PMID- 27212109
OWN - NLM
STAT- MEDLINE
DCOM- 20180416
LR  - 20190318
IS  - 1943-3670 (Electronic)
IS  - 0022-3492 (Linking)
VI  - 87
IP  - 10
DP  - 2016 Oct
TI  - Macrophages Play a Key Role in the Obesity-Induced Periodontal Innate Immune 
      Dysfunction via Nucleotide-Binding Oligomerization Domain-Like Receptor Protein 3 
      Pathway.
PG  - 1195-205
LID - 10.1902/jop.2016.160102 [doi]
AB  - BACKGROUND: Obesity is associated with infiltration of macrophages into adipose 
      tissue. However, effects of obesity on macrophage infiltration and activation in 
      periodontal tissues with periodontitis are still to be elucidated. METHODS: A 
      diet-induced obesity 16-week mouse model was constructed, and periodontitis was 
      induced by periodontal ligation for 10 days. The model consisted of periodontitis 
      (P) and control (C) groups, with high fat (HF) and normal (N) diet conditions. 
      Bone loss (BL) was analyzed by microcomputed tomography. In periodontal tissues, 
      immunohistochemical staining and quantitative polymerase chain reaction (qPCR) 
      detected expressions of: 1) nucleotide-binding oligomerization domain-like 
      receptor protein 3 (NLRP3) pathway; 2) macrophage-specific marker (F4/80); and 3) 
      macrophage chemotactic protein 1 (MCP1). Bone marrow-derived macrophages (BMDMs) 
      from the mouse model were stimulated by Porphyromonas gingivalis 
      lipopolysaccharide (LPS) in vitro (NC/NC + LPS: BMDMs from NC group without/with 
      LPS stimulation; HFC/HFC + LPS: BMDMs from HFC group without/with LPS 
      stimulation). Expressions of NLRP3 pathway in BMDMs were detected by 
      immunocytochemical staining and qPCR. RESULTS: BL increased significantly with 
      periodontitis (NC versus NP; HFC versus HFP) and obesity (NP versus HFP). 
      Expressions of NLRP3 pathway were significantly elevated in gingival tissues with 
      periodontitis (NC versus NP; HFC versus HFP), but not with obesity (NC versus 
      HFC; NP versus HFP). F4/80 and MCP1 expressions were significantly upregulated in 
      gingival tissues with periodontitis (NC versus NP; HFC versus HFP) but 
      significantly downregulated in the context of obesity (NP versus HFP). In vitro, 
      NLRP3 pathway expressions were significantly upregulated in BMDMs after LPS 
      stimulation (NC + LPS versus NC; HFC + LPS versus HFC), but significantly 
      downregulated in HFC groups (HFC versus NC; HFC + LPS versus NC + LPS). 
      CONCLUSION: Obesity may paralyze innate immune response of periodontium via 
      attenuating infiltration and activation of macrophages and further aggravate 
      periodontal disease.
FAU - Huang, Xin
AU  - Huang X
AD  - Department of Periodontology, The Affiliated Hospital of Stomatology, Southern 
      Medical University, Guangzhou, Guangdong, China.
FAU - Yu, Ting
AU  - Yu T
AD  - Key Laboratory of Oral Medicine, Guangzhou Institute of Oral Disease, Stomatology 
      Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
FAU - Ma, Chanjuan
AU  - Ma C
AD  - Department of Periodontology, The Affiliated Hospital of Stomatology, Southern 
      Medical University, Guangzhou, Guangdong, China.
FAU - Wang, Yixiong
AU  - Wang Y
AD  - Department of Periodontology, The Affiliated Hospital of Stomatology, Southern 
      Medical University, Guangzhou, Guangdong, China.
FAU - Xie, Baoyi
AU  - Xie B
AD  - Department of Periodontology, The Affiliated Hospital of Stomatology, Southern 
      Medical University, Guangzhou, Guangdong, China.
FAU - Xuan, Dongying
AU  - Xuan D
AD  - Department of Periodontology, Hangzhou Dental Hospital, Savaid Medical School, 
      University of Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
FAU - Zhang, Jincai
AU  - Zhang J
AD  - Department of Periodontology, The Affiliated Hospital of Stomatology, Southern 
      Medical University, Guangzhou, Guangdong, China.
AD  - Department of Periodontology, Savaid Medical School, University of Chinese 
      Academy of Sciences.
LA  - eng
PT  - Journal Article
DEP - 20160523
PL  - United States
TA  - J Periodontol
JT  - Journal of periodontology
JID - 8000345
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Nod2 Signaling Adaptor Protein)
RN  - 0 (Nucleotides)
SB  - IM
EIN - J Periodontol. 2017 Jun;88(6):614. PMID: 28434282
MH  - Animals
MH  - Lipopolysaccharides
MH  - *Macrophages
MH  - Mice
MH  - Models, Animal
MH  - Nod2 Signaling Adaptor Protein/*metabolism
MH  - Nucleotides/*metabolism
MH  - Obesity/*physiopathology
MH  - Porphyromonas gingivalis
MH  - X-Ray Microtomography
OTO - NOTNLM
OT  - *CIAS1 protein, mouse
OT  - *NLRP3 protein, mouse
OT  - *immunity, innate
OT  - *macrophages
OT  - *obesity
OT  - *periodontitis
OT  - *proteins
EDAT- 2016/05/24 06:00
MHDA- 2018/04/17 06:00
CRDT- 2016/05/24 06:00
PHST- 2016/05/24 06:00 [entrez]
PHST- 2016/05/24 06:00 [pubmed]
PHST- 2018/04/17 06:00 [medline]
AID - 10.1902/jop.2016.160102 [doi]
PST - ppublish
SO  - J Periodontol. 2016 Oct;87(10):1195-205. doi: 10.1902/jop.2016.160102. Epub 2016 
      May 23.