Toll-Like Receptors Responding to Lipoteichoic Acid (LTA)
from the Gram-Positive Cell Wall and Signaling the Synthesis
Inflammatory Cytokines.

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1) Gram-positive bacteria release lipoteichoic acid (LTA) from their cell wall.
2) The LTA binds to a TLR-2/TLR-6 pair on defense cells such as macrophages and dendritic cells.
3) The binding of LTA to TLR-2/TLR-6 enables regulatory molecules within the cell - Mal, MyD88, Tram, and Trif - to trigger reactions that activate a master regulator of inflammation called NF-kappa B. Activated NF-kappa B enters the cell's nucleus and switches on genes coding for cytokines such as:

a. Interleukin-1 (IL-1) and Tumor necrosis factor-alpha (TNF-alpha): enhance inflammatory responses;
b. Interleukin-8 (IL-8): aids in the ability of white blood cells to leave the blood vessels and enter the tissue; a chemoattractant for phagocytes;
c. Interleukin-6 (IL-6) promotes B-lymphocyte activity; and
d. Interleukin-12 (IL-12): promotes T-lymphocyte activity. (5)

4) Cytokine genes are transcribed into mRNA molecules that goe to the cytoplasm to be translated into inflammatory cytokines that are subsequently secreted from the cell.

Flash animation illustrating Toll-Like Receptors Responding to Lipoteichoic Acid (LTA) from the Gram-Positive Cell Wall Signaling the Synthesis Inflammatory Cytokines. .swf
by Gary E. Kaiser, Ph.D.
Professor of Microbiology, The Community College of Baltimore County, Catonsville Campus
This work is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at http://faculty.ccbcmd.edu/~gkaiser/index.html.

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Last updated: August, 2019
Please send comments and inquiries to Dr. Gary Kaiser