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    Apoptosis-induced T-cell lymphopenia is related to COVID-19 severity
    (Wiley, 2021) Cizmecioglu, Ahmet; Cizmecioglu, Hilal Akay; Goktepe, Mevlut Hakan; Emsen, Ayca; Korkmaz, Celalettin; Tasbent, Fatma Esenkaya; Consultant, Fatma Colkesen
    Increased levels of acute-phase reactants and lymphopenia are predictors of disease severity in coronavirus disease 2019 (COVID-19). This study aimed to investigate the role of apoptosis in the etiology of lymphopenia in patients with COVID-19. This multicentered, prospective, and case-control study was conducted with polymerase chain reaction (+) severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) patients, and an age-gender-matched control group. Samples were taken at the time of diagnosis and analyzed via flow cytometry within 24 h. The participants' demographic data and initial laboratory tests were also recorded. In total, 33 patients with COVID-19 (mean age = 45.4 +/- 17.2) and 25 controls (mean age = 43.4 +/- 17.4) participated in the study. All patients were identified as having mild (16), moderate (5), or severe (12) disease severity. Both early and late apoptotic cells in B and T lymphocytes were increased in all patients with COVID-19 (p < .05). Early apoptotic (EA) B and T lymphocytes were also higher in severe cases compared to mild cases (p = .026). There was no significant difference between lymphopenia and apoptosis in patients with COVID-19. However, patients with lymphopenia (n = 14) and severe COVID-19 (p = .013) had increased EA T lymphocytes. This study's results show that B and T lymphocytes' apoptosis increases in patients with COVID-19. In addition, enhanced T lymphocyte apoptosis is associated with disease severity in lymphopenic patients with COVID-19.
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    The change of HLA DR expressions and monocyte subsets in non-small cell lung cancer
    (Wiley, 2021) Emsen, Ayca; Artac, Mehmet; Artac, Hasibe
    [Abstract Not Availabe]
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    Correlation of myeloid-derived suppressor cells with C-reactive protein, ferritin and lactate dehydrogenase levels in patients with severe COVID-19
    (Wiley, 2022) Emsen, Ayca; Sumer, Sua; Tulek, Baykal; Cizmecioglu, Hilal; Vatansev, Husamettin; Goktepe, Mevlut Hakan; Kanat, Fikret
    The novel coronavirus disease 2019 (COVID-19) remains a global health emergency, and understanding the interactions between the virus and host immune responses is crucial to preventing its lethal effects. The expansion of myeloid-derived suppressor cells (MDSCs) in COVID-19, thereby suppressing immune responses, has been described as responsible for the severity of the disease, but the correlation between MDSC subsets and COVID-19 severity remains elusive. Therefore, we classified patients according to clinical and laboratory findings-aiming to investigate the relationship between MDSC subsets and laboratory findings such as high C-reactive protein, ferritin and lactate dehydrogenase levels, which indicate the severity of the disease. Forty-one patients with COVID-19 (26 mild and 15 severe; mean age of 49.7 +/- 15 years) and 26 healthy controls were included in this study. MDSCs were grouped into two major subsets-polymorphonuclear MDSCs (PMN-MDSCs) and monocytic MDSCs-by flow cytometric immunophenotyping, and PMN-MDSCs were defined as mature and immature, according to CD16 expressions, for the first time in COVID-19. Total MDSCs, PMN-MDSCs, mature PMN-MDSCs and monocytic MDSCs were significantly higher in patients with COVID-19 compared with the healthy controls (P < .05). Only PMN-MDSCs and their immature PMN-MDSC subsets were higher in the severe subgroup than in the mild subgroup. In addition, a significant correlation was found between C-reactive protein, ferritin and lactate dehydrogenase levels and MDSCs in patients with COVID-19. These findings suggest that MDSCs play a role in the pathogenesis of COVID-19, while PMN-MDSCs, especially immature PMN-MDSCs, are associated with the severity of the disease.
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    Reduced Monocyte Subsets, Their HLA-DR Expressions, and Relations to Acute Phase Reactants in Severe COVID-19 Cases
    (Mary Ann Liebert, Inc, 2022) Cizmecioglu, Ahmet; Emsen, Ayca; Sumer, Sua; Ergun, Dilek; Akay Cizmecioglu, Hilal; Turk Dagi, Hatice; Artac, Hasibe
    Monocytes are one of the principal immune defense cells that encounter infectious agents. However, an essential role of monocytes has been shown in the spread of viruses throughout the human body. Considering this dilemma, this study aimed to evaluate monocyte subsets and Human Leukocyte Antigen-DR isotype (HLA-DR) expressions in clinical coronavirus disease 2019 (COVID-19) cases. This prospective, multicenter, case-control study was conducted with COVID-19 patients and healthy controls. The patient group was divided into two subgroups according to disease severity (severe and non-severe). Three monocyte subsets (classical, CL; intermediate, INT; non-classical, NC) were analyzed with flow cytometry upon the patients' hospital admission. A total of 42 patients with COVID-19 and 30 controls participated in this study. The patients' conditions were either severe (n = 23) or non-severe (n = 19). All patients' monocyte and HLA-DR expressions were decreased compared with the controls (p < 0.05). Per disease severity, all monocyte subsets were not significant with disease severity; however, the HLA-DR expressions of CL monocytes (p = 0.002) and INT monocytes (p = 0.025) were more decreased in the severe patient group. In patients with various clinical features, NC monocytes were more affected. Based on these results, NC monocytes were more decreased in acute COVID-19 cases, though related various clinics decreased all monocyte subsets in these patients. Decreased monocyte HLA expressions may be a sign of immune suppression in severe patients, even when the percentage of monocyte levels has not decreased yet.
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    Response to trastuzumab and investigation of expression profiles of matrix metalloproteinase-related proteins in primary breast cancer stem cells
    (Springer-Verlag Italia Srl, 2021) Koygun, Gozde Kayadibi; Kars, Meltem Demirel; Emsen, Ayca; Artac, Hasibe; Aksoy, Faruk; Cakir, Murat; Tavli, Lema
    Breast cancer (BC) is the leading cause of cancer deaths in women. One of the reasons for the failure of BC treatment is reportedly the ineffectiveness of chemotherapeutic drugs against breast cancer stem-like cells (BCSCs). HER2 receptors have an important role in the self-renewal of BCSCs. Matrix metalloproteinase (MMP) and cytokine levels were found to be higher in BCSCs, which demonstrates their potential metastatic capacity. Therefore, the aim of this study was to evaluate the response of BCSCs to trastuzumab and to investigate the MMP levels in primary breast cancer cells and HER2(+) BCSCs. Tumour tissue samples were obtained during surgical intervention from ten breast cancer patients, and primary culture cells were established from these tissues. Four major molecular subgroups were sorted from the primary culture: HER2(+) BCSCs (CD44(+)CD24(-)HER2(+)), HER2(-) BCSCs (CD44(+)CD24(-)HER2(-)), HER2(-) primary culture cells (CD44(+)CD24(+)HER2(-)) and triple positive primary culture cells (CD44(+)CD24(+)HER2(+)). These cells were cultured and treated with trastuzumab, paclitaxel, carboplatin, and the combination of those three drugs for 96 h. Cellular responses to these drugs were determined by XTT cytotoxicity test. MMPs and cytokine array analysis showed that MMPs and TIMP-1, TIMP-2 proteins were expressed more in HER2(+) BCSCs than in primary culture. HER2(-) BCSCs were more resistant to drugs than HER2(+) BCSCs. Our findings suggest that the presence of HER2(-) BCSCs may be responsible for primary trastuzumab resistance in HER2(+) BC cell population. Further studies investigating the function of MMPs are needed for drug targeting of BCSCs.