MyD88 and not TRIF knockout is sufficient to abolish LPS‐induced inflammatory responses in bone‐derived macrophages

Abstract

Macrophages play an important role in the response to infection and/or repair of injury in tissues. To examine the NF‐κB pathway in response to an inflammatory stimulus, we used wild‐type bone‐marrow‐derived macrophages (BMDMs) or BMDMs with knockout (KO) of myeloid differentiation primary response 88 (MyD88) and/or Toll/interleukin‐1 receptor domain‐containing adapter‐inducing interferon‐β (TRIF) via CRISPR/Cas9. Following treatment of BMDMs with lipopolysaccharide (LPS) to induce an inflammatory response, translational signalling of NF‐κB was quantified via immunoblot and cytokines were measured. Our findings reveal that MyD88 KO, but not TRIF KO, decreased LPS‐induced NF‐κB signalling, and 10% expression of basal MyD88 expression was sufficient to partially rescue the abolished inflammatory cytokine secretion observed upon MyD88 KO.