PMID- 22144493
OWN - NLM
STAT- MEDLINE
DCOM- 20120409
LR  - 20211021
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Print)
IS  - 0019-9567 (Linking)
VI  - 80
IP  - 3
DP  - 2012 Mar
TI  - Roles of interleukin-17 in an experimental Legionella pneumophila pneumonia 
      model.
PG  - 1121-7
LID - 10.1128/IAI.05544-11 [doi]
AB  - Interleukin-17 (IL-17) is a key factor in T helper type 17 (Th17) lineage host 
      responses and plays critical roles in immunological control of a variety of 
      infectious diseases. Although Legionella pneumophila, an intracellular bacterium 
      found widely in the environment, often causes a serious and life-threatening 
      pneumonia in humans, the contribution of IL-17 to immune function during 
      Legionella pneumonia is unknown. In the present study, we used an experimental 
      Legionella pneumonia infection to clarify the role of IL-17 in the resulting 
      immune response. We observed robust production of pulmonary IL-17A and IL-17F 
      (IL-17A/F), peaking on day 1 and declining thereafter. Upregulated production of 
      tumor necrosis factor alpha (TNF-alpha), IL-6, and IL-1beta, but not monocyte 
      chemotactic protein 1 (MCP-1), was observed in Legionella-infected bone 
      marrow-derived macrophages from BALB/c mice that had been stimulated with IL-17A 
      or IL-17F. A significant decrease in the production of proinflammatory cytokines 
      IL-6 and TNF-alpha was observed in IL-17A/F-deficient mice (BALB/c background) 
      infected with L. pneumophila. Moreover, we found impaired neutrophil migration 
      and lower numbers of chemokines (KC, LIX, and MIP-2) in IL-17A/F-deficient mice. 
      IL-17A/F-deficient mice also eliminated L. pneumophila more slowly and were less 
      likely to survive a lethal challenge. These results demonstrate that IL-17A/F 
      plays a critical role in L. pneumophila pneumonia, probably through induction of 
      proinflammatory cytokines and accumulation of neutrophils at the infection site.
FAU - Kimizuka, Yoshifumi
AU  - Kimizuka Y
AD  - Department of Microbiology and Infectious Disease, Toho University School of 
      Medicine, Tokyo, Japan.
FAU - Kimura, Soichiro
AU  - Kimura S
FAU - Saga, Tomoo
AU  - Saga T
FAU - Ishii, Makoto
AU  - Ishii M
FAU - Hasegawa, Naoki
AU  - Hasegawa N
FAU - Betsuyaku, Tomoko
AU  - Betsuyaku T
FAU - Iwakura, Yoichiro
AU  - Iwakura Y
FAU - Tateda, Kazuhiro
AU  - Tateda K
FAU - Yamaguchi, Keizo
AU  - Yamaguchi K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111205
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-17)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Cytokines/metabolism
MH  - Disease Models, Animal
MH  - Interleukin-17/*immunology
MH  - Legionella pneumophila/*immunology/*pathogenicity
MH  - Legionnaires' Disease/*immunology/microbiology/*pathology
MH  - Macrophages/immunology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Neutrophils/immunology
MH  - Pneumonia/immunology/microbiology/pathology
PMC - PMC3294673
EDAT- 2011/12/07 06:00
MHDA- 2012/04/10 06:00
PMCR- 2012/09/01
CRDT- 2011/12/07 06:00
PHST- 2011/12/07 06:00 [entrez]
PHST- 2011/12/07 06:00 [pubmed]
PHST- 2012/04/10 06:00 [medline]
PHST- 2012/09/01 00:00 [pmc-release]
AID - IAI.05544-11 [pii]
AID - 05544-11 [pii]
AID - 10.1128/IAI.05544-11 [doi]
PST - ppublish
SO  - Infect Immun. 2012 Mar;80(3):1121-7. doi: 10.1128/IAI.05544-11. Epub 2011 Dec 5.