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Alternatively activated alveolar macrophages in pulmonary fibrosis-mediator production and intracellular signal transduction.
Clin Immunol. 2010 Oct; 137(1):89-101.CI

Abstract

Activated macrophages have been characterized as M1 and M2 according to their inflammatory response pattern. Here we analyzed the M2 marker expression and intracellular signal transduction in the course of cytokine-driven differentiation. We found elevated spontaneous production of the chemokines CCL17, CCL18 and CCL22 and increased expression of CD206 by alveolar macrophages from patients with lung fibrosis. Stimulation of normal human AM with Th2 cytokines IL-4 and/or IL-10 in vitro revealed IL-4 as the most powerful inducer of M2-phenotype in AM and monocytes. Importantly, IL-10 enhanced IL-4-induced expression of CCL18 and IL-1RA in a synergistic fashion. IL-4/IL-10 stimulation induces a strong activation of STAT3 in AM from fibrosis patients. These results suggest an important role for M2 polarized AM in the pathogenesis of pulmonary fibrosis and indicate that both IL-4 and IL-10 account for human AM phenotype shift to M2, as seen in patients with fibrotic interstitial lung diseases.

Authors+Show Affiliations

Department of Pneumology, Medical Center, Albert-Ludwigs University, Freiburg, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20674506

Citation

Pechkovsky, Dmitri V., et al. "Alternatively Activated Alveolar Macrophages in Pulmonary Fibrosis-mediator Production and Intracellular Signal Transduction." Clinical Immunology (Orlando, Fla.), vol. 137, no. 1, 2010, pp. 89-101.
Pechkovsky DV, Prasse A, Kollert F, et al. Alternatively activated alveolar macrophages in pulmonary fibrosis-mediator production and intracellular signal transduction. Clin Immunol. 2010;137(1):89-101.
Pechkovsky, D. V., Prasse, A., Kollert, F., Engel, K. M., Dentler, J., Luttmann, W., Friedrich, K., Müller-Quernheim, J., & Zissel, G. (2010). Alternatively activated alveolar macrophages in pulmonary fibrosis-mediator production and intracellular signal transduction. Clinical Immunology (Orlando, Fla.), 137(1), 89-101. https://doi.org/10.1016/j.clim.2010.06.017
Pechkovsky DV, et al. Alternatively Activated Alveolar Macrophages in Pulmonary Fibrosis-mediator Production and Intracellular Signal Transduction. Clin Immunol. 2010;137(1):89-101. PubMed PMID: 20674506.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Alternatively activated alveolar macrophages in pulmonary fibrosis-mediator production and intracellular signal transduction. AU - Pechkovsky,Dmitri V, AU - Prasse,Antje, AU - Kollert,Florian, AU - Engel,Kathrin M Y, AU - Dentler,Jan, AU - Luttmann,Werner, AU - Friedrich,Karlheinz, AU - Müller-Quernheim,Joachim, AU - Zissel,Gernot, Y1 - 2010/07/31/ PY - 2009/05/12/received PY - 2010/06/22/revised PY - 2010/06/29/accepted PY - 2010/8/3/entrez PY - 2010/8/3/pubmed PY - 2010/12/14/medline SP - 89 EP - 101 JF - Clinical immunology (Orlando, Fla.) JO - Clin Immunol VL - 137 IS - 1 N2 - Activated macrophages have been characterized as M1 and M2 according to their inflammatory response pattern. Here we analyzed the M2 marker expression and intracellular signal transduction in the course of cytokine-driven differentiation. We found elevated spontaneous production of the chemokines CCL17, CCL18 and CCL22 and increased expression of CD206 by alveolar macrophages from patients with lung fibrosis. Stimulation of normal human AM with Th2 cytokines IL-4 and/or IL-10 in vitro revealed IL-4 as the most powerful inducer of M2-phenotype in AM and monocytes. Importantly, IL-10 enhanced IL-4-induced expression of CCL18 and IL-1RA in a synergistic fashion. IL-4/IL-10 stimulation induces a strong activation of STAT3 in AM from fibrosis patients. These results suggest an important role for M2 polarized AM in the pathogenesis of pulmonary fibrosis and indicate that both IL-4 and IL-10 account for human AM phenotype shift to M2, as seen in patients with fibrotic interstitial lung diseases. SN - 1521-7035 UR - https://www.unboundmedicine.com/medline/citation/20674506/Alternatively_activated_alveolar_macrophages_in_pulmonary_fibrosis_mediator_production_and_intracellular_signal_transduction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1521-6616(10)00643-1 DB - PRIME DP - Unbound Medicine ER -