PMID- 17034573
OWN - NLM
STAT- MEDLINE
DCOM- 20070117
LR  - 20221207
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 146
IP  - 2
DP  - 2006 Nov
TI  - Innate immune peptide LL-37 displays distinct expression pattern from 
      beta-defensins in inflamed gingival tissue.
PG  - 218-25
AB  - Anti-microbial peptides produced from mucosal epithelium appear to play pivotal 
      roles in the host innate immune defence system in the oral cavity. In particular, 
      human beta-defensins (hBDs) and the cathelicidin-type anti-microbial peptide, 
      LL-37, were reported to kill periodontal disease-associated bacteria. In contrast 
      to well-studied hBDs, little is known about the expression profiles of LL-37 in 
      gingival tissue. In this study, the anti-microbial peptides expressed in gingival 
      tissue were analysed using immunohistochemistry and enxyme-linked immunosorbent 
      assay (ELISA). Immunohistochemistry revealed that neutrophils expressed only 
      LL-37, but not hBD-2 or hBD-3, and that such expression was prominent in the 
      inflammatory lesions when compared to healthy gingivae which showed very few or 
      no LL-37 expressing neutrophils. Gingival epithelial cells (GEC), however, 
      expressed all three examined anti-microbial peptides, irrespective of the 
      presence or absence of inflammation. Moreover, as determined by ELISA, the 
      concentration of LL-37 in the gingival tissue homogenates determined was 
      correlated positively with the depth of the gingival crevice. Stimulation with 
      periodontal bacteria in vitro induced both hBD-2 and LL-37 expressions by GEC, 
      whereas peripheral blood neutrophils produced only LL-37 production, but not 
      hBD-2, in response to the bacterial stimulation. These findings suggest that 
      LL-37 displays distinct expression patterns from those of hBDs in gingival 
      tissue.
FAU - Hosokawa, I
AU  - Hosokawa I
AD  - Department of Immunology, The Forsyth Institute, Boston, Massachusetts, USA.
FAU - Hosokawa, Y
AU  - Hosokawa Y
FAU - Komatsuzawa, H
AU  - Komatsuzawa H
FAU - Goncalves, R B
AU  - Goncalves RB
FAU - Karimbux, N
AU  - Karimbux N
FAU - Napimoga, M H
AU  - Napimoga MH
FAU - Seki, M
AU  - Seki M
FAU - Ouhara, K
AU  - Ouhara K
FAU - Sugai, M
AU  - Sugai M
FAU - Taubman, M A
AU  - Taubman MA
FAU - Kawai, T
AU  - Kawai T
LA  - eng
GR  - R01 DE003420/DE/NIDCR NIH HHS/United States
GR  - R37 DE003420/DE/NIDCR NIH HHS/United States
GR  - K22 DE014551/DE/NIDCR NIH HHS/United States
GR  - DE-14551/DE/NIDCR NIH HHS/United States
GR  - DE-03420/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Antigens, Bacterial)
RN  - 0 (Antimicrobial Cationic Peptides)
RN  - 0 (DEFB103A protein, human)
RN  - 0 (DEFB4A protein, human)
RN  - 0 (RNA, Messenger)
RN  - 0 (beta-Defensins)
RN  - 0 (Cathelicidins)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antigens, Bacterial/immunology
MH  - Antimicrobial Cationic Peptides/genetics/*metabolism
MH  - Bacteria/immunology
MH  - Cells, Cultured
MH  - Enzyme-Linked Immunosorbent Assay/methods
MH  - Female
MH  - Gene Expression Regulation
MH  - Gingiva/metabolism
MH  - Gingivitis/immunology/*metabolism/pathology
MH  - Humans
MH  - Immunoenzyme Techniques
MH  - Male
MH  - Middle Aged
MH  - Neutrophils/metabolism
MH  - RNA, Messenger/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - beta-Defensins/genetics/*metabolism
MH  - Cathelicidins
PMC - PMC1942065
EDAT- 2006/10/13 09:00
MHDA- 2007/01/18 09:00
PMCR- 2007/11/01
CRDT- 2006/10/13 09:00
PHST- 2006/10/13 09:00 [pubmed]
PHST- 2007/01/18 09:00 [medline]
PHST- 2006/10/13 09:00 [entrez]
PHST- 2007/11/01 00:00 [pmc-release]
AID - CEI3200 [pii]
AID - 10.1111/j.1365-2249.2006.03200.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2006 Nov;146(2):218-25. doi: 10.1111/j.1365-2249.2006.03200.x.