The Role of Macrophage Polarization in Infectious and Inflammatory Diseases

Labonte, Adam C.; Tosello‐Trampont, Annie‐Carole; Hahn, Young S.

doi:10.14348/molcells.2014.2374

Cited by 298 publications

(274 citation statements)

References 163 publications

(196 reference statements)

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“…M1 macrophages usually express a high level of cell surface markers such as CCR7, while M2 macrophages express a higher level of the mannose receptor (CD206) [15]. We accessed the expression of these surface markers by flow cytometry.…”

Section: Resultsmentioning

confidence: 99%

Autophagy Inhibition Contributes to ROS-Producing NLRP3-Dependent Inflammasome Activation and Cytokine Secretion in High Glucose-Induced Macrophages

Dai

Zhang

et al. 2017

Cell Physiol Biochem

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Background: Type 2 diabetes is a persistent inflammatory response that impairs the healing process. We hypothesized that stimulation with high glucose following a pro-inflammatory signal would lead to autophagy inhibition, reactive oxygen species (ROS) production and eventually to the activation of the Nod-like receptor protein (NLRP) -3. Methods: Macrophages were isolated from human diabetic wound. We measured the expression of NLRP3, caspase1 and interleukin-1 beta (IL-1β) by western blot and real-time PCR, and the surface markers on cells by flow cytometry. THP-1-derived macrophages exposed to high glucose were applied to study the link between autophagy, ROS and NLRP3 activation. LC3-II, P62, NLRP3 inflammation and IL-1β expression were measured by western blot and real-time PCR. ROS production was measured with a Cellular Reactive Oxygen Species Detection Assay Kit. Results: Macrophages isolated from diabetic wounds exhibited a pro-inflammatory phenotype, including sustained NLRP3 inflammasome activity associated with IL-1β secretion. Our data showed that high glucose inhibited autophagy, induced ROS production, and activated NLRP3 inflammasome and cytokine secretion in THP-1-derived macrophages. To study high glucose-induced NLRP3 inflammasome signalling, we performed studies using an autophagy inducer, a ROS inhibitor and a NLRP3 inhibitor and found that all reduced the NLRP3 inflammasome activation and cytokine secretion. Conclusion: Sustained NLRP3 inflammasome activity in wound-derived macrophages contributes to the hyper-inflammation in human diabetic wounds. Autophagy inhibition and ROS generation play an essential role in high glucose-induced NLRP3 inflammasome activation and cytokine secretion in macrophages.

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Section: Resultsmentioning

confidence: 99%

Autophagy Inhibition Contributes to ROS-Producing NLRP3-Dependent Inflammasome Activation and Cytokine Secretion in High Glucose-Induced Macrophages

Dai

Zhang

et al. 2017

Cell Physiol Biochem

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“…Macrophage phenotype and function are regulated, in large part, by their environmental milieu [42][43][44][45]. On the basis of cell morphology and function, two populations of activated macrophages have been identified [46].…”

Section: Regulation Of Macrophage Functionmentioning

confidence: 99%

“…These cells are pro-inflammatory and secrete inflammatory mediators (TNF-α, IL-1, IL-6, IL-15, IL-18, IL-23, IFN-γ), stimulate inducible nitric oxide synthase (iNOS) and promote the formation of reactive oxygen and nitrogen species [47]. The second macrophage phenotype, the alternatively activated M2 macrophage, is induced by IL-4, IL-10, IL-13 and glucocorticoid hormones [42][43][44][45]. M2 macrophages play an important role in the resolution of inflammation by inhibiting inflammatory cytokine expression and promoting wound healing [42][43][44][45].…”

Section: Regulation Of Macrophage Functionmentioning

confidence: 99%

“…The second macrophage phenotype, the alternatively activated M2 macrophage, is induced by IL-4, IL-10, IL-13 and glucocorticoid hormones [42][43][44][45]. M2 macrophages play an important role in the resolution of inflammation by inhibiting inflammatory cytokine expression and promoting wound healing [42][43][44][45]. HDL and apo A-I have been shown to promote the formation of anti-inflammatory M2 macrophages in human monocyte-derived macrophages [48] and mice [49].…”

Section: Regulation Of Macrophage Functionmentioning

confidence: 99%

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Role of HDL-Associated Proteins and Lipids in the Regulation of Inflammation

White¹,

Giordano²,

Datta³

2017

Advances in Lipoprotein Research

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Lipoproteins are complexes of lipids and proteins that carry water-insoluble cholesterol in the bloodstream. While cholesterol is required for normal cell function, hypercholesterolemia contributes to the development of cardiovascular disease (CVD). Increased low-density lipoprotein (LDL) is a major risk factor for CVD. Reduced high-density lipoprotein (HDL) levels are inversely related to CVD risk, suggesting a protective role for HDL. Several diseases, including atherosclerosis, diabetes, chronic kidney disease and rheumatoid arthritis, have been identified where HDL levels are decreased or function is compromised. HDLs are spherical particles with a hydrophobic core of cholesteryl esters surrounded by a monolayer of phospholipids, proteins and unesterified cholesterol.Apolipoprotein (apo) A-I, the major protein component of HDL, plays an important role in the assembly and function of HDL. One of the major functions of HDL is to mediate cellular cholesterol efflux and the transfer of cholesterol from extrahepatic tissues to the liver for excretion into the bile. In addition to regulating cholesterol metabolism, HDL also exhibits antioxidative, antithrombotic and anti-inflammatory properties. Under certain conditions, however, HDL may undergo biochemical modification resulting in the formation of a particle with pro-inflammatory properties. This review will focus on the variable properties of HDL under normal physiological conditions and in the context of inflammation.

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“…Не-давние исследования свидетельствуют о том, что зараженные вирусом ТОРС мыши, нокаутиро-ванные по STAT1, характеризовались более зна-чительным снижением веса и более выраженной патологией в легких, ассоциированной с повы-шенной продукцией М2-индикаторов, таких как YM1, FIZZ1, IL-4 и IL-13 [76]. Отсутствие выра-женного поражения легких у мышей с двойным нокаутом STAT1/STAT6 -/-также поддерживает концепцию о том, что М2 вносят вклад в патоге-нез ТОРС [51].…”

Section: роль макрофагов в патологии легкихunclassified