Regulation of bone mass by the gut microbiota is dependent on NOD1 and NOD2 signaling.

Abstract:

:Germ-free (GF) mice have increased bone mass that is normalized by colonization with gut microbiota (GM) from conventionally raised (CONV-R) mice. To determine if innate immune signaling pathways mediated the effect of the GM, we studied the skeleton of GF and CONV-R mice with targeted inactivation of MYD88, NOD1 or NOD2. In contrast to WT and Myd88-/- mice, cortical bone thickness in mice lacking Nod1 or Nod2 was not increased under GF conditions. The expression of Tnfα and the osteoclastogenic factor Rankl in bone was reduced in GF compared to CONV-R WT mice but not in Nod1-/- or Nod2-/- mice indicating that the effect of the GM to increase Tnfα and Rankl in bone and to reduce bone mass is dependent on both NOD1 and NOD2 signaling.

journal_name

Cell Immunol

journal_title

Cellular immunology

authors

Ohlsson C,Nigro G,Boneca IG,Bäckhed F,Sansonetti P,Sjögren K

doi

10.1016/j.cellimm.2017.05.003

subject

Has Abstract

pub_date

2017-07-01 00:00:00

pages

55-58

eissn

0008-8749

issn

1090-2163

pii

S0008-8749(17)30076-X

journal_volume

317

pub_type

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