PMID- 19281567
OWN - NLM
STAT- MEDLINE
DCOM- 20090413
LR  - 20220317
IS  - 1574-695X (Electronic)
IS  - 0928-8244 (Linking)
VI  - 55
IP  - 2
DP  - 2009 Mar
TI  - In vitro neutralization of tumor necrosis factor-alpha during Chlamydia 
      pneumoniae infection impairs dendritic cells maturation/function and increases 
      chlamydial progeny.
PG  - 215-25
LID - 10.1111/j.1574-695X.2008.00512.x [doi]
AB  - Dendritic cells (DCs) produce tumor necrosis factor (TNF)-alpha upon infection 
      and contribute in various ways to defense against pathogenic agents. Several 
      biological agents have been designed to inhibit TNF-alpha activity. However, the 
      use of these inhibitors has been associated with an increased rate of certain 
      opportunistic infections. To study the effect of TNF-alpha inhibition, human 
      monocyte-derived DCs were infected with Chlamydia pneumoniae. TNF-alpha was 
      neutralized by adalimumab, a human anti-TNF-alpha monoclonal antibody. Chlamydiae 
      induced the maturation of DC as determined by flow cytometry and quantitative 
      real-time PCR. However, DC maturation was impaired in the presence of adalimumab. 
      Moreover, neutralization of TNF-alpha resulted in a significant increase of 
      infectious progeny, 16S rRNA gene copy number and development of larger 
      inclusions consisting of different stages of chlamydial development. 
      Additionally, chlamydial infection induced secretion of cytokines/chemokines, 
      which were downregulated by adalimumab treatment. Our data reveal an indirect 
      effect on maturation of DC by C. pneumoniae and that maturation is crucial for 
      the restriction of chlamydial development. The results also demonstrate an 
      increase in infectious progeny after TNF-alpha inhibition, suggesting a 
      contribution of TNF-alpha produced by DCs to chlamydial growth arrest. These data 
      suggest a possible mechanism by which TNF-alpha inhibition enhances the risk of 
      intracellular infections.
FAU - Njau, Florence
AU  - Njau F
AD  - Department of Nephrology, Hannover Medical School, Germany. fnjau@yahoo.com
FAU - Wittkop, Ulrike
AU  - Wittkop U
FAU - Rohde, Manfred
AU  - Rohde M
FAU - Haller, Hermann
AU  - Haller H
FAU - Klos, Andreas
AU  - Klos A
FAU - Wagner, Annette Doris
AU  - Wagner AD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - FEMS Immunol Med Microbiol
JT  - FEMS immunology and medical microbiology
JID - 9315554
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antigens, CD)
RN  - 0 (Cytokines)
RN  - 0 (Immunologic Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - FYS6T7F842 (Adalimumab)
SB  - IM
MH  - Adalimumab
MH  - Antibodies, Monoclonal/pharmacology
MH  - Antibodies, Monoclonal, Humanized
MH  - Antigens, CD/analysis
MH  - Cells, Cultured
MH  - Chlamydophila pneumoniae/*growth & development/*immunology
MH  - Colony Count, Microbial/methods
MH  - Cytokines/biosynthesis
MH  - Cytoplasm/microbiology
MH  - Dendritic Cells/chemistry/*immunology/*microbiology
MH  - Flow Cytometry
MH  - Humans
MH  - Immunologic Factors/pharmacology
MH  - Inclusion Bodies/microbiology
MH  - Microscopy, Electron, Transmission
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors/*immunology
EDAT- 2009/03/14 09:00
MHDA- 2009/04/14 09:00
CRDT- 2009/03/14 09:00
PHST- 2009/03/14 09:00 [entrez]
PHST- 2009/03/14 09:00 [pubmed]
PHST- 2009/04/14 09:00 [medline]
AID - FIM512 [pii]
AID - 10.1111/j.1574-695X.2008.00512.x [doi]
PST - ppublish
SO  - FEMS Immunol Med Microbiol. 2009 Mar;55(2):215-25. doi: 
      10.1111/j.1574-695X.2008.00512.x.