Rheumatoid Arthritis Support

In animal studies, LTA has induced arthritis, nephritis, uveitis, encephalomyelitis, meningitis, and periodontal lesions, and also triggered cascades resulting in septic shock and multiorgan failure. Binding of LTA to targets can be inhibited by phospholipids and antibodies directed at LTA, CD14, or Toll-like receptors. In vitro, LTA release can be inhibited by non-bacteriolytic antibiotics and by polysulfates such as heparin.

LTA can be considered a virulence factor that has an important role in infections and in postinfectious sequelae caused by Gram-positive bacteria. The development of effective antibiotics killing the bacteria without lysing them and multidrug strategies to attenuate LTA-induced secretion of proinflammatory agonists is of great importance to combat septic shock and multiorgan failure caused by Gram-positive bacteria.

LTA's molecular structure has been found to have the strongest hydrophobic bonds of an entire bacteria.


Adapted from the Wikipedia article Lipoteichoic acid, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki