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Kılıçoğlu, Bilge Kaan

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Undergraduate Student

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Bilge Kaan

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Kılıçoğlu

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Kılıçoğlu, Bilge Kaan

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2021 - 20222

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Researcher Of Publications: search.filters.isAuthorOfPublication.9ddd1900-c44d-4885-9925-6a75c090bcd8

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    PublicationMetadata only
    Efficacy of amikacin and meropenem on colistin-induced klebsiella pneumoniae persisters
    (Mary Ann Liebert, Inc, 2022) N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; Vatansever, Cansel; Özer, Berna; Ataç, Nazlı; Güler, Orhan Ulaş; Kılıçoğlu, Bilge Kaan; Berkkan, Metehan; Başkurt, Defne; Sever, Egemen; Doğan, Özlem; Can, Füsun; Master Student; Researcher; Researcher; Undergraduate Student; Undergraduate Student; Undergraduate Student; Undergraduate Student; Undergraduate Student; Faculty Member; Graduate School of Health Sciences; N/A; N/A; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; School of Medicine; Koç Üniversitesi İş Bankası Enfeksiyon Hastalıkları Uygulama ve Araştırma Merkezi (EHAM) / Koç University İşbank Center for Infectious Diseases (KU-IS CID); N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 103165
    Colistin-based antibiotic therapies have been recommended for the treatment of multidrug-resistant Klebsiella pneumoniae infections. During colistin treatment, persister cells that tolerate antibiotics may arise. Here we designed an in vitro study to assess the killing activity of colistin, meropenem, and amikacin on colistin-induced K. pneumoniae persisters in comparison with starvation-induced persisters. Colistin-induced persisters were generated under exposure to 10 x minimum inhibitory concentration dose of colistin, whereas starvation-induced persisters were produced by limitation of nutrients. In colistin-induced persisters, amikacin totally inhibited cell growth in 6 hours, whereas 98% of the cell population was inhibited by meropenem, and total eradication with meropenem was observed after 24 hours. Both antibiotics also inhibited metabolic activity >88%. The lack of killing effect under colistin exposure suggested to us that these cells could protect themselves from further colistin stress. There was no significant permeabilization change in the cellular membrane with all antibiotics. There was no killing effect on starvation-induced persister cells with the exposure to all antibiotics. In 6 hours, the metabolic activity of the persisters with meropenem and colistin increased 99% and 40%, respectively, whereas there was no increase with amikacin. The sustained inhibition with amikacin was an important finding for antipersister effect of amikacin. Amikacin had rapid and sustained antipersister activity on colistin-induced persister cells. During the colistin treatment of K. pneumoniae infection, the addition of amikacin to the regimen seems to be an effective approach to prevent a recurrence.
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    PublicationOpen Access
    Virulence determinants of colistin-resistant K. pneumoniae high-risk clones
    (Multidisciplinary Digital Publishing Institute (MDPI), 2021) Department of Industrial Engineering; Ergönül, Önder; Gönen, Mehmet; Can, Füsun; Doğan, Özlem; Vatansever, Cansel; Ataç, Nazlı; Albayrak, Özgür; Karahüseyinoğlu, Serçin; Şahin, Özgün Ekin; Kılıçoğlu, Bilge Kaan; Demiray, Atalay; Faculty Member; Faculty Member; Faculty Member; Faculty Member; Undergraduate Student; Researcher; Faculty Member; Master Student; Department of Industrial Engineering; School of Medicine; Graduate School of Health Sciences; College of Engineering; 110398; 237468; 103165; 170418; N/A; N/A; N/A; 110772; N/A; N/A; N/A
    We proposed the hypothesis that high-risk clones of colistin-resistant K. pneumoniae (ColR-Kp) possesses a high number of virulence factors and has enhanced survival capacity against the neutrophil activity. We studied virulence genes of ColR-Kp isolates and neutrophil response in 142 patients with invasive ColR-Kp infections. The ST101 and ST395 ColR-Kp infections had higher 30-day mortality (58%, p = 0.005 and 75%, p = 0.003). The presence of yersiniabactin biosynthesis gene (ybtS) and ferric uptake operon associated gene (kfu) were significantly higher in ST101 (99%, p <= 0.001) and ST395 (94%, p < 0.012). Being in ICU (OR: 7.9; CI: 1.43-55.98; p = 0.024), kfu (OR:27.0; CI: 5.67-179.65; p < 0.001) and ST101 (OR: 17.2; CI: 2.45-350.40; p = 0.01) were found to be predictors of 30-day mortality. Even the neutrophil uptake of kfu+-ybtS+ ColR-Kp was significantly higher than kfu--ybtS- ColR-Kp (phagocytosis rate: 78% vs. 65%, p < 0.001), and the kfu+-ybtS+ ColR-Kp survived more than kfu--ybtS- ColR-Kp (median survival index: 7.90 vs. 4.22; p = 0.001). The kfu+-ybtS+ ColR-Kp stimulated excessive NET formation. Iron uptake systems in high-risk clones of colistin-resistant K. pneumoniae enhance the success of survival against the neutrophil phagocytic defense and stimulate excessive NET formation. The drugs targeted to iron uptake systems would be a promising approach for the treatment of colistin-resistant high-risk clones of K. pneumoniae infections.