PMID- 23555735
OWN - NLM
STAT- MEDLINE
DCOM- 20130930
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 3
DP  - 2013
TI  - Differential immune responses to Segniliparus rotundus and Segniliparus rugosus 
      infection and analysis of their comparative virulence profiles.
PG  - e59646
LID - 10.1371/journal.pone.0059646 [doi]
LID - e59646
AB  - Two closely related bacterial species, Segniliparus rotundus and Segniliparus 
      rugosus, have emerged as important human pathogens, but little is known about the 
      immune responses they elicit or their comparative pathophysiologies. To determine 
      the virulence and immune responses of the two species, we compared their 
      abilities to grow in phagocytic and non-phagocytic cells. Both species maintained 
      non-replicating states within A549 epithelial cells. S. rugosus persisted longer 
      and multiplied more rapidly inside murine bone marrow-derived macrophages 
      (BMDMs), induced more pro-inflammatory cytokines, and induced higher levels of 
      macrophage necrosis. Activation of BMDMs by both species was mediated by 
      toll-like receptor 2 (TLR2), followed by mitogen-activated protein kinases (MAPK) 
      and nuclear factor kappaB (NF-kappaB) signaling pathways, indicating a critical role for 
      TLR2 in Segniliparus-induced macrophage activation. S. rugosus triggered faster 
      and stronger activation of MAPK signaling and IkappaB degradation, indicating that S. 
      rugosus induces more pro-inflammatory cytokines than S. rotundus. Multifocal 
      granulomatous inflammations in the liver and lung were observed in mice infected 
      with S. rugosus, but S. rotundus was rapidly cleared from all organs tested 
      within 15 days post-infection. Furthermore, S. rugosus induced faster 
      infiltration of innate immune cells such as neutrophils and macrophages to the 
      lung than S. rotundus. Our results suggest that S. rugosus is more virulent and 
      induces a stronger immune response than S. rotundus.
FAU - Kim, Jong-Seok
AU  - Kim JS
AD  - Department of Microbiology and Institute for Immunology and Immunological 
      Diseases, Yonsei University College of Medicine, Seoul, South Korea.
FAU - Kim, Woo Sik
AU  - Kim WS
FAU - Lee, Keehoon
AU  - Lee K
FAU - Won, Choul-Jae
AU  - Won CJ
FAU - Kim, Jin Man
AU  - Kim JM
FAU - Eum, Seok-Yong
AU  - Eum SY
FAU - Koh, Won-Jung
AU  - Koh WJ
FAU - Shin, Sung Jae
AU  - Shin SJ
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130329
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
RN  - 0 (Tlr2 protein, mouse)
RN  - 0 (Toll-Like Receptor 2)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Actinomycetales/growth & development/*pathogenicity/physiology
MH  - Actinomycetales Infections/*immunology/metabolism/pathology
MH  - Animals
MH  - Bone Marrow Cells/cytology
MH  - Cell Death/immunology
MH  - Cytokines/biosynthesis
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Female
MH  - Immunity, Cellular
MH  - Immunity, Humoral
MH  - Intracellular Space/microbiology
MH  - Kinetics
MH  - Lung/immunology/metabolism/microbiology
MH  - Macrophages/immunology/microbiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/metabolism
MH  - Phenotype
MH  - Phosphorylation/immunology
MH  - Signal Transduction/immunology
MH  - Species Specificity
MH  - Toll-Like Receptor 2/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
PMC - PMC3612032
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/04/05 06:00
MHDA- 2013/10/01 06:00
PMCR- 2013/03/29
CRDT- 2013/04/05 06:00
PHST- 2012/10/31 00:00 [received]
PHST- 2013/02/16 00:00 [accepted]
PHST- 2013/04/05 06:00 [entrez]
PHST- 2013/04/05 06:00 [pubmed]
PHST- 2013/10/01 06:00 [medline]
PHST- 2013/03/29 00:00 [pmc-release]
AID - PONE-D-12-34221 [pii]
AID - 10.1371/journal.pone.0059646 [doi]
PST - ppublish
SO  - PLoS One. 2013;8(3):e59646. doi: 10.1371/journal.pone.0059646. Epub 2013 Mar 29.