated a subpopulation of quiescent Cells with high proliferative potential to divide (Elgavish et al., 1996b, J Cell Physiol 169:42–51). Studies were consistent with the possibility that NO-mediated mechanisms were involved (Elgavish et al., 1996c, J Cell Physiol 169:66–77). We postulated that LT-2 may upregulate expression of iNOS. Promoters of the gene encoding iNOS, as well as genes encoding many cytokines, contain elements homologous to consensus sequences for the binding of the transcription factor NF-κB. Based on this, we postulated that: (1) NF-κB activation is an early event following exposure of basal UT to LT-2 and (2) NF-κB activation mediates basal UT proliferation triggered by LT-2. To test these hypotheses, UT maintained for 3 days under growth-restricting conditions, were treated with or without 25 μg/ml LT-2. Nuclear distribution of NF-κB, that is, activated NF-κB, was detected by immunofluorescence microscopy in a subpopulation of basal UT as early as 5–10 min after the beginning of the treatment. In contrast, LT-2 had no effect on cultures containing more differentiated UT. NF-κB activation preceded production of NO, since treatment with 25 μM hemoglobin, a potent inactivator of NO, did not prevent LT-2-triggered NF-κB activation. Treatment with 10 μM pyrrolidine dithiocarbamate (PDTC) inhibited LT-2-triggered activation of NF-κB and prevented the stimulatory effect of LT-2 on proliferation of basal UT. These findings support the possibility that NF-κB activation mediates basal UT proliferation triggered by LT-2. J. Cell. Physiol. 182:232–238, 2000. © 2000 Wiley-Liss, Inc.

  • i a subpopulation of human urothelial Cells is stimulated to proliferate by treatment in vitro with lipoteichoic acid a Cell Wall Component of streptococcus faecalis
    Journal of Cellular Physiology, 1996
    Co-Authors: Ada Elgavish, Keith Lloyd, Rebecca Reed
    Abstract:

    Urinary tract infection with gram-positive bacteria is common. Avenues for ingress of bacteria into the bladder include luminal and suburothelial infection. Terminally differentiated superficial urothelial Cells lining the lumen of the bladder are often shed in response to infection. In contrast, infection-induced altered function of progenitors of urothelial Cells residing in the basal layer of the urothelium is likely to have long lasting effects on the structure and function of the urothelium. The main objective of the present studies was to investigate in vitro the possibility that exposure to lipoteichoic acid, a Cell Wall Component of the gram-positive Streptococcus faecalis (LT-2), stimulates basal urothelial Cells to proliferate. To simulate conditions that restrict proliferation and inhibit terminal differentiation of urothelial Cells in the basal layer, secondary cultures of urothelial Cells (UT) were grown on collagen or fibronectin-coated substrate in medium containing low levels of Ca2+ (0.2 mM) and growth factors (0.005% bovine pituitary extract [BPE]). Under these conditions, UT cultures displayed a highly reproducible colony size distribution, possibly due to the fact that colonies were progeny of basal Cells with various proliferative potentials, retained in vitro. In cultures grown under growth-restricting conditions, the majority of progenitors appeared to be quiescent, just like stem Cells in the basal layer of the urothelium. Thus, the population of large colonies (more than six Cells/colony), was small when a steady state of growth was achieved, 3–7 days after seeding. Growth factors (0.005–0.5% BPE) caused a dose-dependent increase in this population of large colonies. Moreover, treatment of UT grown under growth-restricting conditions (0.005% BPE) with LT-2 increased steady-state levels of the population of large colonies to levels obtained in cultures growing under optimal conditions with respect to growth factors. These results indicated that the subpopulation of progenitors, quiescent under normal conditions, could be stimulated to proliferate. Two lines of evidence were consistent with the possibility that treatment with LT-2 stimulated proliferation of the subpopulation of progenitors and that large colonies were the progeny of this subpopulation of single Cells: (1) treatment with LT-2 increased the percentage of single Cells that incorporated bromodeoxyuridine (i.e., proliferated) in a time-dependent manner; (2) An increase in the percentage of large colonies was found following LT-2-triggered proliferation of single Cells. We propose that, under normal conditions, Cells produced in response to LT-2-triggered proliferation of stem Cells are removed from the system due to an increased rate of differentiation followed by apoptosis. Recurrent infection and inflammation may not allow these processes to proceed effectively, resulting in chronic injury to the bladder. Moreover, under conditions in which stem Cells accumulate mutations that incapacitate their progeny to undergo apoptosis, LT-triggered proliferation could be a contributing factor to tumorigenesis. © 1996 Wiley-Liss, Inc.

Alberto Mantovani - One of the best experts on this subject based on the ideXlab platform.

  • expression of monocyte chemotactic protein 3 in human monocytes exposed to the mycobacterial Cell Wall Component lipoarabinomannan
    Cytokine, 1997
    Co-Authors: Valerie Vouretcraviari, Guido Poli, Salvatore Cenzuales, Alberto Mantovani
    Abstract:

    Abstract Monocyte chemotactic protein-3 (MCP-3) is a C–C chemokine which interacts with the CCR1, CCR2 (MCP-1) and CCR3 receptors and has a distinct spectrum of action. The present study was designed to assess whether mycobacterial Components were able to induce expression and production of MCP-3 in human monocytes. Mycobacterial lipoarabinomannan (LAM) induced expression of MCP-3 mRNA in human peripheral blood mononuclear Cells. The non-mannose-capped version of lipoarabinomannan (AraLAM) was considerably more potent than the mannose-capped version ManLAM or the simpler version phosphatidylinositol mannoside (PLM). Among mononuclear Cells, monocytes were responsible for LAM-induced MCP-3 mRNA expression. Whole mycobacteria ( Mycobacterium bovis BCG) strongly induced MCP-3 expression. Pretreatment with actinomycin D abolished LAM-induced MCP-3 expression, whereas cycloheximide only partially reduced the expression. LAM-induced MCP-3 expression was associated with the production of immunoreactive PTX3. Interleukin 10 (IL-10) and IL-13 inhibited the induction of MCP-3 by LAM. Thus mycobacterial Cell Wall Components induced expression of MCP-3 in human monocytes. MCP-3, a chemokine active on mononuclear phagocytes, NK Cells, T Cells and dendritic Cells, may be relevant to the induction and expression of immunity against mycobacteria.

  • expression of a long pentraxin ptx3 by monocytes exposed to the mycobacterial Cell Wall Component lipoarabinomannan
    Infection and Immunity, 1997
    Co-Authors: Valerie Vouretcraviari, Cristian Matteucci, Giuseppe Peri, Guido Poli, Martino Introna, Alberto Mantovani
    Abstract:

    PTX3 is a prototypic long pentraxin composed of a C-terminal domain similar to those of classical pentraxins (e.g., C reactive protein) and an unrelated N-terminal portion. PTX3 is expressed in a variety of Cell types, notably mononuclear phagocytes and endothelial Cells, after exposure to the inflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). The present study was designed to assess whether mycobacterial Components were able to induce expression and production of PTX3. Mycobacterial lipoarabinomannan (LAM) induced expression of PTX3 mRNA in human peripheral blood mononuclear Cells. The non-mannose-capped version of lipoarabinomannan (AraLAM) was considerably more potent than the mannose-capped version ManLAM or the simpler version phosphatidylinositol mannoside. Among mononuclear Cells, monocytes were responsible for LAM-induced PTX3 mRNA expression. Whole mycobacteria (Mycobacterium bovis BCG) strongly induced PTX3 expression. Pretreatment with actinomycin D abolished LAM-induced PTX3 expression, whereas cycloheximide only partially reduced the expression. LAM-induced PTX3 expression was associated with the production of immunoreactive PTX3. IL-10 and IL-13 did not inhibit the induction of PTX3 by LAM. Under the same conditions, these anti-inflammatory cytokines inhibited MCP-1 expression. In contrast, gamma interferon inhibited LAM-induced PTX3 expression. Thus, in addition to IL-1, TNF, and lipopolysaccharide, mycobacterial Cell Wall Components also induce expression and production of the long pentraxin PTX3. The significance of PTX3 in the immunobiology of mycobacterial infection and its relevance in relation to clinical involvement remain to be determined.