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The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation

(2019) NATURE IMMUNOLOGY. 20(5). p.571-580
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Abstract
Fine control of macrophage activation is needed to prevent inflammatory disease, particularly at barrier sites such as the lungs. However, the dominant mechanisms that regulate the activation of pulmonary macrophages during inflammation are poorly understood. We found that alveolar macrophages (AlvMs) were much less able to respond to the canonical type 2 cytokine IL-4, which underpins allergic disease and parasitic worm infections, than macrophages from lung tissue or the peritoneal cavity. We found that the hyporesponsiveness of AlvMs to IL-4 depended upon the lung environment but was independent of the host microbiota or the lung extracellular matrix components surfactant protein D (SP-D) and mucin 5b (Muc5b). AlvMs showed severely dysregulated metabolism relative to that of cavity macrophages. After removal from the lungs, AlvMs regained responsiveness to IL-4 in a glycolysis-dependent manner. Thus, impaired glycolysis in the pulmonary niche regulates AlvM responsiveness during type 2 inflammation.
Keywords
TISSUE-RESIDENT MACROPHAGES, GLUCOSE-HOMEOSTASIS, FETAL MONOCYTES, TH2, INDUCTION, RESPONSES, IMMUNOMETABOLISM, PROTECTION, PATHWAYS, PROMOTES, CELLS

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Citation

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MLA
Svedberg, Freya, et al. “The Lung Environment Controls Alveolar Macrophage Metabolism and Responsiveness in Type 2 Inflammation.” NATURE IMMUNOLOGY, vol. 20, no. 5, 2019, pp. 571–80.
APA
Svedberg, F., Brown, S. L., Krauss, M. Z., Campbell, L., Sharpe, C., Clausen, M., … MacDonald, A. S. (2019). The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation. NATURE IMMUNOLOGY, 20(5), 571–580.
Chicago author-date
Svedberg, Freya, Sheila L Brown, Maria Z Krauss, Laura Campbell, Catherine Sharpe, Maryam Clausen, Gareth J Howell, et al. 2019. “The Lung Environment Controls Alveolar Macrophage Metabolism and Responsiveness in Type 2 Inflammation.” NATURE IMMUNOLOGY 20 (5): 571–80.
Chicago author-date (all authors)
Svedberg, Freya, Sheila L Brown, Maria Z Krauss, Laura Campbell, Catherine Sharpe, Maryam Clausen, Gareth J Howell, Howard Clark, Jens Madsen, Christopher M Evans, Tara E Sutherland, Alasdair C Ivens, David J Thornton, Richard K Grencis, Tracy Hussell, Danen M Cunoosamy, Peter C Cook, and Andrew S MacDonald. 2019. “The Lung Environment Controls Alveolar Macrophage Metabolism and Responsiveness in Type 2 Inflammation.” NATURE IMMUNOLOGY 20 (5): 571–580.
Vancouver
1.
Svedberg F, Brown SL, Krauss MZ, Campbell L, Sharpe C, Clausen M, et al. The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation. NATURE IMMUNOLOGY. 2019;20(5):571–80.
IEEE
[1]
F. Svedberg et al., “The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation,” NATURE IMMUNOLOGY, vol. 20, no. 5, pp. 571–580, 2019.
@article{8628852,
  abstract     = {Fine control of macrophage activation is needed to prevent inflammatory disease, particularly at barrier sites such as the lungs. However, the dominant mechanisms that regulate the activation of pulmonary macrophages during inflammation are poorly understood. We found that alveolar macrophages (AlvMs) were much less able to respond to the canonical type 2 cytokine IL-4, which underpins allergic disease and parasitic worm infections, than macrophages from lung tissue or the peritoneal cavity. We found that the hyporesponsiveness of AlvMs to IL-4 depended upon the lung environment but was independent of the host microbiota or the lung extracellular matrix components surfactant protein D (SP-D) and mucin 5b (Muc5b). AlvMs showed severely dysregulated metabolism relative to that of cavity macrophages. After removal from the lungs, AlvMs regained responsiveness to IL-4 in a glycolysis-dependent manner. Thus, impaired glycolysis in the pulmonary niche regulates AlvM responsiveness during type 2 inflammation.},
  author       = {Svedberg, Freya and Brown, Sheila L and Krauss, Maria Z and Campbell, Laura and Sharpe, Catherine and Clausen, Maryam and Howell, Gareth J and Clark, Howard and Madsen, Jens and Evans, Christopher M and Sutherland, Tara E and Ivens, Alasdair C and Thornton, David J and Grencis, Richard K and Hussell, Tracy and Cunoosamy, Danen M and Cook, Peter C and MacDonald, Andrew S},
  issn         = {1529-2908},
  journal      = {NATURE IMMUNOLOGY},
  keywords     = {TISSUE-RESIDENT MACROPHAGES,GLUCOSE-HOMEOSTASIS,FETAL MONOCYTES,TH2,INDUCTION,RESPONSES,IMMUNOMETABOLISM,PROTECTION,PATHWAYS,PROMOTES,CELLS},
  language     = {eng},
  number       = {5},
  pages        = {571--580},
  title        = {The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation},
  url          = {http://dx.doi.org/10.1038/s41590-019-0352-y},
  volume       = {20},
  year         = {2019},
}

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