Alteration of gonococcal protein expression in acidic culture

Pettit, Robin K.; Filiatrault, Melanie J.; Martin, Elda S.

doi:10.1128/iai.64.3.1039-1042.1996

Cited by 9 publications

(2 citation statements)

References 26 publications

(34 reference statements)

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“…We have not examined how lactic acid compromises the gonococcal cell wall/membrane integrity. However, previous studies have shown membrane protein expression profile changes in GC cultured in medium acidified with HCl [ 22 , 31 ]. How those protein expression profile changes affect the wall/membrane integrity and bacterial survival have yet to be determined.…”

Section: Discussionmentioning

confidence: 99%

“…However, to the best of our knowledge, the effect of lactic acid on GC survival has not been experimentally documented to date. Although HCl-mediated GC killing has been reported [ 21 , 22 ], studies have demonstrated that lactic acid and HCl differ in their antimicrobial activities [ 23 , 24 ]. We have recently determined the lactic acid susceptibility of Chlamydia trachomatis , another major sexually transmitted bacterial pathogen [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

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Arginine- and Polyamine-Induced Lactic Acid Resistance in Neisseria gonorrhoeae

Gong

Tang

et al. 2016

PLoS ONE

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Microbe-derived lactic acid protects women from pathogens in their genital tract. The purpose of this study was to determine lactic acid susceptibility of Neisseria gonorrhoeae, and identify potential acid resistance mechanisms present in this pathogen. Tested in vitro, lactic acid killed all 10 gonococcal strains analyzed in a low pH-dependent manner. Full inactivation occurred at pH 4.5. At low pH, lactic acid treatment resulted in the entry of the DNA-binding fluorochrome propidium iodide into the microbial cells, suggesting that hydrogen ions from lactic acid compromise the integrity of the bacterial cell wall/membrane. Most likely, hydrogen ions also inactivate intracellular proteins since arginine rendered significant protection against lactic acid presumably through action of the gonococcal arginine decarboxylase, an enzyme located in the bacterial cytoplasm. Surprisingly, arginine also lessened lactic acid-mediated cell wall/membrane disruption. This effect is probably mediated by agmatine, a triamine product of arginine decarboxylase, since agmatine demonstrated a stronger protective effect on GC than arginine at equal molar concentration. In addition to agmatine, diamines cadaverine and putrescine, which are generated by bacterial vaginosis-associated microbes, also induced significant resistance to lactic acid-mediated GC killing and cell wall/membrane disruption. These findings suggest that the arginine-rich semen protects gonococci through both neutralization-dependent and independent mechanisms, whereas polyamine-induced acid resistance contributes to the increased risk of gonorrhea in women with bacterial vaginosis.

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Section: Discussionmentioning

confidence: 99%