Neither Lys- and DAP-type peptidoglycans stimulate mouse or human innate immune cells via Toll-like receptor 2.
Marybeth Langer, Alanson W Girton, Narcis I Popescu, Tarea Burgett, Jordan P Metcalf, K Mark Coggeshall
Author Information
Marybeth Langer: The Oklahoma Medical Research Foundation, Program in Arthritis & Immunology, Oklahoma City, OK, United States of America.
Alanson W Girton: The Oklahoma Medical Research Foundation, Program in Arthritis & Immunology, Oklahoma City, OK, United States of America.
Narcis I Popescu: The Oklahoma Medical Research Foundation, Program in Arthritis & Immunology, Oklahoma City, OK, United States of America.
Tarea Burgett: The Oklahoma Medical Research Foundation, Program in Arthritis & Immunology, Oklahoma City, OK, United States of America.
Jordan P Metcalf: The Department of Medicine, Pulmonary and Critical Care Div., University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States of America.
K Mark Coggeshall: The Oklahoma Medical Research Foundation, Program in Arthritis & Immunology, Oklahoma City, OK, United States of America. ORCID
Peptidoglycan (PGN), a major component of bacterial cell walls, is a pathogen-associated molecular pattern (PAMP) that causes innate immune cells to produce inflammatory cytokines that escalate the host response during infection. In order to better understand the role of PGN in infection, we wanted to gain insight into the cellular receptor for PGN. Although the receptor was initially identified as Toll-like receptor 2 (TLR2), this receptor has remained controversial and other PGN receptors have been reported. We produced PGN from live cultures of Bacillus anthracis and Staphylococcus aureus and tested samples of PGN isolated during the purification process to determine at what point TLR2 activity was removed, if at all. Our results indicate that although live B. anthracis and S. aureus express abundant TLR2 ligands, highly-purified PGN from either bacterial source is not recognized by TLR2.
