PMID- 26241961
OWN - NLM
STAT- MEDLINE
DCOM- 20160510
LR  - 20181113
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 10
IP  - 8
DP  - 2015
TI  - Increased Eotaxin and MCP-1 Levels in Serum from Individuals with Periodontitis 
      and in Human Gingival Fibroblasts Exposed to Pro-Inflammatory Cytokines.
PG  - e0134608
LID - 10.1371/journal.pone.0134608 [doi]
LID - e0134608
AB  - Periodontitis is a chronic inflammatory disease of tooth supporting tissues 
      resulting in periodontal tissue destruction, which may ultimately lead to tooth 
      loss. The disease is characterized by continuous leukocyte infiltration, likely 
      mediated by local chemokine production but the pathogenic mechanisms are not 
      fully elucidated. There are no reliable serologic biomarkers for the diagnosis of 
      periodontitis, which is today based solely on the degree of local tissue 
      destruction, and there is no available biological treatment tool. Prompted by the 
      increasing interest in periodontitis and systemic inflammatory mediators we 
      mapped serum cytokine and chemokine levels from periodontitis subjects and 
      healthy controls. We used multivariate partial least squares (PLS) modeling and 
      identified monocyte chemoattractant protein-1 (MCP-1) and eotaxin as clearly 
      associated with periodontitis along with C-reactive protein (CRP), years of 
      smoking and age, whereas the number of remaining teeth was associated with being 
      healthy. Moreover, body mass index correlated significantly with serum MCP-1 and 
      CRP, but not with eotaxin. We detected higher MCP-1 protein levels in inflamed 
      gingival connective tissue compared to healthy but the eotaxin levels were 
      undetectable. Primary human gingival fibroblasts displayed strongly increased 
      expression of MCP-1 and eotaxin mRNA and protein when challenged with tumor 
      necrosis factor-alpha (TNF-alpha and interleukin-1beta (IL-1beta), key mediators of periodontal 
      inflammation. We also demonstrated that the upregulated chemokine expression was 
      dependent on the NF-kappaBeta pathway. In summary, we identify higher levels of CRP, 
      eotaxin and MCP-1 in serum of periodontitis patients. This, together with our 
      finding that both CRP and MCP-1 correlates with BMI points towards an increased 
      systemic inflammatory load in patients with periodontitis and high BMI. Targeting 
      eotaxin and MCP-1 in periodontitis may result in reduced leukocyte infiltration 
      and inflammation in periodontitis and maybe prevent tooth loss.
FAU - Bostrom, Elisabeth A
AU  - Bostrom EA
AD  - Karolinska Institutet, Division of Periodontology, Department of Dental Medicine, 
      Stockholm, Sweden.
FAU - Kindstedt, Elin
AU  - Kindstedt E
AD  - Umea University, Department of Molecular Periodontology, Umea, Sweden.
FAU - Sulniute, Rima
AU  - Sulniute R
AD  - Umea University, Department of Molecular Periodontology, Umea, Sweden.
FAU - Palmqvist, Py
AU  - Palmqvist P
AD  - Umea University, Department of Molecular Periodontology, Umea, Sweden.
FAU - Majster, Mirjam
AU  - Majster M
AD  - Karolinska Institutet, Division of Periodontology, Department of Dental Medicine, 
      Stockholm, Sweden.
FAU - Holm, Cecilia Koskinen
AU  - Holm CK
AD  - Umea University, Department of Molecular Periodontology, Umea, Sweden.
FAU - Zwicker, Stephanie
AU  - Zwicker S
AD  - Karolinska Institutet, Division of Periodontology, Department of Dental Medicine, 
      Stockholm, Sweden.
FAU - Clark, Reuben
AU  - Clark R
AD  - Karolinska Institutet, Division of Periodontology, Department of Dental Medicine, 
      Stockholm, Sweden.
FAU - Onell, Sebastian
AU  - Onell S
AD  - Umea University, Department of Molecular Periodontology, Umea, Sweden.
FAU - Johansson, Ingegerd
AU  - Johansson I
AD  - Umea University, Department of Cariology, Umea, Sweden.
FAU - Lerner, Ulf H
AU  - Lerner UH
AD  - Umea University, Department of Molecular Periodontology, Umea, Sweden; University 
      of Gothenburg, Sahlgrenska Academy, Centre for Bone and Arthritis Research, 
      Gothenburg, Sweden.
FAU - Lundberg, Pernilla
AU  - Lundberg P
AD  - Umea University, Department of Molecular Periodontology, Umea, Sweden.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150804
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL11)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Adult
MH  - Age Factors
MH  - Body Mass Index
MH  - C-Reactive Protein
MH  - Chemokine CCL11/blood/*metabolism
MH  - Chemokine CCL2/blood/*metabolism
MH  - Cytokines/*pharmacology
MH  - Female
MH  - Fibroblasts/drug effects/*metabolism/pathology
MH  - Gingiva/drug effects/*metabolism/pathology
MH  - Humans
MH  - Inflammation/metabolism/pathology
MH  - Male
MH  - Middle Aged
MH  - Periodontitis/*blood/pathology
MH  - Periodontium/drug effects/metabolism/pathology
MH  - Smoking
PMC - PMC4524692
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2015/08/05 06:00
MHDA- 2016/05/11 06:00
PMCR- 2015/08/04
CRDT- 2015/08/05 06:00
PHST- 2015/04/17 00:00 [received]
PHST- 2015/07/11 00:00 [accepted]
PHST- 2015/08/05 06:00 [entrez]
PHST- 2015/08/05 06:00 [pubmed]
PHST- 2016/05/11 06:00 [medline]
PHST- 2015/08/04 00:00 [pmc-release]
AID - PONE-D-15-16677 [pii]
AID - 10.1371/journal.pone.0134608 [doi]
PST - epublish
SO  - PLoS One. 2015 Aug 4;10(8):e0134608. doi: 10.1371/journal.pone.0134608. 
      eCollection 2015.