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Different engagement of TLR2 and TLR4 in Porphyromonas gingivalis vs. ligature-induced periodontal bone loss.

Abstract This study was conducted to investigate the roles of different Toll-like receptor (TLR) signaling in Porphyromonas gingivalis (P. gingivalis)-induced and ligature-induced experimental periodontal bone resorption in mice. Wild-type (WT), TLR2 knockout (KO), TLR4KO, and TLR2&4 KO mice with C57/BL6 background were divided into three groups: control, P. gingivalis infection, and ligation. Live P. gingivalis or silk ligatures were placed in the sulcus around maxillary second molars over a 2-week period. Images were captured by digital stereomicroscopy, and the bone resorption area was measured with ImageJ software. The protein expression level of gingival RANKL was measured by ELISA. The gingival mRNA levels of RANKL, IL-1β, TNF-α, and IL-10 were detected by RT-qPCR. The results showed that P. gingivalis induced significant periodontal bone resorption in WT mice and TLR2 KO mice but not in TLR4 KO mice or TLR2&4 KO mice. For all four types of mice, ligation induced significant bone loss compared with that in control groups, and this bone loss was significantly higher than that in the P. gingivalis infection group. RANKL protein expression was significantly increased in the ligation group compared with that in the control group for all four types of mice, and in the P. gingivalis infection group of WT, TLR2 KO, and TLR4 KO mice. Expression patterns of RANKL, IL-1β, TNF-α, and IL-10 mRNA were different in the P. gingivalis infection group and the ligation group in different types of mice. In summary, P. gingivalis-induced periodontal bone resorption is TLR4-dependent, whereas ligation-induced periodontal bone resorption is neither TLR2- nor TLR4-dependent.
PMID
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Authors

Mayor MeshTerms

Disease Models, Animal

Keywords
Journal Title brazilian oral research
Publication Year Start




PMID- 28832712
OWN - NLM
STAT- MEDLINE
DA  - 20170823
DCOM- 20170912
LR  - 20170912
IS  - 1807-3107 (Electronic)
IS  - 1806-8324 (Linking)
VI  - 31
DP  - 2017 Aug 21
TI  - Different engagement of TLR2 and TLR4 in Porphyromonas gingivalis vs.
      ligature-induced periodontal bone loss.
PG  - e63
LID - S1806-83242017000100254 [pii]
LID - 10.1590/1807-3107BOR-2017.vol31.0063 [doi]
AB  - This study was conducted to investigate the roles of different Toll-like receptor
      (TLR) signaling in Porphyromonas gingivalis (P. gingivalis)-induced and
      ligature-induced experimental periodontal bone resorption in mice. Wild-type
      (WT), TLR2 knockout (KO), TLR4KO, and TLR2&4 KO mice with C57/BL6 background were
      divided into three groups: control, P. gingivalis infection, and ligation. Live
      P. gingivalis or silk ligatures were placed in the sulcus around maxillary second
      molars over a 2-week period. Images were captured by digital stereomicroscopy,
      and the bone resorption area was measured with ImageJ software. The protein
      expression level of gingival RANKL was measured by ELISA. The gingival mRNA
      levels of RANKL, IL-1beta, TNF-alpha, and IL-10 were detected by RT-qPCR. The
      results showed that P. gingivalis induced significant periodontal bone resorption
      in WT mice and TLR2 KO mice but not in TLR4 KO mice or TLR2&4 KO mice. For all
      four types of mice, ligation induced significant bone loss compared with that in 
      control groups, and this bone loss was significantly higher than that in the P.
      gingivalis infection group. RANKL protein expression was significantly increased 
      in the ligation group compared with that in the control group for all four types 
      of mice, and in the P. gingivalis infection group of WT, TLR2 KO, and TLR4 KO
      mice. Expression patterns of RANKL, IL-1beta, TNF-alpha, and IL-10 mRNA were
      different in the P. gingivalis infection group and the ligation group in
      different types of mice. In summary, P. gingivalis-induced periodontal bone
      resorption is TLR4-dependent, whereas ligation-induced periodontal bone
      resorption is neither TLR2- nor TLR4-dependent.
FAU - Lin, Mei
AU  - Lin M
AD  - Beijing ChaoYang Hospital affiliated with Capital Medical University, Department 
      of Stomatology, Beijing, China.
FAU - Hu, Yang
AU  - Hu Y
AD  - The Forsyth Institute, Department of Immunology and Infectious Diseases,
      Cambridge, MA, USA.
FAU - Wang, Yuhua
AU  - Wang Y
AD  - Ninth People's Hospital, College of Stomatology, Shanghai JiaoTong University
      School of Medicine, Department of Prosthodontics, Shanghai Key Laboratory,
      Shanghai, China.
FAU - Kawai, Toshihisa
AU  - Kawai T
AD  - The Forsyth Institute, Department of Immunology and Infectious Diseases,
      Cambridge, MA, USA.
FAU - Wang, Zuomin
AU  - Wang Z
AD  - Beijing ChaoYang Hospital affiliated with Capital Medical University, Department 
      of Stomatology, Beijing, China.
FAU - Han, Xiaozhe
AU  - Han X
AD  - The Forsyth Institute, Department of Immunology and Infectious Diseases,
      Cambridge, MA, USA.
LA  - eng
PT  - Journal Article
DEP - 20170821
PL  - Brazil
TA  - Braz Oral Res
JT  - Brazilian oral research
JID - 101307187
RN  - 0 (Interleukin-1beta)
RN  - 0 (Receptor Activator of Nuclear Factor-kappa B)
RN  - 0 (Tlr2 protein, mouse)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Tnfrsf11a protein, mouse)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
SB  - D
SB  - IM
MH  - Alveolar Bone Loss/*etiology/microbiology
MH  - Animals
MH  - *Disease Models, Animal
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Interleukin-10/metabolism
MH  - Interleukin-1beta/metabolism
MH  - Ligation
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Periodontitis/*microbiology
MH  - Porphyromonas gingivalis/*pathogenicity
MH  - Real-Time Polymerase Chain Reaction
MH  - Receptor Activator of Nuclear Factor-kappa B/metabolism
MH  - Reproducibility of Results
MH  - Time Factors
MH  - Toll-Like Receptor 2/analysis/genetics/*physiology
MH  - Toll-Like Receptor 4/analysis/genetics/*physiology
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2017/08/24 06:00
MHDA- 2017/09/13 06:00
CRDT- 2017/08/24 06:00
PHST- 2017/02/01 [received]
PHST- 2017/05/30 [accepted]
AID - S1806-83242017000100254 [pii]
AID - 10.1590/1807-3107BOR-2017.vol31.0063 [doi]
PST - epublish
SO  - Braz Oral Res. 2017 Aug 21;31:e63. doi: 10.1590/1807-3107BOR-2017.vol31.0063.