ABSTRACT
The coronavirus disease of 2019 (COVID-19) is an emerging coronavirus that affects people's respiratory systems (Severe acute respiratory syndrome coronavirus) and can the rapidly growing COVID-19 pandemic represents a significant global challenge, It can be considered that lipocalin-2 was highly associated with the severity of COVID-19. Therefore, it may be a useful biomarker for diagnosing disease severity in COVID-19 patients. lipocalin-2 was initially identified as a secreted protein from human neutrophils. Alveolar type II cells that have been damaged primarily express this substance. To verify lipocalin-2's potential as a diagnosing biomarker for COVID-19 patients, Lipocalin-2 levels in the blood were examined in this pilot investigation. To examine the relationship between serum lipocalin-2 levels and the severity of COVID-19 infection to see if this protein may be utilized as a disease indicator. This study was done in a case-control study with One hundred and twenty patients (79 males, 41 females) with COVID-19 who participated in the research. The COVID-19 patients were divided into three groups based on the severity of the illness: critical disease (n = 30), severe disease (n = 30), and mild/moderate disease (n = 60), with (n = 60) healthy volunteers serving as the control group (35 males, 25 females). Between January 2022 and May 2022, the patients were obtained from Al-Amal hospitals and the AL-Shefaa centre in ALNajaf City, Iraq., All of the patients' fundamental clinical and demographic data were collected along with blood samples. Enzyme-linked immunosorbent tests were used to measure the blood's level of LCN2 (ELISA). The levels of total cholesterol, triglycerides, and High-Density lipoprotein were assessed using colorimetric methods. Ichroma was tested for serum ferritin, D-dimer, and CBC by Swelab. ran a statistical study to see if they were related to the severity of the disease. Higher lipocalin-2 levels were observed in the patient group, particularly in cases of mild/moderate (1.32±0.30) (P. 0.001), severe(2.16±0.42) (P. 0.001), and critical(4.71±1.01) (P. 0.001) comparing cases to healthy controls (0.86±0.51) respectively, groupings. (SPO2 %, Hb, TC, HDL, LDL, and lymphocyte) levels were found to significant negative correlation with one another in the COVID-19 patient group, with p-values=0.001 for each of these relationships. Moreover, a significant positive correlation between (TG, VLDL-C, WBCs, neutrophil, platelet, N/L ratio, D-dimer, Ferritin, and CRP, p.value=0.001 for each one of them) levels with lipocalin-2 in the COVID-19 patients group. a cut-off value of 1.215 (ng/mL) for lipocalin-2 predicted severe COVID-19 with a sensitivity of 81.7 % and a specificity of 80.2 % (AUC: 0.9, 95%CI 0.852-0.949;p<0.0001). [ FROM AUTHOR] Copyright of Egyptian Academic Journal of Biological Sciences, C Physiology & Molecular Biology is the property of Egyptian Academic Journal of Biological Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)
ABSTRACT
Background and Aims: All components of the immune system are involved in alleviating severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Further research is required to provide detailed insights into COVID-19-related immune compartments and pathways. In addition, a significant percentage of hospitalized COVID-19 patients suspect bacterial infections and antimicrobial resistance occurs following antibiotics treatment. The aim of this study was to evaluate the possible effects of antibiotics on the response of neutrophil-related genes in SARS-CoV-2 patients by an experimental in silico study. Methods: The two data sets GSE1739 and GSE21802 including 10 SARS positive patients and 35 influenza A (H1N1) patients were analyzed, respectively. Differentially expressed genes (DEGs) between these two data sets were determined by GEO2R analysis and the Venn diagram online tool. After determining the hub genes involved in immune responses, the expression of these genes in 30 COVID-19 patients and 30 healthy individuals was analyzed by real-time polymerase chain reaction (PCR). All patients received antibiotics, including levofloxacin, colistin, meropenem, and ceftazidime. Results: GEO2R analysis detected 240 and 120 DEGs in GSE21802 and GSE1739, respectively. Twenty DEGs were considered as enriched hub genes involved in immune processes such as neutrophil degranulation, neutrophil activation, and antimicrobial humoral response. The central nodes were attributed to the genes of neutrophil elastase (ELANE), arginase 1 (ARG-1), lipocalin 2 (LCN2), and defensin 4 (DEFA4). Compared to the healthy subjects, the expression of LCN2 and DEFA4 were significantly reduced in COVID-19 patients. However, no significant differences were observed in the ELANE and AGR-1 levels between COVID-19 subjects and the control group. Conclusions: Activation and degranulation of neutrophils were observed mainly in SARS, and H1N1 infection processes and antibiotics administration could affect neutrophil activity during viral infection. It can be suggested that antibiotics can decrease inflammation by restoring the expression of neutrophil-related genes in COVID-19 patients.
ABSTRACT
Aim: To elucidate the transcriptional characteristics of COVID-19. Materials & methods: We utilized an integrative approach to comprehensively analyze the transcriptional features of both COVID-19 patients and SARS-CoV-2 infected cells. Results: Widespread infiltration of immune cells was observed. We identified 233 genes that were codifferentially expressed in both bronchoalveolar lavage fluid and lung samples of COVID-19 patients. Functional analysis suggested upregulated genes were related to immune response such as neutrophil activation and antivirus response, while downregulated genes were associated with cell adhesion. Finally, we identified LCN2, STAT1 and UBE2L6 as core genes during SARS-CoV-2 infection. Conclusion: The identification of core genes involved in COVID-19 can provide us with more insights into the molecular features of COVID-19.