PMID- 30176521
OWN - NLM
STAT- MEDLINE
DCOM- 20190327
LR  - 20190327
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 101
DP  - 2018 Sep
TI  - Lipoproteins in Streptococcus gordonii are critical in the infection and 
      inflammatory responses.
PG  - 574-584
LID - S0161-5890(18)30704-1 [pii]
LID - 10.1016/j.molimm.2018.08.023 [doi]
AB  - Gram-positive bacteria such as Streptococcus gordonii causing life-threatening 
      infective endocarditis are mainly recognized by Toll-like receptor 2 (TLR2). 
      Lipoteichoic acid (LTA) and lipoproteins are representative TLR2 ligands that 
      play important roles in bacterial infection and in host inflammatory responses. 
      In the present study, we generated an LTA-deficient mutant (DeltaltaS) and a 
      lipoprotein-deficient mutant (Deltalgt) and investigated the contributions of LTA and 
      lipoproteins to bacterial morphology and their effect on induction of 
      proinflammatory cytokines in THP-1 and mouse bone-marrow derived macrophages 
      (BMDMs). Deletion of ltaS and lgt was confirmed by PCR analysis of genomic DNA 
      from each mutant. The mutants with absence of LTA or lipoproteins were examined 
      by SDS-PAGE followed by Western blotting with anti-LTA antibodies and silver 
      staining, respectively. Interestingly, scanning and transmission electron 
      microscopies showed no difference in the bacterial cell morphology or size 
      between the wild-type and the mutants even though substantial changes in the cell 
      size and/or morphology have been reported in other Gram-positive bacteria such as 
      Staphylococcus aureus, Listeria monocytogenes, and Bacillus subtilis. However, S. 
      gordonii wild-type and DeltaltaS potently induced the expression of proinflammatory 
      cytokines including TNF-alpha, IL-8, and IL-1beta at the mRNA and protein levels, while 
      Deltalgt did not have these effects. Furthermore, lipoproteins purified from S. 
      gordonii also induced the expression of the aforementioned cytokines more 
      potently than the purified LTA. Neither LTA nor lipoprotein induced TNF-alpha, KC 
      (IL-8 counterpart in mouse), and IL-1beta in TLR2-deficient BMDMs. S. gordonii Deltalgt 
      was less virulent than the wild-type or DeltaltaS in a mouse intraperitoneal 
      infection model. Collectively, these results suggest that S. gordonii 
      lipoproteins, but not LTA, are mainly responsible for the infection and 
      inflammatory responses.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Kim, Hyun Young
AU  - Kim HY
AD  - Department of Oral Microbiology and Immunology, DRI and BK21 Plus Program, School 
      of Dentistry, Seoul National University, Seoul 08826, Republic of Korea.
FAU - Kim, A Reum
AU  - Kim AR
AD  - Department of Oral Microbiology and Immunology, DRI and BK21 Plus Program, School 
      of Dentistry, Seoul National University, Seoul 08826, Republic of Korea.
FAU - Seo, Ho Seong
AU  - Seo HS
AD  - Research Division for Biotechnology, Korea Atomic Energy Research Institute, 
      Jeongeup 56212, Republic of Korea.
FAU - Baik, Jung Eun
AU  - Baik JE
AD  - Department of Oral Microbiology and Immunology, DRI and BK21 Plus Program, School 
      of Dentistry, Seoul National University, Seoul 08826, Republic of Korea.
FAU - Ahn, Ki Bum
AU  - Ahn KB
AD  - Department of Oral Microbiology and Immunology, DRI and BK21 Plus Program, School 
      of Dentistry, Seoul National University, Seoul 08826, Republic of Korea; Research 
      Division for Biotechnology, Korea Atomic Energy Research Institute, Jeongeup 
      56212, Republic of Korea.
FAU - Yun, Cheol-Heui
AU  - Yun CH
AD  - Department of Agricultural Biotechnology and Research Institute for Agriculture 
      and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea.
FAU - Han, Seung Hyun
AU  - Han SH
AD  - Department of Oral Microbiology and Immunology, DRI and BK21 Plus Program, School 
      of Dentistry, Seoul National University, Seoul 08826, Republic of Korea. 
      Electronic address: shhan-mi@snu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180831
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Lipoproteins)
RN  - 0 (TLR2 protein, human)
RN  - 0 (Teichoic Acids)
RN  - 0 (Toll-Like Receptor 2)
RN  - 56411-57-5 (lipoteichoic acid)
SB  - IM
MH  - Animals
MH  - Cell Wall/metabolism
MH  - Cytokines/metabolism
MH  - Humans
MH  - Inflammation/*pathology
MH  - Inflammation Mediators/metabolism
MH  - Lipopolysaccharides
MH  - Lipoproteins/isolation & purification/*metabolism
MH  - Mice, Inbred C57BL
MH  - Mutation/genetics
MH  - Streptococcal Infections/*microbiology/pathology
MH  - Streptococcus gordonii/cytology/*physiology/ultrastructure
MH  - THP-1 Cells
MH  - Teichoic Acids
MH  - Toll-Like Receptor 2/metabolism
OTO - NOTNLM
OT  - Lipoprotein
OT  - Lipoteichoic acid
OT  - Macrophage
OT  - Proinflammatory cytokines
OT  - Streptococcus gordonii
OT  - Toll-like receptor 2
EDAT- 2018/09/04 06:00
MHDA- 2019/03/28 06:00
CRDT- 2018/09/04 06:00
PHST- 2018/05/26 00:00 [received]
PHST- 2018/07/29 00:00 [revised]
PHST- 2018/08/23 00:00 [accepted]
PHST- 2018/09/04 06:00 [pubmed]
PHST- 2019/03/28 06:00 [medline]
PHST- 2018/09/04 06:00 [entrez]
AID - S0161-5890(18)30704-1 [pii]
AID - 10.1016/j.molimm.2018.08.023 [doi]
PST - ppublish
SO  - Mol Immunol. 2018 Sep;101:574-584. doi: 10.1016/j.molimm.2018.08.023. Epub 2018 
      Aug 31.