PMID- 16622206
OWN - NLM
STAT- MEDLINE
DCOM- 20060523
LR  - 20220408
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 74
IP  - 5
DP  - 2006 May
TI  - Campylobacter jejuni induces maturation and cytokine production in human 
      dendritic cells.
PG  - 2697-705
AB  - Campylobacter jejuni is a leading bacterial cause of human diarrheal disease in 
      both developed and developing nations. Colonic mucosal invasion and the resulting 
      host inflammatory responses are thought to be the key contributing factors to the 
      dysenteric form of this disease. Dendritic cells (DCs) play an important role in 
      both the innate and adaptive immune responses to microbial infection. In this 
      study, the interaction between human monocyte-derived dendritic cells and C. 
      jejuni was studied. We found that C. jejuni was readily internalized by DCs over 
      a 2-h period. However, after a prolonged infection period (24 or 48 h) with C. 
      jejuni, only a few viable bacteria remained intracellularly. Minimal cytotoxicity 
      of C. jejuni to dendritic cells was observed. C. jejuni induced the maturation of 
      dendritic cells over 24 h, as indicated by up-regulation of cell surface marker 
      proteins CD40, CD80, and CD86. In addition, Campylobacter-infected DCs triggered 
      activation of NF-kappaB and significantly stimulated production of 
      interleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, IL-12, gamma interferon, and 
      tumor necrosis factor alpha (TNF-alpha) compared to uninfected DCs. Active 
      bacterial invasion of DCs was not necessary for the induction of these cytokines, 
      as heat-killed C. jejuni stimulated similar levels of cytokine production as live 
      bacteria. Purified lipooligosaccharide of C. jejuni appears to be the major 
      stimulant for the increased production of cytokines by DCs. Taken together, these 
      data indicate that during infection, Campylobacter triggers an innate 
      inflammatory response through increased production of IL-1beta, IL-6, IL-8, and 
      TNF-alpha and initiates a Th1-polarized adaptive immune response as predicted 
      from the high level of production of IL-12.
FAU - Hu, Lan
AU  - Hu L
AD  - Laboratory of Enteric and Sexually Transmitted Diseases, Center for Biologics 
      Evaluation and Research, Food and Drug Administration, 29 Lincoln Drive, NIH 
      Campus, Bethesda, MD 20892, USA.
FAU - Bray, Mechelle D
AU  - Bray MD
FAU - Osorio, Manuel
AU  - Osorio M
FAU - Kopecko, Dennis J
AU  - Kopecko DJ
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (lipid-linked oligosaccharides)
SB  - IM
MH  - Campylobacter jejuni/*immunology
MH  - Cytokines/*biosynthesis
MH  - Dendritic Cells/*immunology/microbiology/physiology
MH  - Humans
MH  - Lipopolysaccharides/pharmacology
MH  - NF-kappa B/metabolism
PMC - PMC1459697
EDAT- 2006/04/20 09:00
MHDA- 2006/05/24 09:00
PMCR- 2006/09/01
CRDT- 2006/04/20 09:00
PHST- 2006/04/20 09:00 [pubmed]
PHST- 2006/05/24 09:00 [medline]
PHST- 2006/04/20 09:00 [entrez]
PHST- 2006/09/01 00:00 [pmc-release]
AID - 74/5/2697 [pii]
AID - 1751-05 [pii]
AID - 10.1128/IAI.74.5.2697-2705.2006 [doi]
PST - ppublish
SO  - Infect Immun. 2006 May;74(5):2697-705. doi: 10.1128/IAI.74.5.2697-2705.2006.