Document Detail


NF-κB signaling participates in both RANKL- and IL-4-induced macrophage fusion: receptor cross-talk leads to alterations in NF-κB pathways.
MedLine Citation:
PMID:  21734075     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
NF-κB activation is essential for receptor activator for NF-κB ligand (RANKL)-induced osteoclast formation. IL-4 is known to inhibit the RANKL-induced osteoclast differentiation while at the same time promoting macrophage fusion to form multinucleated giant cells (MNG). Several groups have proposed that IL-4 inhibition of osteoclastogenesis is mediated by suppressing the RANKL-induced activation of NF-κB. However, we found that IL-4 did not block proximal, canonical NF-κB signaling. Instead, we found that IL-4 inhibited alternative NF-κB signaling and induced p105/50 expression. Interestingly, in nfκb1(-/-) bone marrow-derived macrophages (BMM), the formation of both multinucleated osteoclast and MNG induced by RANKL or IL-4, respectively, was impaired. This suggests that NF-κB signaling also plays an important role in IL-4-induced macrophage fusion. Indeed, we found that the RANKL-induced and IL-4-induced macrophage fusion were both inhibited by the NF-κB inhibitors IκB kinase 2 inhibitor and NF-κB essential modulator inhibitory peptide. Furthermore, overexpression of p50, p65, p52, and RelB individually in nfκb1(-/-) or nfκb1(+/+) BMM enhanced both giant osteoclast and MNG formation. Interestingly, knockdown of nfκb2 in wild-type BMM dramatically enhanced both osteoclast and MNG formation. In addition, both RANKL- and IL-4-induced macrophage fusion were impaired in NF-κB-inducing kinase(-/-) BMM. These results suggest IL-4 influences NF-κB pathways by increasing p105/p50 and suppressing RANKL-induced p52 translocation and that NF-κB pathways participate in both RANKL- and IL-4-induced giant cell formation.
Authors:
Minjun Yu; Xiulan Qi; Jose L Moreno; Donna L Farber; Achsah D Keegan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-07-06
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  187     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-08-03     Completed Date:  2011-09-29     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1797-806     Citation Subset:  AIM; IM    
Affiliation:
Department of Microbiology and Immunology, Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bone Marrow Cells / immunology*
Cell Fusion
Cells, Cultured
Giant Cells / immunology*
Interleukin-4 / genetics,  immunology*
Mice
Mice, Knockout
NF-kappa B / genetics,  immunology*
Osteoclasts / immunology*
Protein-Serine-Threonine Kinases / genetics,  immunology
RANK Ligand / genetics,  immunology*
Grant Support
ID/Acronym/Agency:
AI038985/AI/NIAID NIH HHS; AI059775/AI/NIAID NIH HHS; R01 AI038985-14/AI/NIAID NIH HHS; R01 AI038985-15/AI/NIAID NIH HHS; R01 AI038985-16/AI/NIAID NIH HHS; R01 AI059775-01A2/AI/NIAID NIH HHS; R01 AI059775-02/AI/NIAID NIH HHS; R01 AI059775-03/AI/NIAID NIH HHS; R01 AI059775-04/AI/NIAID NIH HHS; R01 AI059775-05/AI/NIAID NIH HHS; R01 AI059775-05S1/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/NF-kappa B; 0/RANK Ligand; 0/Tnfsf11 protein, mouse; 207137-56-2/Interleukin-4; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.25/NF-kappa B kinase

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