scholarly journals Trehalose 6, 6dimycolate (cord factor) induced pulmonary granuloma in naive and lymphopenic mice

2012 ◽  
Vol 4 (3) ◽  
pp. 29-35
Author(s):  
Mathai A
2010 ◽  
Vol 192 (7) ◽  
pp. 1751-1760 ◽  
Author(s):  
Esther Julián ◽  
Mónica Roldán ◽  
Alejandro Sánchez-Chardi ◽  
Oihane Astola ◽  
Gemma Agustí ◽  
...  

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.


1984 ◽  
Vol 231 (3) ◽  
pp. 109-111 ◽  
Author(s):  
N. Inoue ◽  
T. Uozumi ◽  
T. Yamamoto ◽  
T. Ohishi ◽  
Y. Murai ◽  
...  

2009 ◽  
Vol 206 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Kerstin Werninghaus ◽  
Anna Babiak ◽  
Olaf Groß ◽  
Christoph Hölscher ◽  
Harald Dietrich ◽  
...  

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.


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

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