PMID- 24402617
OWN - NLM
STAT- MEDLINE
DCOM- 20141028
LR  - 20211021
IS  - 1573-2592 (Electronic)
IS  - 0271-9142 (Print)
IS  - 0271-9142 (Linking)
VI  - 34
IP  - 2
DP  - 2014 Feb
TI  - Mycobacterium massiliense induces inflammatory responses in macrophages through 
      Toll-like receptor 2 and c-Jun N-terminal kinase.
PG  - 212-23
LID - 10.1007/s10875-013-9978-y [doi]
AB  - Mycobacterium massiliense (Mmass) is an emerging, rapidly growing mycobacterium 
      (RGM) that belongs to the M. abscessus (Mabc) group, albeit clearly 
      differentiated from Mabc. Compared with M. tuberculosis, a well-characterized 
      human pathogen, the host innate immune response against Mmass infection is 
      largely unknown. In this study, we show that Mmass robustly activates mRNA and 
      protein expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 in 
      murine bone marrow-derived macrophages (BMDMs). Toll-like receptor (TLR)-2 and 
      myeloid differentiation primary response gene 88 (MyD88), but neither TLR4 nor 
      Dectin-1, are involved in Mmass-induced TNF-alpha or IL-6 production in BMDMs. Mmass 
      infection also activates the mitogen-activated protein kinase (MAPKs; c-Jun 
      N-terminal kinase (JNK), ERK1/2 and p38 MAPK) pathway. Mmass-induced TNF-alpha and 
      IL-6 production was dependent on JNK activation, while they were unaffected by 
      either the ERK1/2 or p38 pathway in BMDMs. Additionally, intracellular reactive 
      oxygen species (ROS), NADPH oxidase-2, and nuclear factor-kappaB are required for 
      Mmass-induced proinflammatory cytokine generation in macrophages. Furthermore, 
      the S morphotype of Mmass showed lower overall induction of pro-inflammatory 
      (TNF-alpha, IL-6, and IL-1beta) and anti-inflammatory (IL-10) cytokines than the R 
      morphotype, suggesting fewer immunogenic characteristics for this clinical 
      strain. Together, these results suggest that Mmass-induced activation of host 
      proinflammatory cytokines is mediated through TLR2-dependent JNK and ROS 
      signaling pathways.
FAU - Kim, Tae Sung
AU  - Kim TS
AD  - Department of Microbiology, College of Medicine, Chungnam National University, 6 
      Munhwa-dong, Jungku, Daejeon, 301-747, South Korea.
FAU - Kim, Yi Sak
AU  - Kim YS
FAU - Yoo, Heekyung
AU  - Yoo H
FAU - Park, Young Kil
AU  - Park YK
FAU - Jo, Eun-Kyeong
AU  - Jo EK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140109
PL  - Netherlands
TA  - J Clin Immunol
JT  - Journal of clinical immunology
JID - 8102137
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lectins, C-Type)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (NF-kappa B)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (dectin 1)
RN  - EC 1.6.3.- (Cybb protein, mouse)
RN  - EC 1.6.3.- (NADPH Oxidase 2)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Cytokines/biosynthesis
MH  - Disease Models, Animal
MH  - Inflammation Mediators/metabolism
MH  - JNK Mitogen-Activated Protein Kinases/*metabolism
MH  - Lectins, C-Type/metabolism
MH  - Macrophages/*immunology/*metabolism
MH  - Membrane Glycoproteins/metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Mycobacterium/*immunology
MH  - Mycobacterium Infections/genetics/*immunology/*metabolism
MH  - Myeloid Differentiation Factor 88/metabolism
MH  - NADPH Oxidase 2
MH  - NADPH Oxidases/metabolism
MH  - NF-kappa B/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction
MH  - Toll-Like Receptor 2/genetics/*metabolism
PMC - PMC3937545
EDAT- 2014/01/10 06:00
MHDA- 2014/10/29 06:00
PMCR- 2014/01/09
CRDT- 2014/01/10 06:00
PHST- 2013/08/22 00:00 [received]
PHST- 2013/12/09 00:00 [accepted]
PHST- 2014/01/10 06:00 [entrez]
PHST- 2014/01/10 06:00 [pubmed]
PHST- 2014/10/29 06:00 [medline]
PHST- 2014/01/09 00:00 [pmc-release]
AID - 9978 [pii]
AID - 10.1007/s10875-013-9978-y [doi]
PST - ppublish
SO  - J Clin Immunol. 2014 Feb;34(2):212-23. doi: 10.1007/s10875-013-9978-y. Epub 2014 
      Jan 9.