Abstract
Metabolic disorders have been identified as major health problems affecting a large portion of the world population. In addition, obesity and insulin resistance are principal risk factors for the development of cardiovascular diseases. Altered immune responses are common features of both hypertension and obesity and, moreover, the involvement of the nervous system in the modulation of immune system is gaining even more attention in both pathophysiological contexts. For these reasons, during the last decades, researches focused their efforts on the comprehension of the molecular mechanisms connecting immune system to cardiovascular and metabolic diseases. On the other hand, it has been reported that in these pathological conditions, central neural pathways modulate the activity of the peripheral nervous system, which is strongly involved in onset and progression of the disease. It is interesting to notice that neural reflex can also participate in the modulation of immune functions. In this scenario, the spleen becomes the crucial hub allowing the interaction of different systems differently involved in metabolic and cardiovascular diseases. Here, we summarize the major findings that dissect the role of the immune system in disorders related to metabolic and cardiovascular dysfunctions, and how this could also be influenced by neural reflexes.
Highlights
Despite initially having been depicted as a blood filter, the spleen is gaining more attention for the pivotal role played in modulating immune responses [1]
A different study with high fat diet (HFD)-fed mice showed that more pro-inflammatory F4/80+CD11c+ macrophages were recruited in adipose tissue of obese mice compared with lean mice and, HFD-fed C–C motif chemokine receptor 2 (CCR2) KO mice showed a decreased content of the same population of immune cells, suggesting that infiltrating cells were recruited through a mechanism mediated by the chemokine monocyte chemoattractant protein-1 (MCP1/CCL2) and CCR2 [38]
As a further mechanism modulating the immune response involved in metabolic disease, it has been shown that adipose tissue releases free fatty acids (FFAs), which enhance inflammation trough Toll-like receptor 4 (TLR4) via Fetuin-A (FET-A) and the consequent activation of Nuclear factor KB (NF-KB) induced insulin resistance (IR)
Summary
Despite initially having been depicted as a blood filter, the spleen is gaining more attention for the pivotal role played in modulating immune responses [1]. A different study with HFD-fed mice showed that more pro-inflammatory F4/80+CD11c+ macrophages were recruited in adipose tissue of obese mice compared with lean mice and, HFD-fed C–C motif chemokine receptor 2 (CCR2) KO mice showed a decreased content of the same population of immune cells, suggesting that infiltrating cells were recruited through a mechanism mediated by the chemokine monocyte chemoattractant protein-1 (MCP1/CCL2) and CCR2 [38]. As a further mechanism modulating the immune response involved in metabolic disease, it has been shown that adipose tissue releases free fatty acids (FFAs), which enhance inflammation trough Toll-like receptor 4 (TLR4) via Fetuin-A (FET-A) and the consequent activation of Nuclear factor KB (NF-KB) induced IR. In response to specific stimuli, a dysregulation of the immune system may become a principal actor in the development of metabolic syndrome
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