Anti-inflammatory actions of lipoxin A4 and aspirin-triggered lipoxin are SOCS-2 dependent
Control of inflammation is crucial to prevent damage to the host during infection. Lipoxins and aspirin-triggered lipoxins are crucial modulators of proinflammatory responses; however, their intracellular mechanisms have not been completely elucidated. We previously showed that lipoxin A4 (LXA4) con...
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Published in | Nature medicine Vol. 12; no. 3; pp. 330 - 334 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Nature Publishing Group
01.03.2006
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Abstract | Control of inflammation is crucial to prevent damage to the host during infection. Lipoxins and aspirin-triggered lipoxins are crucial modulators of proinflammatory responses; however, their intracellular mechanisms have not been completely elucidated. We previously showed that lipoxin A4 (LXA4) controls migration of dendritic cells (DCs) and production of interleukin (IL)-12 in vivo. In the absence of LXA4 biosynthetic pathways, the resulting uncontrolled inflammation during infection is lethal, despite pathogen clearance. Here we show that lipoxins activate two receptors in DCs, AhR and LXAR, and that this activation triggers expression of suppressor of cytokine signaling (SOCS)-2. SOCS-2-deficient DCs are hyper-responsive to microbial stimuli, as well as refractory to the inhibitory actions of LXA4, but not to IL-10. Upon infection with an intracellular pathogen, SOCS-2-deficient mice had uncontrolled production of proinflammatory cytokines, decreased microbial proliferation, aberrant leukocyte infiltration and elevated mortality. We also show that SOCS-2 is a crucial intracellular mediator of the anti-inflammatory actions of aspirin-induced lipoxins in vivo. |
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AbstractList | Control of inflammation is crucial to prevent damage to the host during infection. Lipoxins and aspirin-triggered lipoxins are crucial modulators of proinflammatory responses; however, their intracellular mechanisms have not been completely elucidated. We previously showed that lipoxin A4 (LXA4) controls migration of dendritic cells (DCs) and production of interleukin (IL)-12 in vivo. In the absence of LXA4 biosynthetic pathways, the resulting uncontrolled inflammation during infection is lethal, despite pathogen clearance. Here we show that lipoxins activate two receptors in DCs, AhR and LXAR, and that this activation triggers expression of suppressor of cytokine signaling (SOCS)-2. SOCS-2-deficient DCs are hyper-responsive to microbial stimuli, as well as refractory to the inhibitory actions of LXA4, but not to IL-10. Upon infection with an intracellular pathogen, SOCS-2-deficient mice had uncontrolled production of proinflammatory cytokines, decreased microbial proliferation, aberrant leukocyte infiltration and elevated mortality. We also show that SOCS-2 is a crucial intracellular mediator of the anti-inflammatory actions of aspirin-induced lipoxins in vivo. |
Audience | Academic |
Author | Aliberti, Julio Bafica, Andre Serhan, Charles N Machado, Fabiana S Esper, Lisia Dias, Alexandra Johndrow, James E |
Author_xml | – sequence: 1 givenname: Fabiana S surname: Machado fullname: Machado, Fabiana S organization: Department of Immunology, Duke University Medical Center, Durham, North Carolina 27705, USA – sequence: 2 givenname: James E surname: Johndrow fullname: Johndrow, James E – sequence: 3 givenname: Lisia surname: Esper fullname: Esper, Lisia – sequence: 4 givenname: Alexandra surname: Dias fullname: Dias, Alexandra – sequence: 5 givenname: Andre surname: Bafica fullname: Bafica, Andre – sequence: 6 givenname: Charles N surname: Serhan fullname: Serhan, Charles N – sequence: 7 givenname: Julio surname: Aliberti fullname: Aliberti, Julio |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16415877$$D View this record in MEDLINE/PubMed |
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Snippet | Control of inflammation is crucial to prevent damage to the host during infection. Lipoxins and aspirin-triggered lipoxins are crucial modulators of... |
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SubjectTerms | Animals Anti-Inflammatory Agents, Non-Steroidal - pharmacology Aspirin - pharmacology Basic Helix-Loop-Helix Transcription Factors Biochemistry Brain - cytology Brain - parasitology Cells, Cultured Dendritic Cells - cytology Dendritic Cells - drug effects Infections Inflammation - drug therapy Inflammation - metabolism Interleukin-12 - antagonists & inhibitors Lipoxins - pharmacology Medical research Mice Mice, Inbred C57BL Receptors, Aryl Hydrocarbon - deficiency Receptors, Aryl Hydrocarbon - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Spleen - cytology Spleen - drug effects Suppressor of Cytokine Signaling Proteins - deficiency Suppressor of Cytokine Signaling Proteins - genetics Suppressor of Cytokine Signaling Proteins - metabolism Toxoplasma - pathogenicity |
Title | Anti-inflammatory actions of lipoxin A4 and aspirin-triggered lipoxin are SOCS-2 dependent |
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