Activation of aryl hydrocarbon receptor (AhR) in mesenchymal stem cells modulates macrophage polarization in asthma

Autor: Taoping Li, Zhuang Cui, Peisong Gao, Ting Xu, Danqing Li, Yuan Feng
Rok vydání: 2020
Předmět:
Male
Cockroaches
Cell Communication
010501 environmental sciences
Toxicology
01 natural sciences
Pathogenesis
Mice
Basic Helix-Loop-Helix Transcription Factors
Macrophage
Lung
Cells
Cultured

0303 health sciences
biology
Chemistry
aryl hydrocarbon receptor
Interleukin
respiratory system
Phenotype
Cell biology
Signal Transduction
lcsh:Immunologic diseases. Allergy
CYP1B1
Immunology
Primary Cell Culture
Macrophage polarization
macrophage
cockroach allergen
03 medical and health sciences
lcsh:RA1190-1270
Animals
Humans
030304 developmental biology
0105 earth and related environmental sciences
lcsh:Toxicology. Poisons
Macrophages
Mesenchymal stem cell
Mesenchymal Stem Cells
Allergens
Macrophage Activation
Aryl hydrocarbon receptor
Asthma
Coculture Techniques
respiratory tract diseases
Disease Models
Animal

Receptors
Aryl Hydrocarbon

biology.protein
Pyrazoles
lcsh:RC581-607
Azo Compounds
Zdroj: Journal of Immunotoxicology, Vol 17, Iss 1, Pp 21-30 (2020)
ISSN: 1547-6901
Popis: Macrophage polarization has been demonstrated to exert a vital role on asthma pathogenesis. Mesenchymal stem cells (MSC) have the capacity to modulate macrophage differentiation from a pro-inflammatory M1 phenotype toward an anti-inflammatory M2 phenotype. However, the impact of MSC-macrophage interactions on asthma development and underlying mechanisms responsible for this interaction remain largely unknown. The aim of this study was to investigate the role of AhR expressed on MSC in macrophage polarization in a cockroach extract (CRE)-induced asthma mouse model. The studies here revealed that MSC polarized macrophages from a pro-inflammatory M1 phenotype toward an anti-inflammatory M2 phenotype in this model. The mRNA levels of interleukin (IL)-6, IL-1β, and NOS2 as M1 markers were significantly decreased while those of select M2 markers such as Arg-1, FIZZ1, and YM-1 were significantly enhanced. It was also observed that aryl hydrocarbon receptor (AhR) signaling was significantly increased during asthma pathogenesis as demonstrated by enhanced mRNA expression of AhR, CYP1a1, and CYP1b1. It was also seen that the elevated AhR signaling was able to attenuate the onset of asthma. Use of an AhR antagonist (CH223191) resulted in significant inhibition of the AhR signaling and increases in M2 marker expression, but led to elevation of expression of M1 markers in the CRE-induced asthma model. Taken together, the current study showed that MSC can modulate macrophage polarization, in part, via activation of AhR signaling during CRE-induced asthma.
Databáze: OpenAIRE
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