Inflammatory Cytokines, Redox Status, and Cardiovascular Diseases Risk after Weight Loss via Bariatric Surgery and Lifestyle Intervention.

Background and Objectives: Obesity is a chronic inflammatory condition and is considered a major risk factor for cardiovascular disease (CVD). The effects of obesity management via sleeve gastrectomy (SG) and lifestyle intervention (LS) on inflammatory cytokines, redox status, and CVD risk were studied in this work. Materials and Methods: A total of 92 participants (18 to 60 years old) with obesity (BMI ≥ 35 kg/m2 were divided into two groups: the bariatric surgery (BS) group (n = 30), and the LS group (n = 62). According to the achievement of 7% weight loss after 6 months, the participants were allocated to either the BS group, the weight loss (WL) group, or the weight resistance (WR) group. Assessments were performed for body composition (by bioelectric impedance), inflammatory markers (by ELISA kits), oxidative stress (OS), antioxidants (by spectrophotometry), and CVD risk (by the Framingham risk score (FRS) and lifetime atherosclerotic cardiovascular disease risk (ASCVD)). Measurements were taken before and after six months of either SG or LS (500 kcal deficit balanced diet, physical activity, and behavioral modification). Results: At the final assessment, only 18 participants in the BS group, 14 participants in the WL group, and 24 participants in the WR group remained. The loss in fat mass (FM) and weight loss were greatest in the BS group (p < 0.0001). Levels of IL-6, TNF-a, MCP-1, CRP, and OS indicators were significantly reduced in the BS and WL groups. The WR group had significant change only in MCP-1 and CRP. Significant reductions in the CVD risk in the WL and BS groups were detected only when using FRS rather than ASCVD. The FM loss correlated inversely with FRS-BMI and ASCVD in the BS group, whereas in the WL group, FM loss correlated only with ASCVD. Conclusions: BS produced superior weight and fat mass loss. However, both BS and LS produced a similar reduction in the inflammatory cytokines, relief of OS indicators, and enhancement of antioxidant capacity, and consequently reduced the CVD risk.

Correction: Abulmeaty et al. Effect of Long-Term Continuous Light Exposure and Western Diet on Adropin Expression, Lipid Metabolism, and Energy Homeostasis in Rats. Biology 2021, 10, 413.

In the original publication [...].

Effect of Long-Term Continuous Light Exposure and Western Diet on Adropin Expression, Lipid Metabolism, and Energy Homeostasis in Rats.

Long-term continuous light exposure (CL) and western diet (WD) effects on Adropin expression, RORα, and Rev-erb-α nuclear receptors and energy homeostasis were studied in rats. Thirty-two male Wistar rats (250-290 g) were enrolled for 3 months in the following groups (n = 8/group): (a) Normal control group (NC), (b) CL group, (c) WD group, and (d) CL + WD group. Then, indirect calorimetry and food intake (FI) were measured. Finally, Adropin, hormone-sensitive lipase (HSL), adipocyte triglyceride lipase (ATGL), and free fatty acids (FFA) were measured. Additionally, the histopathology and gene expression of Enho, RORα, and Rev-erb-α genes were done. The CL alone elevated the Adropin plasma level and gene expression, increased RORα expression, and decreased the Rev-erb-α nuclear receptor expression mainly in the liver and kidney. Besides, CL increased the total energy expenditure (TEE) and decreased the respiratory quotient. WD alone or in combination with the CL reversed gene expression of Enho, RORα, and Rev-erb-α. Combined CL and WD increased the TEE, reduced the food intake, increased the ATGL, and reduced the Adropin level in addition to widespread degenerative changes in the liver, spleen, and renal tissues. The deleterious effects of CL and WD on energy homeostasis may include Adropin with the involvement of the RORα and Rev-erb-α nuclear receptors.

Human CD3+ T-Cells with the Anti-ERBB2 Chimeric Antigen Receptor Exhibit Efficient Targeting and Induce Apoptosis in ERBB2 Overexpressing Breast Cancer Cells.

Breast cancer is a common malignancy among women. The innate and adaptive immune responses failed to be activated owing to immune modulation in the tumour microenvironment. Decades of scientific study links the overexpression of human epidermal growth factor receptor 2 (ERBB2) antigen with aggressive tumours. The Chimeric Antigen Receptor (CAR) coding for specific tumour-associated antigens could initiate intrinsic T-cell signalling, inducing T-cell activation, and cytotoxic activity without the need for major histocompatibility complex recognition. This renders CAR as a potentially universal immunotherapeutic option. Herein, we aimed to establish CAR in CD3+ T-cells, isolated from human peripheral blood mononucleated cells that could subsequently target and induce apoptosis in the ERBB2 overexpressing human breast cancer cell line, SKBR3. Constructed CAR was inserted into a lentiviral plasmid containing a green fluorescent protein tag and produced as lentiviral particles that were used to transduce activated T-cells. Transduced CAR-T cells were then primed with SKBR3 cells to evaluate their functionality. Results showed increased apoptosis in SKBR3 cells co-cultured with CAR-T cells compared to the control (non-transduced T-cells). This study demonstrates that CAR introduction helps overcome the innate limitations of native T-cells leading to cancer cell apoptosis. We recommend future studies should focus on in vivo cytotoxicity of CAR-T cells against ERBB2 expressing tumours.