PMID- 20837714
OWN - NLM
STAT- MEDLINE
DCOM- 20101215
LR  - 20240320
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Print)
IS  - 0019-9567 (Linking)
VI  - 78
IP  - 12
DP  - 2010 Dec
TI  - Role of MyD88 and Toll-like receptors 2 and 4 in the sensing of Parachlamydia 
      acanthamoebae.
PG  - 5195-201
LID - 10.1128/IAI.00786-10 [doi]
AB  - Parachlamydia acanthamoebae is a Chlamydia-related organism whose pathogenic role 
      in pneumonia is supported by serological and molecular clinical studies and an 
      experimental mouse model of lung infection. Toll-like receptors (TLRs) play a 
      seminal role in sensing microbial products and initiating innate immune 
      responses. The aim of this study was to investigate the roles of MyD88, TLR2, and 
      TLR4 in the interaction of Parachlamydia with macrophages. Here, we showed that 
      Parachlamydia entered bone-marrow derived macrophages (BMDMs) in a 
      TLR-independent manner but did not multiply intracellularly. Interestingly, 
      compared to live bacteria, heat-inactivated Parachlamydia induced the production 
      of substantial amounts of tumor necrosis factor alpha (TNF), interleukin-6 
      (IL-6), and IL-12p40 by BMDMs and of TNF and IL-6 by peritoneal macrophages as 
      well as RAW 264.7 and J774 macrophage cell lines. Cytokine production by BMDMs, 
      which was partially inhibited upon trypsin treatment of Parachlamydia, was 
      dependent on MyD88, TLR4, and, to a lesser extent, TLR2. Finally, MyD88(-/-), 
      TLR4(-/-), and TLR2(-/-) mice were as resistant as wild-type mice to lung 
      infection following the intratracheal instillation of Parachlamydia. Thus, in 
      contrast to Chlamydia pneumoniae, Parachlamydia acanthamoebae weakly stimulates 
      macrophages, potentially compensating for its low replication capacity in 
      macrophages by escaping the innate immune surveillance.
FAU - Roger, Thierry
AU  - Roger T
AD  - Infectious Diseases Service, Department of Medicine, Centre Hospitalier 
      Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland.
FAU - Casson, Nicola
AU  - Casson N
FAU - Croxatto, Antony
AU  - Croxatto A
FAU - Entenza, Jose Manuel
AU  - Entenza JM
FAU - Pusztaszeri, Marc
AU  - Pusztaszeri M
FAU - Akira, Shizuo
AU  - Akira S
FAU - Reymond, Marlies Knaup
AU  - Reymond MK
FAU - Le Roy, Didier
AU  - Le Roy D
FAU - Calandra, Thierry
AU  - Calandra T
FAU - Greub, Gilbert
AU  - Greub G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100913
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Interleukin-6)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Chlamydia Infections/immunology/microbiology/pathology
MH  - Chlamydiales/immunology/*physiology
MH  - Female
MH  - Host-Pathogen Interactions/immunology/physiology
MH  - Interleukin-6/analysis/blood/physiology
MH  - Lung/chemistry/immunology/pathology
MH  - Macrophages/immunology/microbiology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Myeloid Differentiation Factor 88/immunology/*physiology
MH  - Phagocytosis/physiology
MH  - Pneumonia, Bacterial/immunology/microbiology/pathology
MH  - Signal Transduction/physiology
MH  - Toll-Like Receptor 2/immunology/*physiology
MH  - Toll-Like Receptor 4/immunology/*physiology
MH  - Tumor Necrosis Factor-alpha/analysis/blood/physiology
PMC - PMC2981336
EDAT- 2010/09/15 06:00
MHDA- 2010/12/16 06:00
PMCR- 2011/06/01
CRDT- 2010/09/15 06:00
PHST- 2010/09/15 06:00 [entrez]
PHST- 2010/09/15 06:00 [pubmed]
PHST- 2010/12/16 06:00 [medline]
PHST- 2011/06/01 00:00 [pmc-release]
AID - IAI.00786-10 [pii]
AID - 0786-10 [pii]
AID - 10.1128/IAI.00786-10 [doi]
PST - ppublish
SO  - Infect Immun. 2010 Dec;78(12):5195-201. doi: 10.1128/IAI.00786-10. Epub 2010 Sep 
      13.