Biomarkers of Inflammation in Obesity-Psoriatic Patients

Abstract

Psoriasis is a common chronic inflammatory multisystemic disease with a complex pathogenesis consisting of genetic, immunological, and environmental components. It is associated with a number of comorbidities, including diabetes, metabolic syndrome, obesity, and myocardial infarction. In addition, the severity of psoriasis seems to be related to the severity of obesity. Patients with higher levels of obesity show poorer response to systemic treatments of psoriasis. Several studies have demonstrated that white adipose tissue is a crucial site of the formation of proinflammatory adipokines such as leptin, adiponectin, and resistin and classical cytokines such as interleukin- (IL-) 6 and tumour necrosis factor-α. In psoriasis, due to the proliferation of Th1, Th17, and Th22 cells, IL-22, among others, is produced in addition to the abovementioned cytokines. With respect to leptin and resistin, both of these adipokines are present in high levels in obese persons with psoriasis. Further, the plasma levels of leptin and resistin are related to the severity of psoriasis. These results strongly suggest that obesity, through proinflammatory pathways, is a predisposing factor to the development of psoriasis and that obesity aggravates existing psoriasis. Different inflammatory biomarkers link psoriasis and obesity. In this paper, the most important ones are described.

Figure 1

Metabolic pathway of lipoinflammation. The interactive association among psoriasis, obesity, type 2 diabetes, cardiovascular disease, and mortality would be based on the inflammation observed in each of these diseases and transported systemically, especially to other inflammatory processes.

Figure 2

IL-22 stimulation leads to lymphocyte proliferation, which in turn accelerates the synthesis of molecules, elimination of germs, and desquamation. Thus, the epidermis can participate in innate and adaptive immunity in response to infection or stimulation with cytokines. This is due to an increase in the levels of molecules, such as AMP; in the production of chemokines, such as IFN-α, TSL, and TSLP; and in the number of Th17 and IL-17-producing CD4+ and CD8+ T cells and T- helper cells (Th). This mechanism responds to the pathogenesis of psoriasis.