Background: Minimal change disease (MCD) has a high recurrence rate, but currently, no biomarker can predict its recurrence. To this end, this study aimed at identifying potential serum cytokines as valuable biomarkers for predicting the risk of MCD recurrence.
Materials And Methods: Raybiotech 440 cytokine antibody microarray was used to detect the serum samples of eight relapsed, eight non-relapsed MCD patients after glucocorticoid treatment, and eight healthy controls. The differentially expressed cytokines were confirmed by enzyme-linked immunosorbent assay (ELISA) with serum samples from 29 non-relapsed and 35 relapsed MCD patients. The study used the receiver operating characteristic (ROC) curve analysis to investigate the sensitivity and specificity of a serum biomarker for predicting the MCD relapse.
Results: Serum IL-12p40 levels increased significantly in the relapsed group. The Area Under the ROC Curve (AUC) of IL-12p40 was 0.727 (95%CI: 0.597-0.856; < 0.01). The RNA-sequencing analysis and qPCR assay performed on the IL-12 treated mouse podocytes and the control group showed increased expression of podocyte damage genes, such as connective tissue growth factor (CTGF), matrix metallopeptidase 9 (MMP9), secreted phosphoprotein 1 (SPP1), and cyclooxygenase-2 (COX-2) in the former group.
Conclusion: IL-12p40 may serve as a new biomarker for predicting the risk of MCD recurrence after glucocorticoid treatment, and it may be involved in the pathogenesis and recurrence of MCD.
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http://dx.doi.org/10.3389/fmed.2022.922193 | DOI Listing |
Medicina (Kaunas)
November 2024
Department of Internal Medicine and Nephrology, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania.
Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most frequent genetic renal disease with a complex physiopathology. More and more studies sustain that inflammation plays a crucial role in ADPKD pathogenesis and progression. We evaluated IL-12 involvement in ADPKD pathophysiology by assessing the serum levels of its monomers and heterodimers.
View Article and Find Full Text PDFBMC Psychiatry
November 2024
Department of Psychiatry, The Fourth People's Hospital of Lianyungang, The Affiliated KangDa College of Nanjing Medical University, No. 316, Jiefangdong Road, Lianyungang, Jiangsu, 222003, PR China.
Background: Immune dysregulation has been identified as a contributing factor in the pathophysiology of schizophrenia. This study aimed to investigate variations in specific immune regulators and their correlation with psychopathology and cognitive functions in male patients with chronic schizophrenia.
Methods: Employing a cross-sectional design, this study included 72 male patients with chronic schizophrenia.
Int J Alzheimers Dis
September 2024
Center for Life Sciences National Laboratory Astana Nazarbayev University, Astana, Kazakhstan.
Recent studies strongly suggest that gut microbiome can influence brain functions and contribute to the development of Alzheimer's disease (AD). However, reported changes in the gut microbiomes in AD patients from different countries are not similar, and more research is needed to reveal the relationships between human microbiomes and AD in diverse ethnic populations. There is also an assumption that microbiome-associated peripheral inflammation might drive the development of sporadic AD.
View Article and Find Full Text PDFCytokine
November 2024
Department of Urology, Beijing Friendship Hospital, Capital Medical University, China; Institute of Urology, Beijing Municipal Health Commission, China. Electronic address:
UFMylation, a novel ubiquitin-like protein modification system, has been recently found to be activated in inflammation. However, the effects of UFMylation activation on inflammation in vivo remains unclear. In the present study, we generated a UFMylation activated mice using transgenic (TG) techniques.
View Article and Find Full Text PDFNanomaterials (Basel)
September 2024
Research Center for Macromolecules and Biomaterials, National Institute for Materials Science (NIMS), Tsukuba 305-0047, Japan.
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