Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. FFA4 activation does not cause airway contraction in murine PCLS.
  • Fig. S2. TUG-891-mediated relaxation in precontracted PCLS was reduced by the FFA4 antagonist AH7614.
  • Fig. S3. FFA4 agonist compound A mediates ASM relaxation in precontracted PCLS.
  • Fig. S4. FFA4 agonism mediates relaxation in airways precontracted with serotonin.
  • Fig. S5. FFA4 agonist TUG-891 reduces airway resistance in wild-type C57BL6/N mice.
  • Fig. S6. FFA4 agonism did not alter transcript abundance of 5-Lox, BLT1, BLT2, or IL17a but increased expression of LTB4 in a chronic ozone exposure model.
  • Fig. S7. FFA4 is expressed in Gr-1+, CD11c+, and Siglec-F+ immune cells.
  • Fig. S8. FFA4 is normally expressed and fully functional in ozone-exposed mice.
  • Fig. S9. Expression of FFA4 in human lung.
  • Fig. S10. PGE2 receptors are expressed in HBECs and human ASM cells.
  • Fig. S11. FFA4 agonism up-regulates COX-2 but not other PGE2-related transcripts in a chronic ozone model.
  • Fig. S12. FFA4 activation mimics the anti-inflammatory effects of a COX-2 inhibitor but is not altered by the presence of COX-2 inhibition.
  • Table S1. FFA4 agonists do not act as off-target agonists at prostanoid receptors.
  • Table S2. FFA4 agonists do not act as off-target antagonists at prostanoid receptors.
  • References (6265)

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Raw data from figures.