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Possible association of rotavirus IgG with cytokine expression levels and dyslipidemia in rotavirus-infected type 1 diabetic children

Rehab G. Khalil; Adel Abdel-Moneim; Amany A. Arafa; Gamal Allam; Waled M. El-Senousy; Doaa Mabrouk
Molecular Biology Reports · Vol. 49, Issue 8 · pp. 7587-7599 · 2022

Abstract

Background Rotavirus (RV) has been postulated as a viral trigger for the onset of autoimmune disorders, such as type 1 diabetes (T1D). This study aimed to examine the conceivable association of RV IgG with cytokine levels and dyslipidemia in the pathogenesis of pediatric T1D. Methods This study included 30 healthy controls and 80 children with T1D who were divided into two groups based on the time since their T1D diagnosis: newly diagnosed (ND ≤ 1 year; n = 30) and previously diagnosed (PD > 1 year; n = 50). ND and PD patients were also separated into negative and positive according to IgG detection (RV IgG − , ND − , and PD − ; RV IgG + , ND + , and PD + ). Results Positive polymerase chain reaction for RVs was evidenced in 7.5% of children with T1D. Anti-RV IgG was 30% and 36% in ND and PD, respectively, compared to healthy controls (2 of 30, 6.6%; P < 0.05). Fasting blood sugar and hemoglobin A1c significantly increased in PD + compared to PD − . Interferon-γ and interleukin (IL)-15 levels significantly increased. IL-12 and IL-22 mRNA expression was upregulated in ND + patients compared to that in ND − patients. IL-37 mRNA expression was significantly downregulated in ND − and ND + patients compared to that in healthy controls. Total cholesterol and high- and low-density lipoprotein-cholesterol levels were significantly lower in PD + than in PD − ; whereas triglyceride levels were higher than those in healthy controls. Conclusions This study suggested that anti-RV IgG may have a role in the pathogenesis, development, and progression of T1D, and RV infections are implicated in dyslipidemia and inflammation status.

Bibliographic Information

JournalMolecular Biology Reports
PublisherSpringer
Publication Date2022-08-01
Publication Year2022
Volume49
Issue8
Pages7587-7599
Document TypeJournal Article
Print ISSN0301-4851
eISSN1573-4978
DOI10.1007/s11033-022-07573-0

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NARA Access Coverage1973-01-01~Current
Journal Homepagehttps://www.springer.com/journal/11033
Publisher PageOpen Publisher Page
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