Supplementary Materials

The PDF file includes:

  • Supplementary Materials and Methods
  • Fig. S1. PUFA metabolites produced by human MDM in response to treatment with HpbE and impact of HpbE-treated Ptgs2−/− BMDM on eosinophilic airway inflammation.
  • Fig. S2. HpbE has stronger eicosanoid-modulatory effects than glucocorticosteroids.
  • Fig. S3. HpbE has a distinct potential to induce type-2–suppressive mediators compared to other helminth products or helminth-associated bacteria.
  • Fig. S4. Viability and LTA4H expression in human eosinophils and neutrophils and PUFA metabolites produced by human PMNs in response to treatment with HpbE.
  • Fig. S5. HpbE induces a regulatory eicosanoid and cytokine profile in mixed and isolated CD14+ human PBMCs.
  • Fig. S6. Effect of COX-2, NF-κB, PI3K, PTEN, or PKA inhibition on HpbE-driven modulation of cytokines and eicosanoid pathways.
  • Fig. S7. Effect of neutralizing antibodies against PRRs (TLR2 and dectin-1/2) or IL-1β on HpbE-driven modulation of eicosanoids and IL-10 in human MDM.
  • Fig. S8. Bithionol does not affect cell viability and L3 stage HpbE shows a higher GDH activity as compared to L4 or L5 extracts.
  • Fig. S9. Newly generated monoclonal antibodies recognize Hpb GDH, clone 4F8 reduces HpbE-induced PGE2 and IL-10 production, and bithionol partially inhibits activity of recombinant Hpb GDH.
  • Fig. S10. Sequence of Hpb GDH is distinct from human GDH and contains potential predicted glycosylation sites.
  • Legends for tables S1 and S2
  • Table S3. Primer sequences for qPCR.
  • Table S4. Reagents and resources.
  • References (5963)

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Other Supplementary Material for this manuscript includes the following:

  • Table S1 (Microsoft Excel format). LC-MS/MS panel of PUFAs and PUFA metabolites.
  • Table S2 (Microsoft Excel format). Proteins present in active fractions of HpbE identified by MS.
  • Data file S1 (Microsoft Excel format). Primary data.