Ability of Monomeric Peptidoglycan Fragments from Neisseria gonorrhoeae to Damage Human Fallopian-Tube Mucosa

Abstract

Purified disaccharide peptide monomers obtained from Neisseria gonorrhoeae by enzymatic digestion of gonococcal peptidoglycan damaged the mucosa of human fallopian tubes in organ culture. Two peptidoglycan fragments were tested: a nonreducing, anhydromuramyl-containing monomer (the principal fragment shed by growing gonococci) and the analogous reducing, muramidase-derived monomer. The damage produced by either of these peptidoglycan monomers resulted in sloughing of ciliated cells from the mucosa and resembled the damage observed in active gonococcal infection and that produced by filter-sterilized toxic supernatant fluids from gonococcal-infected organ cultures. The minimal toxic dose of peptidoglycan monomers was 0.75 micrograms/ml. Neither lipopolysaccharide, sodium dodecyl sulfate, nor Triton X-100, possible contaminants from the monomer-purification procedures, was present in sufficient quantity to account for the damage. Both of the gonococcal peptidoglycan monomers may be present in vivo and thus may play a role in the pathogenesis of gonococcal infection.

Neisseria gonorrhoeae-derived heptose elicits an innate immune response and drives HIV-1 expression

“…Although neither of these factors appears to contribute to the effect of Ng on HIV-1, it seems likely that they work in concert to make the mucosal tissues receptive to infection by and/or the persistence of the bacteria. Supporting this model, released peptidoglycan fragments are selectively toxic to mucosal ciliary cells so as to stop mucus flow and provide the bacteria access to the subepithelial space (48). Future efforts must consider the cumulative effect of these factors on the mucosal epithelia and their respective roles during Ng infection.…”

Bacterial Growth and Cell Division: a Mycobacterial Perspective

“…The degree to which PG material is sloughed off by bacteria can greatly affect the host response to the infection. For instance, release of PG from Bordetella pertussis (153), Neisseria gonorrhoeae (274), Helicobacter pylori (423), and Vibrio fischeri (223) acts to stimulate inflammatory processes by binding specific pathogen recognition molecules.…”

Mutation of a Single Lytic Transglycosylase Causes Aberrant Septation and Inhibits Cell Separation of Neisseria gonorrhoeae

“…The major fragments released are the 1,6-anhydrodisaccharide tripeptide monomer and the 1,6-anhydrodisaccharide tetrapeptide monomer (16). These PG fragments have potent biological effects, including killing ciliated fallopian tube cells (13), inducing inflammatory cytokine production (4), and causing arthritis (5). Previous studies in our laboratory found that mutations affecting lytic transglycosylases LtgA and LtgB lower PG monomer production but do not alter cell division (2; K. A.…”