Cord Factor and Related Synthetic Trehalose Diesters

1980 ◽  
pp. 95-110
Author(s):  
Edgar Lederer
Keyword(s):  
Cord Factor

scholarly journals Microscopic Cords, a Virulence-Related Characteristic of Mycobacterium tuberculosis, Are Also Present in Nonpathogenic Mycobacteria

2010 ◽  
Vol 192 (7) ◽  
pp. 1751-1760 ◽  
Author(s):  
Esther Julián ◽  
Mónica Roldán ◽  
Alejandro Sánchez-Chardi ◽  
Oihane Astola ◽  
Gemma Agustí ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Trehalose Dimycolate ◽  
Cord Factor ◽  
Ideal Tool ◽  
Colonial Morphology ◽  
Related Characteristic ◽  
Microscopy Images ◽  
Scanning Electron ◽  
The Ideal

ABSTRACT The aggregation of mycobacterial cells in a definite order, forming microscopic structures that resemble cords, is known as cord formation, or cording, and is considered a virulence factor in the M ycobacterium tuberculosis complex and the species M ycobacterium marinum. In the 1950s, cording was related to a trehalose dimycolate lipid that, consequently, was named the cord factor. However, modern techniques of microbial genetics have revealed that cording can be affected by mutations in genes not directly involved in trehalose dimycolate biosynthesis. Therefore, questions such as “How does mycobacterial cord formation occur?” and “Which molecular factors play a role in cord formation?” remain unanswered. At present, one of the problems in cording studies is the correct interpretation of cording morphology. Using optical microscopy, it is sometimes difficult to distinguish between cording and clumping, which is a general property of mycobacteria due to their hydrophobic surfaces. In this work, we provide a new way to visualize cords in great detail using scanning electron microscopy, and we show the first scanning electron microscopy images of the ultrastructure of mycobacterial cords, making this technique the ideal tool for cording studies. This technique has enabled us to affirm that nonpathogenic mycobacteria also form microscopic cords. Finally, we demonstrate that a strong correlation exists between microscopic cords, rough colonial morphology, and increased persistence of mycobacteria inside macrophages.

scholarly journals Adjuvanticity of a synthetic cord factor analogue for subunit Mycobacterium tuberculosis vaccination requires FcRγ–Syk–Card9–dependent innate immune activation

2009 ◽  
Vol 206 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Kerstin Werninghaus ◽  
Anna Babiak ◽  
Olaf Groß ◽  
Christoph Hölscher ◽  
Harald Dietrich ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Subunit Vaccine ◽  
Vaccine Development ◽  
Adaptor Protein ◽  
Synthetic Analogue ◽  
Dependent Manner ◽  
Immunostimulatory Activity ◽  
Adjuvant Activity ◽  
Cord Factor

Novel vaccination strategies against Mycobacterium tuberculosis (MTB) are urgently needed. The use of recombinant MTB antigens as subunit vaccines is a promising approach, but requires adjuvants that activate antigen-presenting cells (APCs) for elicitation of protective immunity. The mycobacterial cord factor Trehalose-6,6-dimycolate (TDM) and its synthetic analogue Trehalose-6,6-dibehenate (TDB) are effective adjuvants in combination with MTB subunit vaccine candidates in mice. However, it is unknown which signaling pathways they engage in APCs and how these pathways are coupled to the adaptive immune response. Here, we demonstrate that these glycolipids activate macrophages and dendritic cells (DCs) via Syk–Card9–Bcl10–Malt1 signaling to induce a specific innate activation program distinct from the response to Toll-like receptor (TLR) ligands. APC activation by TDB and TDM was independent of the C-type lectin receptor Dectin-1, but required the immunoreceptor tyrosine-based activation motif–bearing adaptor protein Fc receptor γ chain (FcRγ). In vivo, TDB and TDM adjuvant activity induced robust combined T helper (Th)-1 and Th-17 T cell responses to a MTB subunit vaccine and partial protection against MTB challenge in a Card9-dependent manner. These data provide a molecular basis for the immunostimulatory activity of TDB and TDM and identify the Syk–Card9 pathway as a rational target for vaccine development against tuberculosis.

scholarly journals Occurrence of 3-Oxo-acyl Groups in the 6,6'-Diesters of alpha-d-Trehalose. New Glycolipids Related to Cord Factor from Corynebacterium diphtheriae

1979 ◽  
Vol 98 (1) ◽  
pp. 99-105 ◽  
Author(s):  
Germain PUZO ◽  
Gerard TISSIE ◽  
Helene AURELLE ◽  
Charlotte LACAVE ◽  
Jean-Claude PROME
Keyword(s):  
Corynebacterium Diphtheriae ◽  
Cord Factor

scholarly journals Lactoferrin modulation of mycobacterial cord factor trehalose 6-6'-dimycolate induced granulomatous response

2010 ◽  
Vol 156 (4) ◽  
pp. 207-215 ◽  
Author(s):  
Kerry J. Welsh ◽  
Shen-An Hwang ◽  
Robert L. Hunter ◽  
Marian L. Kruzel ◽  
Jeffrey K. Actor
Keyword(s):  
Cord Factor ◽  
Granulomatous Response

Treatment of Mycosis fungoides with Heat-Killed BCG and Cord Factor

Dermatology ◽  
1979 ◽  
Vol 158 (2) ◽  
pp. 104-116 ◽  
Author(s):  
Haim A. Cohen ◽  
Adam Bekierkunst
Keyword(s):  
Mycosis Fungoides ◽  
Cord Factor

scholarly journals Trehalose 6,6′-Dimycolate (Cord Factor) of Mycobacterium tuberculosis Induces Corneal Angiogenesis in Rats

2000 ◽  
Vol 68 (10) ◽  
pp. 5991-5997 ◽  
Author(s):  
Norio Saita ◽  
Nagatoshi Fujiwara ◽  
Ikuya Yano ◽  
Kazuhiko Soejima ◽  
Kazuo Kobayashi
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Neutralizing Antibodies ◽  
Early Stage ◽  
Vascular Endothelial ◽  
Cytokine Network ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cord Factor ◽  
Factor Alpha ◽  
Endothelial Growth Factor

ABSTRACT Neovascularization or angiogenesis is required for the progression of chronic inflammation. The mechanism of inflammatory neovascularization in tuberculosis remains unknown. Trehalose 6,6′-dimycolate (TDM) purified from Mycobacterium tuberculosis was injected into rat corneas. TDM challenge provoked a local granulomatous response in association with neovascularization. Neovascularization was seen within a few days after the challenge, with the extent of neovascularization being dose dependent, although granulomatous lesions developed 14 days after the challenge. Cytokines, including tumor necrosis factor alpha (TNF-α), interleukin-8 (IL-8), IL-1β, and vascular endothelial growth factor (VEGF), were found in lesions at the early stage (within a few days after the challenge) and were detectable until day 21. Neovascularization was inhibited substantially by neutralizing antibodies to VEGF and IL-8 but not IL-1β. Treatment with anti-TNF-α antibodies resulted in partial inhibition. TDM possesses pleiotropic activities, and the cytokine network plays an important role in the process of neovascularization.

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