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E-cadherin expression in macrophages dampens their inflammatory responsiveness in vitro, but does not modulate M2-regulated pathologies in vivo

Jan Van den Bossche, Damya Laoui, Thomas Naessens (UGent) , Hermelijn H Smits, Cornelis H Hokke, Benoit Stijlemans, Johan Grooten (UGent) , Patrick De Baetselier and Jo A Van Ginderachter
(2015) SCIENTIFIC REPORTS. 5.
Author
Organization
Abstract
IL-4/IL-13-induced alternatively activated macrophages (M(IL-4/IL-13), AAMs or M2) are known to express E-cadherin, enabling them to engage in heterotypic cellular interactions and IL-4-driven macrophage fusion in vitro. Here we show that E-cadherin overexpression in Raw 264.7 macrophages inhibits their inflammatory response to LPS stimulation, as demonstrated by a reduced secretion of inflammatory mediators like interleukin (IL)-6, tumor necrosis factor (TNF) and nitric oxide (NO). To study the function of E-cadherin in M(IL-4/IL-13) macrophages in vivo, we generated macrophage-specific E-cadherin-deficient C57BL/6 mice. Using this new tool, we analyzed immunological parameters during two typical AAM-associated Th2-driven diseases and assessed Th2-associated granuloma formation. Although E-cadherin is strongly induced in AAMs during Taenia crassiceps helminth infections and allergic airway inflammation, its deletion in macrophages does not affect the course of both Th2 cytokine-driven diseases. Moreover, macrophage E-cadherin expression is largely redundant for granuloma formation around Schistosoma mansoni ova. Overall, we conclude that E-cadherin is a valuable AAM marker which suppresses the inflammatory response when overexpressed. Yet E-cadherin deletion in macrophages does not affect M(LPS+IFN gamma) and M(IL-4) polarization in vitro, nor in vivo macrophage function, at least in the conditions tested.
Keywords
RESPONSES, MECHANISM, FUSION, LUNG, RESISTANCE, MICE, GIANT-CELLS, MYELOID CELLS, ALTERNATIVELY ACTIVATED MACROPHAGES, PARASITE TAENIA-CRASSICEPS

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MLA
Van den Bossche, Jan, et al. “E-Cadherin Expression in Macrophages Dampens Their Inflammatory Responsiveness in Vitro, but Does Not Modulate M2-Regulated Pathologies in Vivo.” SCIENTIFIC REPORTS, vol. 5, 2015, doi:10.1038/srep12599.
APA
Van den Bossche, J., Laoui, D., Naessens, T., Smits, H. H., Hokke, C. H., Stijlemans, B., … Van Ginderachter, J. A. (2015). E-cadherin expression in macrophages dampens their inflammatory responsiveness in vitro, but does not modulate M2-regulated pathologies in vivo. SCIENTIFIC REPORTS, 5. https://doi.org/10.1038/srep12599
Chicago author-date
Van den Bossche, Jan, Damya Laoui, Thomas Naessens, Hermelijn H Smits, Cornelis H Hokke, Benoit Stijlemans, Johan Grooten, Patrick De Baetselier, and Jo A Van Ginderachter. 2015. “E-Cadherin Expression in Macrophages Dampens Their Inflammatory Responsiveness in Vitro, but Does Not Modulate M2-Regulated Pathologies in Vivo.” SCIENTIFIC REPORTS 5. https://doi.org/10.1038/srep12599.
Chicago author-date (all authors)
Van den Bossche, Jan, Damya Laoui, Thomas Naessens, Hermelijn H Smits, Cornelis H Hokke, Benoit Stijlemans, Johan Grooten, Patrick De Baetselier, and Jo A Van Ginderachter. 2015. “E-Cadherin Expression in Macrophages Dampens Their Inflammatory Responsiveness in Vitro, but Does Not Modulate M2-Regulated Pathologies in Vivo.” SCIENTIFIC REPORTS 5. doi:10.1038/srep12599.
Vancouver
1.
Van den Bossche J, Laoui D, Naessens T, Smits HH, Hokke CH, Stijlemans B, et al. E-cadherin expression in macrophages dampens their inflammatory responsiveness in vitro, but does not modulate M2-regulated pathologies in vivo. SCIENTIFIC REPORTS. 2015;5.
IEEE
[1]
J. Van den Bossche et al., “E-cadherin expression in macrophages dampens their inflammatory responsiveness in vitro, but does not modulate M2-regulated pathologies in vivo,” SCIENTIFIC REPORTS, vol. 5, 2015.
@article{6901316,
  abstract     = {{IL-4/IL-13-induced alternatively activated macrophages (M(IL-4/IL-13), AAMs or M2) are known to express E-cadherin, enabling them to engage in heterotypic cellular interactions and IL-4-driven macrophage fusion in vitro. Here we show that E-cadherin overexpression in Raw 264.7 macrophages inhibits their inflammatory response to LPS stimulation, as demonstrated by a reduced secretion of inflammatory mediators like interleukin (IL)-6, tumor necrosis factor (TNF) and nitric oxide (NO). To study the function of E-cadherin in M(IL-4/IL-13) macrophages in vivo, we generated macrophage-specific E-cadherin-deficient C57BL/6 mice. Using this new tool, we analyzed immunological parameters during two typical AAM-associated Th2-driven diseases and assessed Th2-associated granuloma formation. Although E-cadherin is strongly induced in AAMs during Taenia crassiceps helminth infections and allergic airway inflammation, its deletion in macrophages does not affect the course of both Th2 cytokine-driven diseases. Moreover, macrophage E-cadherin expression is largely redundant for granuloma formation around Schistosoma mansoni ova. Overall, we conclude that E-cadherin is a valuable AAM marker which suppresses the inflammatory response when overexpressed. Yet E-cadherin deletion in macrophages does not affect M(LPS+IFN gamma) and M(IL-4) polarization in vitro, nor in vivo macrophage function, at least in the conditions tested.}},
  articleno    = {{12599}},
  author       = {{Van den Bossche, Jan and Laoui, Damya and Naessens, Thomas and Smits, Hermelijn H and Hokke, Cornelis H and Stijlemans, Benoit and Grooten, Johan and De Baetselier, Patrick and Van Ginderachter, Jo A}},
  issn         = {{2045-2322}},
  journal      = {{SCIENTIFIC REPORTS}},
  keywords     = {{RESPONSES,MECHANISM,FUSION,LUNG,RESISTANCE,MICE,GIANT-CELLS,MYELOID CELLS,ALTERNATIVELY ACTIVATED MACROPHAGES,PARASITE TAENIA-CRASSICEPS}},
  language     = {{eng}},
  pages        = {{12}},
  title        = {{E-cadherin expression in macrophages dampens their inflammatory responsiveness in vitro, but does not modulate M2-regulated pathologies in vivo}},
  url          = {{http://dx.doi.org/10.1038/srep12599}},
  volume       = {{5}},
  year         = {{2015}},
}
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