The Influence of Obesity and Weight Loss on the Bioregulation of Innate/Inflammatory Responses: Macrophages and Immunometabolism

Abstract

Obesity is characterized by low-grade inflammation and more susceptibility to infection, particularly viral infections, as clearly demonstrated in COVID-19. In this context, immunometabolism and metabolic flexibility of macrophages play an important role. Since inflammation is an inherent part of the innate response, strategies for decreasing the inflammatory response must avoid immunocompromise the innate defenses against pathogen challenges. The concept “bioregulation of inflammatory/innate responses” was coined in the context of the effects of exercise on these responses, implying a reduction in excessive inflammatory response, together with the preservation or stimulation of the innate response, with good transitions between pro- and anti-inflammatory macrophages adapted to each individual’s inflammatory set-point in inflammatory diseases, particularly in obesity. The question now is whether these responses can be obtained in the context of weight loss by dietary interventions (low-fat diet or abandonment of the high-fat diet) in the absence of exercise, which can be especially relevant for obese individuals with difficulties exercising such as those suffering from persistent COVID-19. Results from recent studies are controversial and do not point to a clear anti-inflammatory effect of these dietary interventions, particularly in the adipose tissue. Further research focusing on the innate response is also necessary.

An Exploratory Critical Review on TNF-α as a Potential Inflammatory Biomarker Responsive to Dietary Intervention with Bioactive Foods and Derived Products

“…Increased levels of TNF-α have been linked with obesity and the associated low-grade chronic inflammatory status as well as with the derived cardiometabolic disorders [ 10 , 11 ]. Inversely, the reduction in body weight has been associated with a decrease in the levels of this and other cytokines [ 12 ]. Intriguingly, TNF-α also relates to metabolic dysfunctions such as anorexia and cachexia which share with obesity overlapping inflammatory mediators and IR but opposite relationship with fat mass [ 13 , 14 , 15 ].…”

The Role of Some Cytokines (Il-1, Il-6, Il-18, Il-22, TNF-Α) in the Genesis of Obesity

“…В 2000 г. группой исследователей была открыта новая молекула -интерлейкин-22 (ИЛ-22) -представитель семейства ИЛ-10, который вырабатывается преимущественно СD4+ Тхелперами (Th1, Th17, Th22) [40]. Ряд исследователей предполагают, что ИЛ-22, полученный из Т-клеток, усиливает воспаление в жировой ткани посредством ИЛ-1β и снижает чувствительность к инсулину в гепатоцитах, способствуя развитию ожирения и сахарного диабета [41,42]. ИЛ-22 выполняет различные функции, включая регуляцию воспалительных реакций, координацию между врожденным и адаптивным иммунитетом, модуляцию метаболических изменений, целостность эпителиальных клеток и выживание клеток.…”

Do Intestinal Unicellular Parasites Have a Role in the Inflammatory and Redox Status among the Severely Obese?

“…The lack of impactful behavioral or pharmacological interventions will only aggravate the situation soon [ 1 ]. Numerous research papers have established a relationship between a situation of low-level systemic inflammation (which is a recognized hallmark of obesity), the development of the metabolic syndrome, and the related chronic pathologies [ 2 , 3 , 4 ]. Lipoinflammation is a phenomenon that takes place among insulin-resistant obese individuals, in which immune cells inhabiting the white adipose tissue increase the delivery of pro-inflammatory cytokines (TNFα, IL-6) to the bloodstream [ 5 ].…”