PMID- 28585206
OWN - NLM
STAT- MEDLINE
DCOM- 20170912
LR  - 20220331
IS  - 0065-2598 (Print)
IS  - 0065-2598 (Linking)
VI  - 960
DP  - 2017
TI  - Adipocyte-Macrophage Cross-Talk in Obesity.
PG  - 327-343
LID - 10.1007/978-3-319-48382-5_14 [doi]
AB  - Obesity is characterized by the chronic low-grade activation of the innate immune 
      system. In this respect, macrophage-elicited metabolic inflammation and 
      adipocyte-macrophage interaction has a primary importance in obesity. Large 
      amounts of macrophages are accumulated by different mechanisms in obese adipose 
      tissue. Hypertrophic adipocyte-derived chemotactic monocyte chemoattractant 
      protein-1 (MCP-1)/C-C chemokine receptor 2 (CCR2) pathway also promotes more 
      macrophage accumulation into the obese adipose tissue. However, increased local 
      extracellular lipid concentrations is a final mechanism for adipose tissue 
      macrophage accumulation. A paracrine loop involving free fatty acids and tumor 
      necrosis factor-alpha (TNF-alpha) between adipocytes and macrophages establishes 
      a vicious cycle that aggravates inflammatory changes in the adipose tissue. 
      Adipocyte-specific caspase-1 and production of interleukin-1beta (IL-1beta) by 
      macrophages; both adipocyte and macrophage induction by toll like receptor-4 
      (TLR4) through nuclear factor-kappaB (NF-kappaB) activation; free fatty 
      acid-induced and TLR-mediated activation of c-Jun N-terminal kinase (JNK)-related 
      pro-inflammatory pathways in CD11c+ immune cells; are effective in macrophage 
      accumulation and in the development of adipose tissue inflammation. Old 
      adipocytes are removed by macrophages through trogocytosis or sending an "eat me" 
      signal. The obesity-induced changes in adipose tissue macrophage numbers are 
      mainly due to increases in the triple-positive CD11b+ F4/80+ CD11c+ adipose 
      tissue macrophage subpopulation. The ratio of M1-to-M2 macrophages is increased 
      in obesity. Furthermore, hypoxia along with higher concentrations of free fatty 
      acids exacerbates macrophage-mediated inflammation in obesity. The metabolic 
      status of adipocytes is a major determinant of macrophage inflammatory output. 
      Macrophage/adipocyte fatty-acid-binding proteins act at the interface of 
      metabolic and inflammatory pathways. Both macrophages and adipocytes are the 
      sites for active lipid metabolism and signaling.
FAU - Engin, Ayse Basak
AU  - Engin AB
AD  - Faculty of Pharmacy, Department of Toxicology, Gazi University, Hipodrom, Ankara, 
      Turkey. abengin@gmail.com.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Adv Exp Med Biol
JT  - Advances in experimental medicine and biology
JID - 0121103
SB  - IM
MH  - Adipocytes/*pathology
MH  - Adipose Tissue/pathology
MH  - Animals
MH  - Humans
MH  - Inflammation/pathology
MH  - Macrophages/*pathology
MH  - Obesity/*pathology
MH  - Signal Transduction/physiology
OTO - NOTNLM
OT  - C-C chemokine receptor 2 (CCR2)
OT  - Chemokine (C-C motif) ligand 2 (CCL2)
OT  - Free fatty acids
OT  - Hypoxia-inducible factor-1 alpha (HIF-1alpha)
OT  - Insulin-like growth factor-1 (IGF1)
OT  - Interleukin-6 (IL-6)
OT  - M1 macrophages
OT  - M2 macrophages
OT  - Monocyte chemoattractant protein-1 (MCP-1)
OT  - NOD-like receptor (NLR) family protein (NLRP3)
OT  - Obesity
OT  - Toll like receptor 4 (TLR4)
OT  - Tumor necrosis factor-alpha (TNF-alpha)
OT  - Visceral adipose tissue
EDAT- 2017/06/07 06:00
MHDA- 2017/09/13 06:00
CRDT- 2017/06/07 06:00
PHST- 2017/06/07 06:00 [entrez]
PHST- 2017/06/07 06:00 [pubmed]
PHST- 2017/09/13 06:00 [medline]
AID - 10.1007/978-3-319-48382-5_14 [doi]
PST - ppublish
SO  - Adv Exp Med Biol. 2017;960:327-343. doi: 10.1007/978-3-319-48382-5_14.