Peptidoglycan fragment release and NOD activation by commensal species from humans and other animals.

, a human restricted pathogen, releases inflammatory peptidoglycan (PG) fragments that contribute to the pathophysiology of pelvic inflammatory disease. The genus is also home to multiple species of human- or animal-associated that form part of the normal microbiota. Here we characterized PG release from the human-associated nonpathogenic species and and animal-associated from macaques and wild mice.

Mutation of increases peptidoglycan fragment release, cell size, and antibiotic susceptibility in .

is unusual in that the bacteria release larger amounts of cell wall material as they grow as compared to related bacteria, and the released cell wall fragments induce inflammation that leads to tissue damage in infected people. The study of MltG revealed the importance of this enzyme for controlling cell wall growth, cell wall fragment production, and bacterial cell size and suggests a role for MltG in a cell wall synthesis and degradation complex. The increased antibiotic sensitivities of mutants suggest that an antimicrobial drug inhibiting MltG would be useful in combination therapy to restore the sensitivity of the bacteria to cell wall targeting antibiotics to which the bacteria are currently resistant.

Mutation of increases peptidoglycan fragment release, cell size, and antibiotic susceptibility in .

Infection with the Gram-negative species leads to inflammation that is responsible for the disease symptoms of gonococcal urethritis, cervicitis, and pelvic inflammatory disease. During growth these bacteria release significant amounts of peptidoglycan (PG) fragments which elicit inflammatory responses in the human host. To better understand the mechanisms involved in PG synthesis and breakdown in , we characterized the effects of mutation of .