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All Trans Retinoic Acid, Transforming Growth Factor beta and Prostaglandin E.sub.2 in Mouse Plasma Synergize with Basophil-Secreted Interleukin-4 to M2 Polarize Murine Macrophages
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All Trans Retinoic Acid, Transforming Growth Factor beta and Prostaglandin E.sub.2 in Mouse Plasma Synergize with Basophil-Secreted Interleukin-4 to M2 Polarize Murine Macrophages
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Journal Article
All Trans Retinoic Acid, Transforming Growth Factor beta and Prostaglandin E.sub.2 in Mouse Plasma Synergize with Basophil-Secreted Interleukin-4 to M2 Polarize Murine Macrophages
2016
Overview
In previous studies we found that macrophages (M[PHI]s) from SH2-containing inositol-5'-phosphatase (SHIP) deficient mice are M2 polarized while their wild type (WT) counterparts are M1 polarized and that this difference in M[PHI] phenotype can be recapitulated during in vitro derivation from bone marrow if mouse plasma (MP), but not fetal calf serum, is added to standard M-CSF-containing cultures. In the current study we investigated the mechanism by which MP skews SHIP-/- but not +/+ M[PHI]s to an M2 phenotype. Our results suggest that SHIP-/- basophils constitutively secrete higher levels of IL-4 than SHIP+/+ basophils and this higher level of IL-4 is sufficient to skew both SHIP+/+ and SHIP-/- M[PHI]s to an M2 phenotype, but only when MP is present to increase the sensitivity of the M[PHI]s to this level of IL-4. MP increases the IL-4 sensitivity of both SHIP+/+ and -/- M[PHI]s not by increasing cell surface IL-4 or CD36 receptor levels, but by triggering the activation of Erk and Akt and the production of ROS, all of which play a critical role in sensitizing M[PHI]s to IL-4-induced M2 skewing. Studies to identify the factor(s) in MP responsible for promoting IL-4-induced M2 skewing suggests that all-trans retinoic acid (ATRA), TGF[beta] and prostaglandin E.sub.2 (PGE.sub.2) all play a role. Taken together, these results indicate that basophil-secreted IL-4 plays an essential role in M2 skewing and that ATRA, TGF[beta] and PGE.sub.2 within MP collaborate to dramatically promote M2 skewing by acting directly on M[PHI]s to increase their sensitivity to IL-4.
Publisher
Public Library of Science
