Genetic Mechanisms Promote Antimicrobial Resistance in Gonorrhea - News Center
Briefly

Genetic Mechanisms Promote Antimicrobial Resistance in Gonorrhea - News Center
"N. gonorrhoeae is the bacteria that causes the sexually transmitted infection gonorrhea. The disease, which is treated with antibiotics, can cause epididymitis in men and pelvic inflammatory disease in women. If left untreated, it can also lead to infertility, pregnancy complications and sepsis. The N. gonorrhoeae Type IV pilus - a hairlike structure found on the bacteria's surface - helps the bacteria securely attach to host cells and evade immune responses from neutrophils, white blood cells produced by bone marrow and the body's first line of defense against infection."
"Previous work led by Hu discovered that the Type IV pilus regulates iron homeostasis, which promotes resistance to antimicrobial agents including hydrogen peroxide and the antimicrobial peptide LL-37. To further understand this mechanism, Hu's team used in vitro evolution to grow N. gonorrhoeae in the laboratory and, using whole genome sequencing, identified genetic mutations that promoted antimicrobial resistance after exposing the bacteria to streptonigrin, an antibiotic which kills cells with high levels of iron."
Northwestern Medicine scientists identified previously unknown genetic mechanisms that promote antimicrobial resistance in Neisseria gonorrhoeae. The Type IV pilus facilitates attachment to host cells and helps the bacteria evade neutrophil-mediated immune responses while regulating iron homeostasis, which enhances resistance to agents such as hydrogen peroxide and the antimicrobial peptide LL-37. In vitro evolution with streptonigrin exposure followed by whole-genome sequencing uncovered mutations that confer resistance, including a mutation in hpaC that promotes streptonigrin resistance. These findings illuminate interconnected resistance pathways and may inform development of more effective therapeutic strategies against gonorrhea.
Read at News Center
Unable to calculate read time
[
|
]