PMID- 16027056
OWN - NLM
STAT- MEDLINE
DCOM- 20060124
LR  - 20071114
IS  - 8756-3282 (Print)
IS  - 1873-2763 (Linking)
VI  - 37
IP  - 4
DP  - 2005 Oct
TI  - Osteoblasts produce monocyte chemoattractant protein-1 in a murine model of 
      Staphylococcus aureus osteomyelitis and infected human bone tissue.
PG  - 504-12
AB  - Incidences of osteomyelitis caused by Staphylococcus aureus have increased 
      dramatically in recent years, in part, due to the appearance of 
      community-acquired antibiotic-resistant strains. Therefore, understanding the 
      pathogenesis of this organism has become imperative. Recently, we have described 
      the surprising ability of bone-forming osteoblasts to secrete a number of 
      important immune mediators when exposed to S. aureus in vitro. In the present 
      study, we provide the first evidence for the in vivo production of the pivotal 
      inflammatory chemokine, monocyte chemoattractant protein-1 (MCP-1), by 
      osteoblasts during S. aureus-associated bone infection. Quantitative real-time 
      PCR was employed to determine levels of mRNA encoding MCP-1 in vivo using a mouse 
      model that closely resembles the pathology of trauma-induced staphylococcal 
      osteomyelitis. Expression of this inflammatory chemokine and osteoblast-specific 
      markers was investigated by confocal laser scanning microscopy in bone tissue 
      from organ cultures of neonatal mouse calvaria and from the in vivo mouse model. 
      Furthermore, the clinical relevancy of these findings was investigated by 
      performing similar studies on infected human bone tissue from patients with S. 
      aureus-associated osteomyelitis. Here, we confirm that expression of mRNA 
      encoding MCP-1 is elevated in bacterially infected murine bone tissue. 
      Importantly, we show that these increases translate into marked elevations in the 
      expression of MCP-1 protein that co-localizes with osteoblast markers in infected 
      bone tissue. Such increases could not be attributed solely to mechanical damage 
      as a similar response was observed in infected but otherwise undamaged organ 
      cultures. Finally, we have demonstrated the in vivo production of MCP-1 by 
      osteoblasts in bone specimens from patients with S. aureus-associated 
      osteomyelitis. As such, these studies demonstrate that bacterial challenge of 
      osteoblasts during bone diseases such as staphylococcal osteomyelitis induces 
      cells to produce a key inflammatory chemokine that can direct appropriate host 
      responses or may contribute to progressive inflammatory damage.
FAU - Marriott, Ian
AU  - Marriott I
AD  - Department of Biology, University of North Carolina at Charlotte, 9201 University 
      City Boulevard, Charlotte, NC 28223, USA. imarriot@uncc.edu
FAU - Gray, David L
AU  - Gray DL
FAU - Rati, Dana M
AU  - Rati DM
FAU - Fowler, Vance G Jr
AU  - Fowler VG Jr
FAU - Stryjewski, Martin E
AU  - Stryjewski ME
FAU - Levin, L Scott
AU  - Levin LS
FAU - Hudson, Michael C
AU  - Hudson MC
FAU - Bost, Kenneth L
AU  - Bost KL
LA  - eng
GR  - AI59111/AI/NIAID NIH HHS/United States
GR  - AR48842/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Bone
JT  - Bone
JID - 8504048
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Disease Models, Animal
MH  - Humans
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Microscopy, Confocal
MH  - Osteoblasts/*metabolism
MH  - Osteomyelitis/*metabolism/microbiology
MH  - RNA, Messenger/genetics
MH  - Staphylococcal Infections/*metabolism/microbiology
MH  - Staphylococcus aureus/*isolation & purification
EDAT- 2005/07/20 09:00
MHDA- 2006/01/25 09:00
CRDT- 2005/07/20 09:00
PHST- 2004/12/11 00:00 [received]
PHST- 2005/05/17 00:00 [revised]
PHST- 2005/05/17 00:00 [accepted]
PHST- 2005/07/20 09:00 [pubmed]
PHST- 2006/01/25 09:00 [medline]
PHST- 2005/07/20 09:00 [entrez]
AID - S8756-3282(05)00224-3 [pii]
AID - 10.1016/j.bone.2005.05.011 [doi]
PST - ppublish
SO  - Bone. 2005 Oct;37(4):504-12. doi: 10.1016/j.bone.2005.05.011.