Hypersensitivity of Aryl Hydrocarbon Receptor-Deficient Mice to Lipopolysaccharide-Induced Septic Shock

The Nuclear Receptor AhR Controls Bone Homeostasis by Regulating Osteoclast Differentiation via the RANK/c-Fos Signaling Axis

“…Therefore, AhR may be indispensable for initiating the inflammatory response after fracture. These results are consistent with those of previous studies indicating that AhR plays a crucial role in inflammation-driven disorders such as septic shock, psoriasis, and rheumatoid arthritis; AhR has also been found to stimulate the infiltration, differentiation, and activation of monocytes and macrophages (26,52,53). Note that macrophages infiltrate at a fracture site in the early stages following trauma and likely initiate secondary responses.…”

LeA(H)Rning self-control

“…In this study, Bessede et al [7] found that LPS stimulation induces TDO2 expression and consequently the production of L-Kyn, which then activates an AhR-dependent pathway that protects against endotoxin challenge ( Figure 1). The authors also investigated the role of AhR-dependent signaling in endotoxin tolerance, a state characterized by reduced inflammatory responses to LPS challenge following previous exposure to low levels of LPS.…”

“…In addition, AhR in macrophages modulates their activation by lipopolysaccharide (LPS) [5,6] but the molecular mechanisms involved are not clearly understood. A study by Puccetti and colleagues describes a pathway by which AhR limits the inflammatory response to LPS [7].…”

Aryl hydrocarbon receptor negatively regulates NLRP3 inflammasome activity by inhibiting NLRP3 transcription

“…AhR in combination with STAT1 negatively regulates proinflammatory cytokine production by inhibiting NF-kB activation in macrophages after LPS stimulation 25 . AhR knockout mice are hypersensitive to LPS-induced septic shock, mainly due to macrophage dysfunction 36 . AhR interacts with RORgt, promotes AhR binding at the IL-22 locus and promotes the development of RORgt þ innate lymphoid cells 37 .…”