ABSTRACT
Defensins, crucial components of the innate immune system, play a vital role against infection as part of frontline immunity. Association of SARS-CoV-2 infection with defensins has not been investigated till date. In this study, we have investigated the expression of defensin genes in the buccal cavity during COVID-19 infection. Nasopharyngeal/Oropharyngeal swab samples collected for screening SARS-CoV-2 infection were analyzed for the expression of major defensin genes by the quantitative real-time reverse transcription polymerase chain reaction, qRT-PCR. 40 SARS-CoV-2 infected positive and 40 negative swab samples were selected for the study. Based on the RT-PCR analysis involving gene specific primer for defensin genes, 10 defensin genes were found to be expressed in the Nasopharyngeal/Oropharyngeal cavity. Six defensin genes were further found to be significantly downregulated in SARS-CoV-2 infected patients as against the control, negative samples based on differential expression analysis. The genes significantly downregulated were defensin beta 4A, 4B, 106B, 107B, 103A and defensin alpha 1B. Downregulation of several defensin genes suggests that innate immunity provided by defensins is or may be compromised in SARS-CoV-2 infection resulting in progression of the disease caused by the virus. Upregulation of defensin gene expression and use of defensin peptides could be attractive therapeutic interventions.
ABSTRACT
WDR13 - a WD repeat protein, is abundant in pancreas, liver, ovary and testis. Absence of this protein in mice has been seen to be associated with pancreatic β-cell proliferation, hyperinsulinemia and age dependent mild obesity. Previously, we have reported that the absence of WDR13 in diabetic Leprdb/db mice helps in amelioration of fatty liver phenotype along with diabetes and systemic inflammation. This intrigued us to study direct liver injury and hepatic regeneration in Wdr13−/0 mice using hepatotoxin CCl4. In the present study we report slower hepatic regeneration in Wdr13−/0 mice as compared to their wild type littermates after CCl4 administration. Interestingly, during the regeneration phase, hepatic hypertriglyceridemia was observed in Wdr13 −/0 mice. Further analyses revealed an upregulation of PPAR pathway in the liver of CCl4- administered Wdr13 −/0 mice, causing de novo lipogenesis. The slower hepatic regeneration observed in CCl4 administered Wdr13 −/0 mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway.
ABSTRACT
WDR13 - a WD repeat protein, is abundant in pancreas, liver, ovary and testis. Absence of this protein in mice has been seen to be associated with pancreatic β-cell proliferation, hyperinsulinemia and age dependent mild obesity. Previously, we have reported that the absence of WDR13 in diabetic Leprdb/db mice helps in amelioration of fatty liver phenotype along with diabetes and systemic inflammation. This intrigued us to study direct liver injury and hepatic regeneration in Wdr13−/0 mice using hepatotoxin CCl4. In the present study we report slower hepatic regeneration in Wdr13−/0 mice as compared to their wild type littermates after CCl4 administration. Interestingly, during the regeneration phase, hepatic hypertriglyceridemia was observed in Wdr13 −/0 mice. Further analyses revealed an upregulation of PPAR pathway in the liver of CCl4- administered Wdr13 −/0 mice, causing de novo lipogenesis. The slower hepatic regeneration observed in CCl4 administered Wdr13 −/0 mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway.
