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:
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.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)
Flash animation illustrating of The Harmful
Effects of Peptidoglycan Fragments
and Lipoteichoic Acid Released During Gram-Positive Infections.jpg 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.
Last updated: August, 2018
Please send comments and inquiries to Dr.
Gary Kaiser