In a reciprocal manner, adipocytes and their precursors interact with the immune system through the release of various cytokines, potentially linking fat and inflammation [2]. Interleukin-17A (IL-17A) is a recently discovered cytokine produced primarily in T-helper 17 (Th17) cells which play a role in a variety of inflammatory conditions [3] and HIV infection [4]. In adipose tissue, IL-17A is
an important regulator of adipogenesis in murine models, and in vitro it acts on preadipocytes and adipocytes to inhibit adipogenesis [5, 6]. However, the relevance of IL-17 to human obesity remains to be established. The pathway regulating the association between IL-17A and obesity remains controversial, and the association between Th17 cells and adipose tissue inflammation remains to be determined. There are no data on the role of IL-17A Navitoclax in adipogenesis or obesity in HIV-1-infected subjects. The aim of the study was to assess the correlation between IL-7A plasma level and visceral obesity in HIV-1-infected patients. Eighty-four patients between 18 and 70 years of age with a chronic HIV-1 infection, who had been
on highly active antiretroviral therapy (HAART) for more than 6 months, were consecutively recruited. An in-depth assessment was performed, including HIV disease history, duration of HAART and infection, viral load, metabolic parameters, BMI, abdominal waist circumference, smoking status and blood Protein Tyrosine Kinase inhibitor pressure. Subjects were excluded from participating if they had any of the following clinical conditions: active AIDS-defining illness, active drug abuse or alcohol abuse. HIV-1-infected patients were divided into two groups. The first group comprised patients with a diagnosis of visceral obesity. The second group included patients for whom a diagnosis of visceral obesity had been excluded. Forty-six subjects (23 with visceral obesity and 23 without) Tyrosine-protein kinase BLK negative for HIV infection were also selected to match HIV-positive patients in terms of age range and gender distribution as a control
group. The diagnosis of central obesity was confirmed by measurement of visceral fat thickness based on ultrasound measurement of the PRFD/BMI ratio according to previously published data [7-9]. For ultrasound measurement, a Logiq 5 ultrasound scanner (General Electric Medical Systems, Wallingford, CT) equipped with a 3.75-MHz convex probe was used. Sonographic evaluation of visceral obesity was performed by a single trained sonographer blinded to the patients’ data. For each subject, an aliquot of serum sample was collected and stored at −80°C. Serum IL-17 was measured by enzyme-linked immunosorbent assay (ELISA; R&D Systems, Abingdon, UK) in duplicate, adding 100 μL of serum per well following the manufacturer’s recommendations.