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( Eun Hye Lee ),( Ah Young Leem ),( Sang Hoon Lee ),( Joo Han Song ),( Song Yee Kim ),( Kyung Soo Chung ),( Ji Ye Jung ),( Moo Suk Park ),( Young Sam Kim ),( Joon Chang ),( Young Ae Kang ) 대한결핵 및 호흡기학회 2018 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.126 No.-
Background: The prevalence of nontuberculous mycobacteria lung disease (NTM-LD) is increasing worldwide. However, there is limited information about the NTM-LD of young age people. Methods: Patients diagnosed with NTM-LD at severance hospital between January 2006 and December 2016 were retrospectively reviewed. Clinical characteristics and microbiologic features of patients under 40 years were compared with patients over 40 years. Results: Total 906 patients were identified NTM-LD. Of these, 29 patients (3.2%) were under 40 years of age (young age group) and the remaining 877 were over 40 years of age (old age group). Mean age of the two groups were 32 (IQR 24-33) and 64 (IQR 56-72), respectively. Female was predominant in both groups and about half of the patients had a history of tuberculosis (51.7% vs.51.5%, p=0.984). 7 patients (24.1%) of the young age group had malignancy history and among them, 6 patients were hematologic cancer who subsequently received bone marrow transplantation. The proportion of the nodular bronchiectatic form of NTM-LD is significantly higher in old age group (67.5%) compared to young age group (31.0%) (p=<0.001). M.avium complex (MAC) was the most common etiologic organism in both groups, however, it was less common in the young age group (44.8% vs. 65.3%, p=0.023). Identification of M.abscessus complex (MABC) was higher in young age group although statistically insignificant (24.1% vs. 17.0%, p=0.318). Conclusion: This study could help to better understand the characteristics and microbial features of NTM-LD of young age people.
Ye Ji Son,Eun Jung Thak,Dong-Jik Lee,Hyun Ah Kang 한국당과학회 2022 한국당과학회 학술대회 Vol.2022 No.07
The human fungal pathogen Cryptococcus neoformans assembles O-linked mannosyl glycans on its proteins in two types; Ktr3p-meidated major-O-glycans without xylose and Cap6-mediated minor-O-glycans without xylose, respectively1. The C. neoformans ktr3Δcap6Δ double mutant strain was constructed to block completely O-mannosylation extension in the Golgi. The ktr3Δcap6Δ strain accumulated the O-glycans carrying only a single mannose and displayed defective growth under several stress conditions, accompanied with completely attenuated virulence in a mouse model of cryptococcosis. By RNA-Seq-based transcriptome analysis, we investigated the effect of defective O-mannosylation on the stress-responsive signaling pathways associated with virulence. The comparative transcriptome analysis of the wild-type (WT) and ktr3Δcap6Δ cells under normal growth and tunicamycin (TM) treatment conditions, respectively, revealed the decreased induction of Mpk1p-and calcineurin-Crz1-mediated cell wall integrity (CWI) signaling pathways. Furthermore, we examined the possible change of physiochemical properties of cell surface in the ktr3Δcap6Δ cells, by profile analysis of N-linked glycans assembled on cell wall proteins, flow cytometry analysis of cell wall components, and filipin-staining analysis of erogosterol. Although no apparent difference in the total amount and overall length of N-glycans was observed, the N-glycan profile of ktr3Δ cap6Δ showed a marginal change with the decreased neutral glycan peaks and increased acidic glycan peaks compared to that of the WT strain. We also observed the slightly increased amount of chitin in ktr3Δ cap6Δ, which might reflect the compensation mechanism of defective CWI. Notably, the ktr3Δ cap6Δ cells showed defective trafficking of ergosterol, an immunoactive fungal molecule, from the ER to the plasma membrane. In conclusion, our results demonstrate the importance of extended O-glycan structure for cell wall integrity signaling and physiochemical properties of cell surface, which critically affect the survival in the host cell environments and the interaction with host cells of C. neoformans during infection process.
Novel pendrin inhibitor attenuates lipopolysaccharide-induced acute lung injury in mice
( Eun Hye Lee ),( Jae Young Choi ),( Mi Hwa Shin ),( Wan Namkung ),( Ji Soo Choi ),( Su Hwan Lee ),( Ah Young Leem ),( Sang Hoon Lee ),( Kyung Soo Chung ),( Song Yee Kim ),( Ji Ye Jung ),( Young Ae Ka 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.0
Background: Pendrin is encoded by SLC26A4 and its mutation leads to congenital hearing loss. Additionally, pendrin is up-regulated in inflammatory airway diseases such as chronic obstructive pulmonary disease, allergic rhinitis, and asthma. In this study, the effects of a novel pendrin inhibitor, YS-01, were investigated in an LPS-induced acute lung injury (ALI) mice model, and the mechanism underlying the effect of YS-01 was examined. Methods: LPS (10 mg/kg) was intranasally instilled in wild type (WT) and pendrin-null mice. Lung injury parameters were assessed in the lung tissue and bronchoalveolar lavage fluid (BALF). Pendrin levels in the BALF of 41 pneumonia/ARDS patients and 25 control (solitary pulmonary nodule) patients were also measured. Results: LPS instillation induced lung injury in WT mice but not in pendrin-null mice. YS-01 treatment dramatically attenuated lung injury and reduced BALF cell counts and protein concentration after LPS instillation in WT mice. Proinflammatory cytokines and NF-κB activation were suppressed by YS-01 treatment in LPS-induced ALI mice. However, the protective effects of pendrin inhibitor lost after SCN- instillation. Furthermore, pendrin expression was upregulated in pneumonia/ARDS patient compared to that in control patient BALF (mean, 24.86 vs. 6.83 ng/mL, p < 0.001). Conclusions: A novel Pendrin inhibitor, YS-01, suppressed lung injury in LPS-induced ALI mice and our data provide a new strategy for the treatment of inflammatory airway diseases including sepsis-induced ALI.
( Eun Kyong Goag ),( Ah Young Leem ),( Song Yee Kim ),( Joo Han Song ),( Kyung Soo Chung ),( Ji Ye Jung ),( Moo Suk Park ),( Young Sam Kim ),( Se Kyu Kim ),( Joon Chang ),( Eun Young Kim ) 대한결핵 및 호흡기학회 2016 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.121 No.-
Background: The EGFR mutation T790M is reported in approximately 50% of NSCLC patients with acquired resistance to EGFR-TKI. Recently, its assessment become more important because the 3rd generation EGFR-TKIs targeting T790M mutant NSCLC are developed and become available in the real world. We aim to investigate the feasibility of bronchoscopy as rebiopsy tool and prevalence of T790M mutations after failure of EGFR-TKI. Methods: We investigated 139 patients who had undergone rebiopsy by flexible bronchoscopy (endobronchial biopsy and transbronchial biopsy) and EBUS-TBNA between Sep 2014 and Jul 2016. Results: Of 139 patients, 102(73.4%) were pathologically diagnosed successfully by bronchoscopic rebiopsy. The most common method used for rebiopsy was transbronchial biopsy(41.5%). The EBUS-TBNA and endobronchial biopsy were used in 26.8% and 19.5%. Among them, we selected a total of 41 EGFR-mutant lung adenocarcinoma patients, who had a history of acquired resistance to EGFR-TKI and available tumor tissue for reassessment of EGFR mutations at rebiopsy. Median duration of EGFR-TKI treatment was 10.0 months. Initial EGFR mutation was E19 del(56.1%), L858R or L861Q(34.1%), and others. The T790M mutation was identified in 18(43.9%) patients. The E19 del was most significant factors for T790M development( p=0.002). There was no significant difference in the incidence of T790M according to the type of EGFR-TKI. Conclusion: Bronchoscopic biopsy is feasible for rebiopsy after failure of EGFR-TKI. The T790M mutation is more frequently induced with E19 deletion than L858R and others.
( Eun Hye Lee ),( Mi Hwa Shin ),( Jong-min Park ),( Sang-guk Lee ),( Nam Su Ku ),( Ah Young Leem ),( Sang Hoon Lee ),( Joo Han Song ),( Song Yee Kim ),( Kyung Soo Chung ),( Ji Ye Jung ),( Young Ae Kan 대한결핵 및 호흡기학회 2018 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.126 No.-
Purpose: Sepsis remains a critical problem worldwide and one of the main causes of death in intensive care units (ICU). We investigated plasma lysophosphatidylcholine (LPC) 16:0 level using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) in ICU sepsis patients. Methods: Patients admitted medical ICU were prospectively enrolled from March 2017 through June 2018 at Severance Hospital. The inclusion criteria for the study were a fulfillment of at least 2 criteria of systemic inflammatory response syndrome (SIRS) or presence of sepsis. The definition of sepsis followed the revised sepsis 3-definition. Results: Of the 120 enrolled patients, 15 patients were non-infectious SIRS, 37 patients were classified as sepsis and 68 were septic shock. Of these 105 patients who meet the sepsis diagnostic criteria, 70 patients survived and 35 patients were dead at 28-day. Mean plasma LPC concentration (μmol/L) of septic shock patients was significantly lower than those of non-infectious SIRS (26.55 vs. 70.65, p<0.001) and sepsis patients (26.55 vs. 48.50, p<0.01). The area under the curve (AUC) predicting 28-day mortality of ΔLPC16:0 (D7-D0) was 0.792 that was higher than APACHE II score (AUC;0.694) and SOFA score (AUC;0.678). In the multivariate analysis, LPC16:0 change less than cut-off value (Δ LPC16:0 (D7-D0) ≤14.859; HR, 5.467) were associated with increased 28-day mortality. Conclusion: Our results indicate that Δ LPC16:0 in sepsis patients using MALDI-TOF MS could help to better predict prognosis and mortality of sepsis patients in ICU.
Eun Jung Thak,Dong-Jik Lee,Hyunah Kim,Ye Ji Son,Jung Ho Kim,Su-Bin Lee,Yong-Sun Bahn,Hyun Ah Kang 한국당과학회 2021 한국당과학회 학술대회 Vol.2021 No.01
The human fungal pathogen Cryptococcus neoformans assembles N-/O-linked glycans on its proteins in two types with and without xylose (1, 2). In this study, the CAP6 gene, encoding an α1,3-mannosyltransferase responsible for the second mannose addition to the minor O-glycans with xylose, was identified and functionally analyzed. The CAP6 deletion in the ktr3Δ strain, in which the α1,2-mannose addition to the major O-glycans is defected, resulted in almost complete blockage of O-glycan extension. Notably, the putative two cell surface sensor proteins, Wml (Wsc/Mid2-Like)1p and Wml2p, were shown to be subjected to minor and major O-mannosylation by Cap6 and Ktr3, respectively. The proteins levels of Wml1 and Wml2 were remarkably decreased in the ktr3Δ cap6Δ mutant, indicating that proper O-mannosylation is essential for their stability. The phosphorylation of Mpk1, induced by tunicamycin, was greatly decreased in the ktr3Δcap6Δ and the wml1Δwml2Δ, supporting an essential role of O-glycans on cell surface sensors in cell wall integrity signaling. As reflecting its defective growth under several stress conditions, the ktr3Δcap6Δ strain showed fully attenuated virulence in a mouse model of cryptococcosis. The delineation of the roles of protein glycosylation in fungal pathogenesis will not only provide a deep insight into the glycan-based fungal infection mechanism but also aid in the development of novel antifungal agents.