Abstract:
:Skeletal complications are common features of neonatal-onset multisystem inflammatory disease (NOMID), a disorder caused by NLRP3-activating mutations. NOMID mice in which NLRP3 is activated globally exhibit several characteristics of the human disease, including systemic inflammation and cartilage dysplasia, but the mechanisms of skeletal manifestations remain unknown. In this study, we find that activation of NLRP3 in myeloid cells, but not mesenchymal cells triggers chronic inflammation, which ultimately, causes growth plate and epiphyseal dysplasia in mice. These responses are IL-1 signaling-dependent, but independent of PARP1, which also functions downstream of NLRP3 and regulates skeletal homeostasis. Mechanistically, inflammation causes severe anemia and hypoxia in the bone environment, yet down-regulates the HIF-1α pathway in chondrocytes, thereby promoting the demise of these cells. Thus, activation of NLRP3 in hematopoietic cells initiates IL-1β-driven paracrine cascades, which promote abnormal growth plate development in NOMID mice.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Wang C,Xu CX,Alippe Y,Qu C,Xiao J,Schipani E,Civitelli R,Abu-Amer Y,Mbalaviele Gdoi
10.1038/s41598-017-05033-5subject
Has Abstractpub_date
2017-07-07 00:00:00pages
4880issue
1issn
2045-2322pii
10.1038/s41598-017-05033-5journal_volume
7pub_type
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