Gingival tissue human beta-defensin levels in relation to infection and inflammation

Meltem Özdemir; Feriha Caglayan; Floris J. Bikker; Pirkko Pussinen; Eija Könönen; Nermin Yamalik; Mervi Gürsoy; Dareen Fteita; Kamran Nazmi; Güliz N. Güncü; Milla Pietiäinen; Mimmi Tolvanen; Ulvi Kahraman Gürsoy

doi:10.1111/jcpe.13227

Gingival tissue human beta-defensin levels in relation to infection and inflammation

Meltem Özdemir, Feriha Caglayan, Floris J. Bikker, Pirkko Pussinen, Eija Könönen, Nermin Yamalik, Mervi Gürsoy, Dareen Fteita, Kamran Nazmi, Güliz N. Güncü, Milla Pietiäinen, Mimmi Tolvanen, Ulvi Kahraman Gürsoy^*

^*Corresponding author for this work

Research output: Contribution to Journal › Article › Academic › peer-review

Abstract

Aim: To profile gingival tissue levels of human beta-defensin (hBD)-2 and hBD-3 in relation to gingival inflammation, Th17-related cytokine concentrations, Porphyromonas gingivalis counts, and gingipain and total protease activities. Materials and Methods: Gingival tissue and subgingival plaque samples were collected from 21 periodontitis patients including 48 periodontal pocket sites with marginal, mild, or moderate to severe inflammation. hBD levels were determined by immunodetection, P. gingivalis counts with real-time polymerase chain reaction, protease activities with fluorogenic substrates, and cytokine concentrations with Luminex technique. Data were statistically analysed using Kruskal–Wallis and Mann–Whitney U tests and Spearman correlation coefficients. Results: Subgingival plaque counts of P. gingivalis (p =.001) and gingipain activity (p <.001), as well as interleukin (IL)-1β (p =.012), IL-10 (p =.024), IL-17A (p =.002), IL-17F (p =.006), and IL-23 (p =.036) concentrations were elevated in severely inflamed sites, whereas no change was observed in hBD-2 and hBD-3 levels. Negative correlations were found between protease activity and hBD-2 (p =.033) and hBD-3(p =.003) levels. Conclusions: Shift in gingival inflammation from marginal to mild stage is related to elevations in subgingival plaque P. gingivalis counts and gingipain activity, but not to tissue hBD levels. Negative correlations between hBDs and total protease activity suggest the degradation of these antimicrobial peptides in progressed inflammation.

Original language	English
Pages (from-to)	309-318
Number of pages	10
Journal	Journal of Clinical Periodontology
Volume	47
Issue number	3
Early online date	3 Dec 2019
DOIs	https://doi.org/10.1111/jcpe.13227
Publication status	Published - Mar 2020

Bibliographical note

Funding Information:
This study is supported by TUBITAK, Turkey (M.?, Grant no: BIDEB- 1059B141700759), Finnish Dental Society Apollonia, Finland (UKG and PP), Turku University Foundation (D.F. Grant no: 12194), Hacettepe University Scientific Research Projects Coordination Units (M?, THD-16531), Sigrid Juselius foundation (PP), and Paulo foundation (PP). The authors are grateful for the skilful technical assistances of Katja Sampalahti from University of Turku. Authors confirm that they have no conflict of interest.

Funding Information:
This study is supported by TUBITAK, Turkey (M.Ö, Grant no: BIDEB‐ 1059B141700759), Finnish Dental Society Apollonia, Finland (UKG and PP), Turku University Foundation (D.F. Grant no: 12194), Hacettepe University Scientific Research Projects Coordination Units (MÖ, THD‐16531), Sigrid Juselius foundation (PP), and Paulo foundation (PP). The authors are grateful for the skilful technical assistances of Katja Sampalahti from University of Turku. Authors confirm that they have no conflict of interest.

Publisher Copyright:
© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

Funding

This study is supported by TUBITAK, Turkey (M.?, Grant no: BIDEB- 1059B141700759), Finnish Dental Society Apollonia, Finland (UKG and PP), Turku University Foundation (D.F. Grant no: 12194), Hacettepe University Scientific Research Projects Coordination Units (M?, THD-16531), Sigrid Juselius foundation (PP), and Paulo foundation (PP). The authors are grateful for the skilful technical assistances of Katja Sampalahti from University of Turku. Authors confirm that they have no conflict of interest. This study is supported by TUBITAK, Turkey (M.Ö, Grant no: BIDEB‐ 1059B141700759), Finnish Dental Society Apollonia, Finland (UKG and PP), Turku University Foundation (D.F. Grant no: 12194), Hacettepe University Scientific Research Projects Coordination Units (MÖ, THD‐16531), Sigrid Juselius foundation (PP), and Paulo foundation (PP). The authors are grateful for the skilful technical assistances of Katja Sampalahti from University of Turku. Authors confirm that they have no conflict of interest.

Funders	Funder number
Türkiye Bilimsel ve Teknolojik Araştirma Kurumu	BIDEB‐ 1059B141700759
Hacettepe Üniversitesi	THD‐16531
Turun Yliopisto	12194
Suomen Hammaslääkäriseura Apollonia
Sigrid Juséliuksen Säätiö
Paulon Säätiö

Keywords

antimicrobial peptides
gingipain
hBD-2
hBD-3
inflammatory cytokines
periodontitis
Porphyromonas gingivalis

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@article{6761d409bb6f4d4c91fdd6475b47ab7c,

title = "Gingival tissue human beta-defensin levels in relation to infection and inflammation",

abstract = "Aim: To profile gingival tissue levels of human beta-defensin (hBD)-2 and hBD-3 in relation to gingival inflammation, Th17-related cytokine concentrations, Porphyromonas gingivalis counts, and gingipain and total protease activities. Materials and Methods: Gingival tissue and subgingival plaque samples were collected from 21 periodontitis patients including 48 periodontal pocket sites with marginal, mild, or moderate to severe inflammation. hBD levels were determined by immunodetection, P. gingivalis counts with real-time polymerase chain reaction, protease activities with fluorogenic substrates, and cytokine concentrations with Luminex technique. Data were statistically analysed using Kruskal–Wallis and Mann–Whitney U tests and Spearman correlation coefficients. Results: Subgingival plaque counts of P. gingivalis (p =.001) and gingipain activity (p <.001), as well as interleukin (IL)-1β (p =.012), IL-10 (p =.024), IL-17A (p =.002), IL-17F (p =.006), and IL-23 (p =.036) concentrations were elevated in severely inflamed sites, whereas no change was observed in hBD-2 and hBD-3 levels. Negative correlations were found between protease activity and hBD-2 (p =.033) and hBD-3(p =.003) levels. Conclusions: Shift in gingival inflammation from marginal to mild stage is related to elevations in subgingival plaque P. gingivalis counts and gingipain activity, but not to tissue hBD levels. Negative correlations between hBDs and total protease activity suggest the degradation of these antimicrobial peptides in progressed inflammation.",

keywords = "antimicrobial peptides, gingipain, hBD-2, hBD-3, inflammatory cytokines, periodontitis, Porphyromonas gingivalis",

author = "Meltem {\"O}zdemir and Feriha Caglayan and Bikker, {Floris J.} and Pirkko Pussinen and Eija K{\"o}n{\"o}nen and Nermin Yamalik and Mervi G{\"u}rsoy and Dareen Fteita and Kamran Nazmi and G{\"u}nc{\"u}, {G{\"u}liz N.} and Milla Pieti{\"a}inen and Mimmi Tolvanen and G{\"u}rsoy, {Ulvi Kahraman}",

note = "Funding Information: This study is supported by TUBITAK, Turkey (M.?, Grant no: BIDEB- 1059B141700759), Finnish Dental Society Apollonia, Finland (UKG and PP), Turku University Foundation (D.F. Grant no: 12194), Hacettepe University Scientific Research Projects Coordination Units (M?, THD-16531), Sigrid Juselius foundation (PP), and Paulo foundation (PP). The authors are grateful for the skilful technical assistances of Katja Sampalahti from University of Turku. Authors confirm that they have no conflict of interest. Funding Information: This study is supported by TUBITAK, Turkey (M.{\"O}, Grant no: BIDEB‐ 1059B141700759), Finnish Dental Society Apollonia, Finland (UKG and PP), Turku University Foundation (D.F. Grant no: 12194), Hacettepe University Scientific Research Projects Coordination Units (M{\"O}, THD‐16531), Sigrid Juselius foundation (PP), and Paulo foundation (PP). The authors are grateful for the skilful technical assistances of Katja Sampalahti from University of Turku. Authors confirm that they have no conflict of interest. Publisher Copyright: {\textcopyright} 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd",

year = "2020",

month = mar,

doi = "10.1111/jcpe.13227",

language = "English",

volume = "47",

pages = "309--318",

journal = "Journal of Clinical Periodontology",

issn = "0303-6979",

publisher = "Blackwell Munksgaard",

number = "3",

}

TY - JOUR

T1 - Gingival tissue human beta-defensin levels in relation to infection and inflammation

AU - Özdemir, Meltem

AU - Caglayan, Feriha

AU - Bikker, Floris J.

AU - Pussinen, Pirkko

AU - Könönen, Eija

AU - Yamalik, Nermin

AU - Gürsoy, Mervi

AU - Fteita, Dareen

AU - Nazmi, Kamran

AU - Güncü, Güliz N.

AU - Pietiäinen, Milla

AU - Tolvanen, Mimmi

AU - Gürsoy, Ulvi Kahraman

N1 - Funding Information: This study is supported by TUBITAK, Turkey (M.?, Grant no: BIDEB- 1059B141700759), Finnish Dental Society Apollonia, Finland (UKG and PP), Turku University Foundation (D.F. Grant no: 12194), Hacettepe University Scientific Research Projects Coordination Units (M?, THD-16531), Sigrid Juselius foundation (PP), and Paulo foundation (PP). The authors are grateful for the skilful technical assistances of Katja Sampalahti from University of Turku. Authors confirm that they have no conflict of interest. Funding Information: This study is supported by TUBITAK, Turkey (M.Ö, Grant no: BIDEB‐ 1059B141700759), Finnish Dental Society Apollonia, Finland (UKG and PP), Turku University Foundation (D.F. Grant no: 12194), Hacettepe University Scientific Research Projects Coordination Units (MÖ, THD‐16531), Sigrid Juselius foundation (PP), and Paulo foundation (PP). The authors are grateful for the skilful technical assistances of Katja Sampalahti from University of Turku. Authors confirm that they have no conflict of interest. Publisher Copyright: © 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

PY - 2020/3

Y1 - 2020/3

N2 - Aim: To profile gingival tissue levels of human beta-defensin (hBD)-2 and hBD-3 in relation to gingival inflammation, Th17-related cytokine concentrations, Porphyromonas gingivalis counts, and gingipain and total protease activities. Materials and Methods: Gingival tissue and subgingival plaque samples were collected from 21 periodontitis patients including 48 periodontal pocket sites with marginal, mild, or moderate to severe inflammation. hBD levels were determined by immunodetection, P. gingivalis counts with real-time polymerase chain reaction, protease activities with fluorogenic substrates, and cytokine concentrations with Luminex technique. Data were statistically analysed using Kruskal–Wallis and Mann–Whitney U tests and Spearman correlation coefficients. Results: Subgingival plaque counts of P. gingivalis (p =.001) and gingipain activity (p <.001), as well as interleukin (IL)-1β (p =.012), IL-10 (p =.024), IL-17A (p =.002), IL-17F (p =.006), and IL-23 (p =.036) concentrations were elevated in severely inflamed sites, whereas no change was observed in hBD-2 and hBD-3 levels. Negative correlations were found between protease activity and hBD-2 (p =.033) and hBD-3(p =.003) levels. Conclusions: Shift in gingival inflammation from marginal to mild stage is related to elevations in subgingival plaque P. gingivalis counts and gingipain activity, but not to tissue hBD levels. Negative correlations between hBDs and total protease activity suggest the degradation of these antimicrobial peptides in progressed inflammation.

AB - Aim: To profile gingival tissue levels of human beta-defensin (hBD)-2 and hBD-3 in relation to gingival inflammation, Th17-related cytokine concentrations, Porphyromonas gingivalis counts, and gingipain and total protease activities. Materials and Methods: Gingival tissue and subgingival plaque samples were collected from 21 periodontitis patients including 48 periodontal pocket sites with marginal, mild, or moderate to severe inflammation. hBD levels were determined by immunodetection, P. gingivalis counts with real-time polymerase chain reaction, protease activities with fluorogenic substrates, and cytokine concentrations with Luminex technique. Data were statistically analysed using Kruskal–Wallis and Mann–Whitney U tests and Spearman correlation coefficients. Results: Subgingival plaque counts of P. gingivalis (p =.001) and gingipain activity (p <.001), as well as interleukin (IL)-1β (p =.012), IL-10 (p =.024), IL-17A (p =.002), IL-17F (p =.006), and IL-23 (p =.036) concentrations were elevated in severely inflamed sites, whereas no change was observed in hBD-2 and hBD-3 levels. Negative correlations were found between protease activity and hBD-2 (p =.033) and hBD-3(p =.003) levels. Conclusions: Shift in gingival inflammation from marginal to mild stage is related to elevations in subgingival plaque P. gingivalis counts and gingipain activity, but not to tissue hBD levels. Negative correlations between hBDs and total protease activity suggest the degradation of these antimicrobial peptides in progressed inflammation.

KW - antimicrobial peptides

KW - gingipain

KW - hBD-2

KW - hBD-3

KW - inflammatory cytokines

KW - periodontitis

KW - Porphyromonas gingivalis

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U2 - 10.1111/jcpe.13227

DO - 10.1111/jcpe.13227

M3 - Article

C2 - 31799742

AN - SCOPUS:85078437608

SN - 0303-6979

VL - 47

SP - 309

EP - 318

JO - Journal of Clinical Periodontology

JF - Journal of Clinical Periodontology

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ER -

Gingival tissue human beta-defensin levels in relation to infection and inflammation

Abstract

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Keywords

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