PMID- 26940588
OWN - NLM
STAT- MEDLINE
DCOM- 20161111
LR  - 20170103
IS  - 2049-632X (Electronic)
IS  - 2049-632X (Linking)
VI  - 74
IP  - 3
DP  - 2016 Apr
TI  - Mycobacterium fortuitum induces A20 expression that impairs macrophage 
      inflammatory responses.
LID - ftw015 [pii]
LID - 10.1093/femspd/ftw015 [doi]
AB  - Mycobacterium fortuitum is a rapidly growing mycobacterium that has been regarded 
      as an etiological agent of a variety of human infections. However, little is 
      known about the host inflammatory responses and the molecular mechanisms by which 
      MF-induced inflammation is regulated in macrophages. In this study, we report 
      that MF infection leads to the induction of an anti-inflammatory molecule, A20 
      (also known as TNFAIP3), which is essential for the regulation of MF-induced 
      inflammatory responses in murine bone marrow-derived macrophages (BMDMs). MF 
      triggered the expression of tumor necrosis factor-alpha and interleukin-6 in BMDMs 
      through signaling of the Toll-like receptor 2 (TLR2)-myeloid differentiation 
      primary response gene 88. Additionally, MF rapidly induced the expression of A20, 
      which inhibited proinflammatory cytokine expression and nuclear factor (NF)-kappaB 
      reporter gene activities in BMDMs. Notably, MF-induced activation of NF-kappaB 
      signaling was required for A20 expression and proinflammatory responses in BMDMs. 
      Furthermore, the rough morphotype of the MF clinical strain induced a higher 
      level of proinflammatory signaling activation, but less A20 induction in BMDMs, 
      compared to the smooth morphotype. Taken together, these results suggest that 
      MF-induced activation of host proinflammatory responses is negatively regulated 
      through TLR2-dependent A20 expression.
CI  - (c) FEMS 2016. All rights reserved. For permissions, please e-mail: 
      journals.permissions@oup.com.
FAU - Lee, Gippeum Joy
AU  - Lee GJ
AD  - Department of Microbiology, College of Medicine, Chungnam National University, 
      Daejeon 301-747, South Korea Infection Signaling Network Research Center, College 
      of Medicine, Chungnam National University, Daejeon 301-747, South Korea.
FAU - Lee, Hye-Mi
AU  - Lee HM
AD  - Department of Microbiology, College of Medicine, Chungnam National University, 
      Daejeon 301-747, South Korea Infection Signaling Network Research Center, College 
      of Medicine, Chungnam National University, Daejeon 301-747, South Korea.
FAU - Kim, Tae Sung
AU  - Kim TS
AD  - Department of Microbiology, College of Medicine, Chungnam National University, 
      Daejeon 301-747, South Korea Infection Signaling Network Research Center, College 
      of Medicine, Chungnam National University, Daejeon 301-747, South Korea.
FAU - Kim, Jin Kyung
AU  - Kim JK
AD  - Department of Microbiology, College of Medicine, Chungnam National University, 
      Daejeon 301-747, South Korea Infection Signaling Network Research Center, College 
      of Medicine, Chungnam National University, Daejeon 301-747, South Korea.
FAU - Sohn, Kyung Mok
AU  - Sohn KM
AD  - Division of Infectious Diseases, Chungnam National University Hospital, Daejeon 
      35015, South Korea.
FAU - Jo, Eun-Kyeong
AU  - Jo EK
AD  - Department of Microbiology, College of Medicine, Chungnam National University, 
      Daejeon 301-747, South Korea Infection Signaling Network Research Center, College 
      of Medicine, Chungnam National University, Daejeon 301-747, South Korea 
      hayoungj@cnu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160302
PL  - United States
TA  - Pathog Dis
JT  - Pathogens and disease
JID - 101595366
RN  - 0 (Interleukin-6)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Rela protein, mouse)
RN  - 0 (Tlr2 protein, mouse)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3)
RN  - EC 3.4.22.- (Cysteine Endopeptidases)
RN  - EC 3.4.22.- (Tnfaip3 protein, mouse)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells/immunology
MH  - Cell Line
MH  - Cysteine Endopeptidases/biosynthesis/genetics/*immunology
MH  - Inflammation/immunology
MH  - Interleukin-6/biosynthesis
MH  - Intracellular Signaling Peptides and Proteins/biosynthesis/genetics/*immunology
MH  - Macrophages/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mycobacterium Infections, Nontuberculous/*immunology/microbiology
MH  - Mycobacterium fortuitum/*immunology
MH  - Myeloid Differentiation Factor 88/immunology
MH  - RNA Interference
MH  - RNA, Small Interfering/genetics
MH  - Toll-Like Receptor 2/*immunology
MH  - Transcription Factor RelA/immunology
MH  - Tumor Necrosis Factor alpha-Induced Protein 3
MH  - Tumor Necrosis Factor-alpha/biosynthesis
OTO - NOTNLM
OT  - A20
OT  - MyD88
OT  - Mycobacterium fortuitum
OT  - NF-kappaB
OT  - TLR
OT  - proinflammatory cytokines
EDAT- 2016/03/05 06:00
MHDA- 2016/11/12 06:00
CRDT- 2016/03/05 06:00
PHST- 2016/02/24 00:00 [accepted]
PHST- 2016/03/05 06:00 [entrez]
PHST- 2016/03/05 06:00 [pubmed]
PHST- 2016/11/12 06:00 [medline]
AID - ftw015 [pii]
AID - 10.1093/femspd/ftw015 [doi]
PST - ppublish
SO  - Pathog Dis. 2016 Apr;74(3):ftw015. doi: 10.1093/femspd/ftw015. Epub 2016 Mar 2.