IL-10 regulation of macrophage VEGF production is dependent on macrophage polarisation and hypoxia

Wu, Weikang; Llewellyn, Oliver; Bates, David O.; Nicholson, Lindsay B.; Dick, Andrew D.

doi:10.1016/j.imbio.2010.05.025

Cited by 137 publications

(120 citation statements)

References 42 publications

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“…A previous report indicated that M2 macrophages are associated with production of TGF-b1 and IL-10 production and M2 macrophages promote IL-10 production in the presence of LPS (Gordon, 2003;Wu et al, 2010). Inversely, by inhibiting C-X-C motif chemokine 10 production, IL-10 induces differentiation into M2 macrophages (Park-Min et al, 2005) and modulates the resultant inflammatory response (Lang et al, 2002).…”

Section: Resultsmentioning

confidence: 98%

Flagellin or Lipopolysaccharide Treatment Modified Macrophage Populations after Colorectal Radiation of Rats

Lacave-Lapalun¹,

Benderitter²,

Linard³

2013

J Pharmacol Exp Ther

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Radiation-induced acute intestinal toxicity remains a major limitation to the delivery of tumoricidal doses of colorectal irradiation. Recent reports indicate that Toll-like receptor (TLR) agonists TLR4 and TLR5 protect against toxicity due to intestinal irradiation. The phenotype (M1 or M2) of macrophages expressing TLRs may play a role in tissue repair. The aim was to investigate whether administration of TLR4 agonist lipopolysaccharide (LPS) or TLR5 agonist flagellin after irradiation modified the recruitment and phenotype of colonic macrophages and improved tissue damage. Rats were exposed to single 20-or 27-Gy doses of colorectal irradiation. TLR4 agonist LPS or TLR5 agonist flagellin (at 50 or 200 mg/rat) was administered i.p. 3 days after irradiation. Flow cytometric analysis, immunostaining, and real-time polymerase chain reaction analysis were used to assess the M1/M2 phenotype and crypt cell proliferation 7 days after irradiation. Irradiation (20 and 27 Gy) increased TLR4 1 and TLR51 macrophage frequency in the mucosa. LPS or flagellin administration maintained this elevated frequency after the 27-Gy irradiation. LPS and flagellin drove macrophages toward the anti-inflammatory M2 phenotype by increasing Arg1 and CD163 expression and microenvironmental effector molecules (C-C motif chemokine 22, transforming growth factor-b1, and interleukin-10). Proliferating cell nuclear antigen immunostaining, Ki67 expression, and antimicrobial factor Reg3g showed that the M2 shift correlated with epithelial regeneration. In conclusion, administration of either LPS or flagellin after colorectal irradiation may provide effective protection against epithelial remodeling. This tissue repair was associated with an M2 macrophage shift. Using TLR agonists to moderately activate innate immunity should be considered as a strategy for protecting healthy tissue from irradiation.

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Section: Resultsmentioning

confidence: 98%

Flagellin or Lipopolysaccharide Treatment Modified Macrophage Populations after Colorectal Radiation of Rats

Lacave-Lapalun¹,

Benderitter²,

Linard³

2013

J Pharmacol Exp Ther

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“…45 In relation to TAMs, IL-10 stimulation of TAMs/ macrophages promotes VEGFA release via STAT3 signaling, as reported for both tumoral and nontumoral conditions. 46,47 Likewise, glioblastoma-derived C-reactive protein promotes IL-6 and IL-1β production by COX2+ TAMs. 48 IL-1β is known to promote the proliferation of endothelial cells and enhances endothelial expression of pro-angiogenic factors including IL-8, VEGFA, and hypoxia-inducible factor (HIF)-1α, 49,50 which stimulate tip and stalk cell activity during the sprouting process (Fig.…”

Section: Neurooncologymentioning

confidence: 99%

The contribution of tumor-associated macrophages in glioma neo-angiogenesis and implications for anti-angiogenic strategies

et al. 2017

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"Tumor-associated macrophages" (TAMs) form a significant cell population in malignant tumors and contribute to tumor growth, metastasis, and neovascularization. Gliomas are characterized by extensive neo-angiogenesis, and knowledge of the role of TAMs in neovascularization is important for future anti-angiogenic therapies. The phenotypes and functions of TAMs are heterogeneous and more complex than a classification into M1 and M2 inflammation response types would suggest. In this review, we provide an update on the current knowledge of the ontogeny of TAMs, focusing on diffuse gliomas. The role of TAMs in the regulation of the different processes in tumor angiogenesis is highlighted and the most recently discovered mechanisms by which TAMs mediate resistance against current antivascular therapies are mentioned. Novel compounds tested in clinical trials are discussed and brought in relation to different TAM-related angiogenesis pathways. In addition, potential therapeutic targets used to intervene in TAM-regulated tumor angiogenesis are summarized.

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“…The paradigm of M1 and M2 macrophages has been studied with respect to angiogenesis. [89][90][91][92] Classical activation generates M1 macrophages, which have proinflammatory functions as we have discussed, operative during inflammation in EAU and impart tissue destruction that is effectively neutralized via blocking TNF-alpha activity. Alternatively activated M2 macrophages confer responses related to wound healing, and are capable of generating VEGF and promoting angiogenesis.…”

Section: Macrophage Conditioning Angiogenesis and Tissue Viabilitymentioning

confidence: 99%

Doyne lecture 2016: intraocular health and the many faces of inflammation

Dick

2016

Eye

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Dogma for reasons of immune privilege including sequestration (sic) of ocular antigen, lack of lymphatic and immune competent cells in the vital tissues of the eye has long evaporated. Maintaining tissue and cellular health to preserve vision requires active immune responses to prevent damage and respond to danger. A priori the eye must contain immune competent cells, undergo immune surveillance to ensure homoeostasis as well as an ability to promote inflammation. By interrogating immune responses in non-infectious uveitis and compare with age-related macular degeneration (AMD), new concepts of intraocular immune health emerge. The role of macrophage polarisation in the two disorders is a tractable start. TNF-alpha regulation of macrophage responses in uveitis has a pivotal role, supported via experimental evidence and validated by recent trial data. Contrast this with the slow, insidious degeneration in atrophic AMD or in neovasular AMD, with the compelling genetic association with innate immunity and complement, highlights an ability to attenuate pathogenic immune responses and despite known inflammasome activation. Yolk sac-derived microglia maintains tissue immune health. The result of immune cell activation is environmentally dependent, for example, on retinal cell bioenergetics status, autophagy and oxidative stress, and alterations that skew interaction between macrophages and retinal pigment epithelium (RPE). For example, dead RPE eliciting macrophage VEGF secretion but exogenous IL-4 liberates an anti-angiogenic macrophage sFLT-1 response. Impaired autophagy or oxidative stress drives inflammasome activation, increases cytotoxicity, and accentuation of neovascular responses, yet exogenous inflammasome-derived cytokines, such as IL-18 and IL-33, attenuate responses.

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IL-10 regulation of macrophage VEGF production is dependent on macrophage polarisation and hypoxia

Cited by 137 publications

References 42 publications

Flagellin or Lipopolysaccharide Treatment Modified Macrophage Populations after Colorectal Radiation of Rats

Flagellin or Lipopolysaccharide Treatment Modified Macrophage Populations after Colorectal Radiation of Rats

The contribution of tumor-associated macrophages in glioma neo-angiogenesis and implications for anti-angiogenic strategies

Doyne lecture 2016: intraocular health and the many faces of inflammation

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