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Immunological Profiling of Obesity.

Ignacio RM, Kim CS, Kim SK - J Lifestyle Med (2014)

Bottom Line: It is widely accepted that chronic inflammation contributes to the pathogenesis of obesity.This immunologic dysregulation has led to the development of the classical pro-inflammatory paradigm.However, since chronic inflammation associated with obesity is more than just the overproduction of pro-inflammatory cytokines, precise dissection requires beyond the classical pro-inflammatory cytokines.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental Medical Biology, Yonsei University Wonju College of Medicine, Wonju, Korea.

ABSTRACT
It is widely accepted that chronic inflammation contributes to the pathogenesis of obesity. Researchers have recently discovered that increased inflammatory cytokines and the infiltration and activation of macrophage cells in the adipose tissue are related to chronic obesity. This immunologic dysregulation has led to the development of the classical pro-inflammatory paradigm. However, since chronic inflammation associated with obesity is more than just the overproduction of pro-inflammatory cytokines, precise dissection requires beyond the classical pro-inflammatory cytokines. The purpose of this review is to summarize the immunological profiling of obesity for theragnostic convenience, focusing on the cytokine and adipokine network in obesity and the significance of the balance of Th1/Th2 immunity.

No MeSH data available.


Related in: MedlinePlus

The human host immune response to a variety of inflammatory states involves a balance between pro-inflammatory and anti-inflammatory cytokines. Adiponectin can act in an autocrine fashion and leads to proliferation, differentiation and activation from preadipocytes to adipocytes. One hallmark of obesity is inflamed adipose tissue leading to macrophage recruitment. Activated adipose tissue is responsible for the secretion of leptin and adiponectin, while increased numbers of macrophages cause phenotypic and morphological changes. These changes include the polarization of adipose tissue macrophages toward a classical M1 or alternatively-activated M2 phenotype, which are associated with potent pro-inflammatory and anti-inflammatory activities, respectively. M1 arises in response to IFN-γ and IL-2, while M2 macrophages arise in response to various immunomodulatory factors such as IL-4, IL-10 and IL-13. In low-grade chronic inflammation associated with obesity, there is a phenotypic shift from M2 to M1, with a prominent M1 macrophage infiltration, consequently augmenting the release of T helper type-1 cytokines such as IL-1, IL-2, IL-6, TNF, monocyte chemo-attractant protein (MCP)-1 and interferon gamma (IFN-γ). Adipocytes can directly and indirectly interact with a wide variety of circulating immunocytes such as granulocytes, NK cells, and monocytes as part of the pro-inflammatory response; and eosinophils, mast cells and B cells as part of the anti-inflammatory response, eventually leading to aberrant immune homeostasis.
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f1-jlm-04-01: The human host immune response to a variety of inflammatory states involves a balance between pro-inflammatory and anti-inflammatory cytokines. Adiponectin can act in an autocrine fashion and leads to proliferation, differentiation and activation from preadipocytes to adipocytes. One hallmark of obesity is inflamed adipose tissue leading to macrophage recruitment. Activated adipose tissue is responsible for the secretion of leptin and adiponectin, while increased numbers of macrophages cause phenotypic and morphological changes. These changes include the polarization of adipose tissue macrophages toward a classical M1 or alternatively-activated M2 phenotype, which are associated with potent pro-inflammatory and anti-inflammatory activities, respectively. M1 arises in response to IFN-γ and IL-2, while M2 macrophages arise in response to various immunomodulatory factors such as IL-4, IL-10 and IL-13. In low-grade chronic inflammation associated with obesity, there is a phenotypic shift from M2 to M1, with a prominent M1 macrophage infiltration, consequently augmenting the release of T helper type-1 cytokines such as IL-1, IL-2, IL-6, TNF, monocyte chemo-attractant protein (MCP)-1 and interferon gamma (IFN-γ). Adipocytes can directly and indirectly interact with a wide variety of circulating immunocytes such as granulocytes, NK cells, and monocytes as part of the pro-inflammatory response; and eosinophils, mast cells and B cells as part of the anti-inflammatory response, eventually leading to aberrant immune homeostasis.

Mentions: In the point of innate immunology, obesity is widely characterized by macrophage infiltration into the adipose tissue. This tissue-resident macrophage has two different phenotypes: M1 (pro-inflammatory) and M2 (anti-inflammatory) [28–31]. Chronic obesity involves the accumulation of M1-polarized macrophages [29–31] and a switch from the M2 to the M1 phenotype. That is, chronic obesity leads to a more pro-inflammatory profile (Fig. 1) [28]. Thus, the absence of the anti-inflammatory macrophage response is linked to a higher risk of obesity, inflammation and insulin resistance [32]. The M1/M2 polarization paradigm describes the macrophage activation directed against pro-inflammatory M1 driven by the Th-1 type cytokine such as interferon-gamma (IFN-γ) (Fig. 1) [33]. This “phenotype switch” from M2 to M1 made it plausible that T cells and Th1/2 cytokines would act as orchestrators of adipose tissue-resident macrophage responses during the development of obesity-associated adipose tissue inflammation and insulin resistance [28,34,35].


Immunological Profiling of Obesity.

Ignacio RM, Kim CS, Kim SK - J Lifestyle Med (2014)

The human host immune response to a variety of inflammatory states involves a balance between pro-inflammatory and anti-inflammatory cytokines. Adiponectin can act in an autocrine fashion and leads to proliferation, differentiation and activation from preadipocytes to adipocytes. One hallmark of obesity is inflamed adipose tissue leading to macrophage recruitment. Activated adipose tissue is responsible for the secretion of leptin and adiponectin, while increased numbers of macrophages cause phenotypic and morphological changes. These changes include the polarization of adipose tissue macrophages toward a classical M1 or alternatively-activated M2 phenotype, which are associated with potent pro-inflammatory and anti-inflammatory activities, respectively. M1 arises in response to IFN-γ and IL-2, while M2 macrophages arise in response to various immunomodulatory factors such as IL-4, IL-10 and IL-13. In low-grade chronic inflammation associated with obesity, there is a phenotypic shift from M2 to M1, with a prominent M1 macrophage infiltration, consequently augmenting the release of T helper type-1 cytokines such as IL-1, IL-2, IL-6, TNF, monocyte chemo-attractant protein (MCP)-1 and interferon gamma (IFN-γ). Adipocytes can directly and indirectly interact with a wide variety of circulating immunocytes such as granulocytes, NK cells, and monocytes as part of the pro-inflammatory response; and eosinophils, mast cells and B cells as part of the anti-inflammatory response, eventually leading to aberrant immune homeostasis.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4390759&req=5

f1-jlm-04-01: The human host immune response to a variety of inflammatory states involves a balance between pro-inflammatory and anti-inflammatory cytokines. Adiponectin can act in an autocrine fashion and leads to proliferation, differentiation and activation from preadipocytes to adipocytes. One hallmark of obesity is inflamed adipose tissue leading to macrophage recruitment. Activated adipose tissue is responsible for the secretion of leptin and adiponectin, while increased numbers of macrophages cause phenotypic and morphological changes. These changes include the polarization of adipose tissue macrophages toward a classical M1 or alternatively-activated M2 phenotype, which are associated with potent pro-inflammatory and anti-inflammatory activities, respectively. M1 arises in response to IFN-γ and IL-2, while M2 macrophages arise in response to various immunomodulatory factors such as IL-4, IL-10 and IL-13. In low-grade chronic inflammation associated with obesity, there is a phenotypic shift from M2 to M1, with a prominent M1 macrophage infiltration, consequently augmenting the release of T helper type-1 cytokines such as IL-1, IL-2, IL-6, TNF, monocyte chemo-attractant protein (MCP)-1 and interferon gamma (IFN-γ). Adipocytes can directly and indirectly interact with a wide variety of circulating immunocytes such as granulocytes, NK cells, and monocytes as part of the pro-inflammatory response; and eosinophils, mast cells and B cells as part of the anti-inflammatory response, eventually leading to aberrant immune homeostasis.
Mentions: In the point of innate immunology, obesity is widely characterized by macrophage infiltration into the adipose tissue. This tissue-resident macrophage has two different phenotypes: M1 (pro-inflammatory) and M2 (anti-inflammatory) [28–31]. Chronic obesity involves the accumulation of M1-polarized macrophages [29–31] and a switch from the M2 to the M1 phenotype. That is, chronic obesity leads to a more pro-inflammatory profile (Fig. 1) [28]. Thus, the absence of the anti-inflammatory macrophage response is linked to a higher risk of obesity, inflammation and insulin resistance [32]. The M1/M2 polarization paradigm describes the macrophage activation directed against pro-inflammatory M1 driven by the Th-1 type cytokine such as interferon-gamma (IFN-γ) (Fig. 1) [33]. This “phenotype switch” from M2 to M1 made it plausible that T cells and Th1/2 cytokines would act as orchestrators of adipose tissue-resident macrophage responses during the development of obesity-associated adipose tissue inflammation and insulin resistance [28,34,35].

Bottom Line: It is widely accepted that chronic inflammation contributes to the pathogenesis of obesity.This immunologic dysregulation has led to the development of the classical pro-inflammatory paradigm.However, since chronic inflammation associated with obesity is more than just the overproduction of pro-inflammatory cytokines, precise dissection requires beyond the classical pro-inflammatory cytokines.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental Medical Biology, Yonsei University Wonju College of Medicine, Wonju, Korea.

ABSTRACT
It is widely accepted that chronic inflammation contributes to the pathogenesis of obesity. Researchers have recently discovered that increased inflammatory cytokines and the infiltration and activation of macrophage cells in the adipose tissue are related to chronic obesity. This immunologic dysregulation has led to the development of the classical pro-inflammatory paradigm. However, since chronic inflammation associated with obesity is more than just the overproduction of pro-inflammatory cytokines, precise dissection requires beyond the classical pro-inflammatory cytokines. The purpose of this review is to summarize the immunological profiling of obesity for theragnostic convenience, focusing on the cytokine and adipokine network in obesity and the significance of the balance of Th1/Th2 immunity.

No MeSH data available.


Related in: MedlinePlus