The Immune Response in Adipocytes and Their Susceptibility to Infection: A Possible Relationship with Infectobesity

Abstract

The current obesity pandemic has been expanding in both developing and developed countries. This suggests that the factors contributing to this condition need to be reconsidered since some new factors are arising as etiological causes of this disease. Moreover, recent clinical and experimental findings have shown an association between the progress of obesity and some infections, and the functions of adipose tissues, which involve cell metabolism and adipokine release, among others. Furthermore, it has recently been reported that adipocytes could either be reservoirs for these pathogens or play an active role in this process. In addition, there is abundant evidence indicating that during obesity, the immune system is exacerbated, suggesting an increased susceptibility of the patient to the development of several forms of illness or death. Thus, there could be a relationship between infection as a trigger for an increase in adipose cells and the impact on the metabolism that contributes to the development of obesity. In this review, we describe the findings concerning the role of adipose tissue as a mediator in the immune response as well as the possible role of adipocytes as infection targets, with both roles constituting a possible cause of obesity.

Presence of human adenovirus 36 in visceral fat tissue, viral load, and analysis of its genetic variability

“…Although it has been argued that Ad36 infection is a marker of “low risk” to develop obesity, 10 in the present study, we found this virus to be associated with patients with obesity at a high frequency. In agreement with previous studies, 13–15,21 our results strengthen the need to continue studying the molecular mechanisms involved in infectobesity, particularly the host‒pathogen relationship, in accordance with other authors 39,43 . In light of our results, we consider it important to reconsider whether Ad36 infection is truly a low‐risk factor for developing obesity.…”

“…In agreement with previous studies, [13][14][15]21 our results strengthen the need to continue studying the molecular mechanisms involved in infectobesity, particularly the host-pathogen relationship, in accordance with other authors. 39,43 In light of our results, we consider it important to reconsider whether Ad36 infection is truly a low-risk factor for developing obesity.…”

“…38 However, the complexity of this phenomenon based on the host-pathogen relationship is not entirely clear. 39 Barrera-Alcocer et al 24 with obesity from a total of 131 male and female participants. Similar to Barrera-Alcocer et al 24 we did not find associations among clinical or metabolic measurements from Ad36-positive versus Ad36negative individuals.…”

“…(i) increasing differentiation and proliferation of preadipocytes into adipocytes, (ii) promoting activation of a noninsulin‐dependent process that increases glucose uptake, and (iii) stimulating activation of glucose transporter protein isoform 4 (GLUT4) and glucose transporter protein isoform 1 (GLUT1) 38 . However, the complexity of this phenomenon based on the host‒pathogen relationship is not entirely clear 39 …”

Susceptibility of Fat Tissue to SARS-CoV-2 Infection in Female hACE2 Mouse Model

“…Loss of body weight is linked with body fat mass and the pathophysiology of fat cells. Adipocytes, also known as fat cells, regulate inflammatory signaling and immune response [ 19 , 20 , 21 , 22 , 23 , 24 ]. It is well known that body fat levels and distribution patterns differ between the sexes and races [ 25 , 26 , 27 ], which may influence the susceptibility to SARS-CoV-2 infection, COVID-19-associated symptoms, and side effects.…”