BioAcyl Corp
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Newson, J., Motwani, M. P., & Kendall, A. C. (2017). Inflammatory Resolution Triggers a Prolonged Phase of Immune Suppression through COX-1/mPGES-1-Derived Prostaglandin E2. Cell Rep. 20(13), 3162–3175. Added by: Dr. Enrique Feoli (22/01/2021, 14:38) Last edited by: Dr. Enrique Feoli (10/05/2023, 17:58) |
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| Resource type: Journal Article DOI: 10.1016/j.celrep.2017.08.098 ID no. (ISBN etc.): 2211-1247 BibTeX citation key: Newson2017 View all bibliographic details  |
Categories: BioAcyl Corp, BioAcyl Corp, BioAcyl Corp Subcategories: Adaptive homeostasis, Inflammation Post resolution, Inflammation resolution Creators: Kendall, Motwani, Newson Collection: Cell Rep. |
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| Abstract |
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Acute inflammation is characterized by granulocyte infiltration followed by efferocytosing mononuclear phagocytes, which pave the way for inflammatory resolution. Until now, it was believed that resolution then leads back to homeostasis, the physiological state tissues experience before inflammation occurred. However, we discovered that resolution triggered a prolonged phase of immune suppression mediated by prostanoids. Specifically, once inflammation was switched off, natural killer cells, secreting interferon γ (IFNγ), infiltrated the post-inflamed site. IFNγ upregulated microsomal prostaglandin E synthase-1 (mPGES-1) alongside cyclo-oxygenase (COX-1) within macrophage populations, resulting in sustained prostaglandin (PG)E2 biosynthesis. Whereas PGE2 suppressed local innate immunity to bacterial infection, it also inhibited lymphocyte function and generated myeloid-derived suppressor cells, the net effect of which was impaired uptake/presentation of exogenous antigens. Therefore, we have defined a sequence of post-resolution events that dampens the propensity to develop autoimmune responses to endogenous antigens at the cost of local tissue infection.
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