| Literature DB >> 35483374 |
Xiaofei Li1, Hui Wang1, Xiang Yu2, Gundappa Saha1, Lydia Kalafati3, Charalampos Ioannidis3, Ioannis Mitroulis4, Mihai G Netea5, Triantafyllos Chavakis6, George Hajishengallis7.
Abstract
Bone marrow (BM)-mediated trained innate immunity (TII) is a state of heightened immune responsiveness of hematopoietic stem and progenitor cells (HSPC) and their myeloid progeny. We show here that maladaptive BM-mediated TII underlies inflammatory comorbidities, as exemplified by the periodontitis-arthritis axis. Experimental-periodontitis-related systemic inflammation in mice induced epigenetic rewiring of HSPC and led to sustained enhancement of production of myeloid cells with increased inflammatory preparedness. The periodontitis-induced trained phenotype was transmissible by BM transplantation to naive recipients, which exhibited increased inflammatory responsiveness and disease severity when subjected to inflammatory arthritis. IL-1 signaling in HSPC was essential for their maladaptive training by periodontitis. Therefore, maladaptive innate immune training of myelopoiesis underlies inflammatory comorbidities and may be pharmacologically targeted to treat them via a holistic approach.Entities:
Keywords: arthritis; bone marrow transplantation; comorbidities; epigenetic rewiring; hematopoietic stem and progenitor cells; inflammation; myelopoiesis; periodontitis; trained immunity
Mesh:
Year: 2022 PMID: 35483374 PMCID: PMC9106933 DOI: 10.1016/j.cell.2022.03.043
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 66.850