TY - JOUR
T1 - Effect of leukocyte hydrolases on bacteria - IX. The release of lipoteichoic acid from group A streptococci and from Strep, mutans by leukocyte extracts and by lysozyme
T2 - Relation to tissue damage in inflammatory sites
AU - Sela, Michael N.
AU - Lahav, Meir
AU - Ginsburg, Isaac
PY - 1977/6
Y1 - 1977/6
N2 - Human leukocyte extracts, egg white lysozyme, cationic proteins, polymyxin, colimycin, and phenol are capable of releasing lipoteichoic acids (LTA) from group A streptococci and Strep, mutans. While the extraction of LTA by phenol is optimal at pH 4.7, the release of LTA from streptococci by the other agents is optimal at pH 7.4. LTA released by all agents was found to have the same sensitizing abilities, as determined by passive hemagglutination, and to have a similar chemical composition, as shown by thin-layer chromatography and radioactive scanning. The LTA-releasing capacity of all the agents is strongly inhibited by normal human serum. The possible role played by LTA released by leukocyte factors in the pathogenesis of tissue damage during bacterial infections is discussed.
AB - Human leukocyte extracts, egg white lysozyme, cationic proteins, polymyxin, colimycin, and phenol are capable of releasing lipoteichoic acids (LTA) from group A streptococci and Strep, mutans. While the extraction of LTA by phenol is optimal at pH 4.7, the release of LTA from streptococci by the other agents is optimal at pH 7.4. LTA released by all agents was found to have the same sensitizing abilities, as determined by passive hemagglutination, and to have a similar chemical composition, as shown by thin-layer chromatography and radioactive scanning. The LTA-releasing capacity of all the agents is strongly inhibited by normal human serum. The possible role played by LTA released by leukocyte factors in the pathogenesis of tissue damage during bacterial infections is discussed.
UR - https://www.scopus.com/pages/publications/0017499158
U2 - 10.1007/BF00918677
DO - 10.1007/BF00918677
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
C2 - 33119
AN - SCOPUS:0017499158
SN - 0360-3997
VL - 2
SP - 151
EP - 164
JO - Inflammation
JF - Inflammation
IS - 2
ER -