Human β-defensin 3 binds to hemagglutinin B (rHagB), a non-fimbrial adhesin from Porphyromonas gingivalis, and attenuates a pro-inflammatory cytokine response

Lindsey C. Pingel, Karl G. Kohlgraf, Christopher J. Hansen, Christopher G. Eastman, Deborah E. Dietrich, Kindra K. Burnell, Rupasree N. Srikantha, Xiangjun Xiao, Myriam Bélanger, Ann Progulske-Fox, Joseph E. Cavanaugh, Janet M. Guthmiller, Georgia K. Johnson, Sophie Joly, Zoya B. Kurago, Deborah V. Dawson, Kim A. Brogden

Research output: Contribution to journalArticle

54 Citations (Scopus)

Abstract

Regulatory mechanisms in mucosal secretions and tissues recognize antigens and attenuate pro-inflammatory cytokine responses. Here, we asked whether human β-defensin 3 (HBD3) serves as an upstream suppressor of cytokine signaling that binds and attenuates pro-inflammatory cytokine responses to recombinant hemagglutinin B (rHagB), a non-fimbrial adhesin from Porphyromonas gingivalis strain 381. We found that HBD3 binds to immobilized rHagB and produces a significantly higher resonance unit signal in surface plasmon resonance spectroscopic analysis, than HBD2 and HBD1 that are used as control defensins. Furthermore, we found that HBD3 significantly attenuates (P<0.05) the interleukin (IL)-6, IL-10, granulocyte macrophage colony stimulating factor (GM-CSF) and tumor-necrosis factor-α (TNF-α) responses induced by rHagB in human myeloid dendritic cell culture supernatants and the extracellular signal-regulated kinases (ERK 1/2) response in human myeloid dendritic cell lysates. Thus, HBD3 binds rHagB and this interaction may be an important initial step to attenuate a pro-inflammatory cytokine response and an ERK 1/2 response.

Original languageEnglish (US)
Pages (from-to)643-649
Number of pages7
JournalImmunology and Cell Biology
Volume86
Issue number8
DOIs
StatePublished - Nov 1 2008

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Defensins
Porphyromonas gingivalis
Hemagglutinins
Cytokines
Myeloid Cells
Dendritic Cells
Mitogen-Activated Protein Kinase 3
Surface Plasmon Resonance
Granulocyte-Macrophage Colony-Stimulating Factor
Interleukin-10
Interleukin-6
Mucous Membrane
Cell Culture Techniques
Tumor Necrosis Factor-alpha
Antigens

Keywords

  • Defensin
  • HBD3
  • Innate immunity
  • Pro-inflammatory cytokine suppression

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

Cite this

Human β-defensin 3 binds to hemagglutinin B (rHagB), a non-fimbrial adhesin from Porphyromonas gingivalis, and attenuates a pro-inflammatory cytokine response. / Pingel, Lindsey C.; Kohlgraf, Karl G.; Hansen, Christopher J.; Eastman, Christopher G.; Dietrich, Deborah E.; Burnell, Kindra K.; Srikantha, Rupasree N.; Xiao, Xiangjun; Bélanger, Myriam; Progulske-Fox, Ann; Cavanaugh, Joseph E.; Guthmiller, Janet M.; Johnson, Georgia K.; Joly, Sophie; Kurago, Zoya B.; Dawson, Deborah V.; Brogden, Kim A.

In: Immunology and Cell Biology, Vol. 86, No. 8, 01.11.2008, p. 643-649.

Research output: Contribution to journalArticle

Pingel, LC, Kohlgraf, KG, Hansen, CJ, Eastman, CG, Dietrich, DE, Burnell, KK, Srikantha, RN, Xiao, X, Bélanger, M, Progulske-Fox, A, Cavanaugh, JE, Guthmiller, JM, Johnson, GK, Joly, S, Kurago, ZB, Dawson, DV & Brogden, KA 2008, 'Human β-defensin 3 binds to hemagglutinin B (rHagB), a non-fimbrial adhesin from Porphyromonas gingivalis, and attenuates a pro-inflammatory cytokine response', Immunology and Cell Biology, vol. 86, no. 8, pp. 643-649. https://doi.org/10.1038/icb.2008.56
Pingel, Lindsey C. ; Kohlgraf, Karl G. ; Hansen, Christopher J. ; Eastman, Christopher G. ; Dietrich, Deborah E. ; Burnell, Kindra K. ; Srikantha, Rupasree N. ; Xiao, Xiangjun ; Bélanger, Myriam ; Progulske-Fox, Ann ; Cavanaugh, Joseph E. ; Guthmiller, Janet M. ; Johnson, Georgia K. ; Joly, Sophie ; Kurago, Zoya B. ; Dawson, Deborah V. ; Brogden, Kim A. / Human β-defensin 3 binds to hemagglutinin B (rHagB), a non-fimbrial adhesin from Porphyromonas gingivalis, and attenuates a pro-inflammatory cytokine response. In: Immunology and Cell Biology. 2008 ; Vol. 86, No. 8. pp. 643-649.
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AU - Pingel, Lindsey C.

AU - Kohlgraf, Karl G.

AU - Hansen, Christopher J.

AU - Eastman, Christopher G.

AU - Dietrich, Deborah E.

AU - Burnell, Kindra K.

AU - Srikantha, Rupasree N.

AU - Xiao, Xiangjun

AU - Bélanger, Myriam

AU - Progulske-Fox, Ann

AU - Cavanaugh, Joseph E.

AU - Guthmiller, Janet M.

AU - Johnson, Georgia K.

AU - Joly, Sophie

AU - Kurago, Zoya B.

AU - Dawson, Deborah V.

AU - Brogden, Kim A.

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N2 - Regulatory mechanisms in mucosal secretions and tissues recognize antigens and attenuate pro-inflammatory cytokine responses. Here, we asked whether human β-defensin 3 (HBD3) serves as an upstream suppressor of cytokine signaling that binds and attenuates pro-inflammatory cytokine responses to recombinant hemagglutinin B (rHagB), a non-fimbrial adhesin from Porphyromonas gingivalis strain 381. We found that HBD3 binds to immobilized rHagB and produces a significantly higher resonance unit signal in surface plasmon resonance spectroscopic analysis, than HBD2 and HBD1 that are used as control defensins. Furthermore, we found that HBD3 significantly attenuates (P<0.05) the interleukin (IL)-6, IL-10, granulocyte macrophage colony stimulating factor (GM-CSF) and tumor-necrosis factor-α (TNF-α) responses induced by rHagB in human myeloid dendritic cell culture supernatants and the extracellular signal-regulated kinases (ERK 1/2) response in human myeloid dendritic cell lysates. Thus, HBD3 binds rHagB and this interaction may be an important initial step to attenuate a pro-inflammatory cytokine response and an ERK 1/2 response.

AB - Regulatory mechanisms in mucosal secretions and tissues recognize antigens and attenuate pro-inflammatory cytokine responses. Here, we asked whether human β-defensin 3 (HBD3) serves as an upstream suppressor of cytokine signaling that binds and attenuates pro-inflammatory cytokine responses to recombinant hemagglutinin B (rHagB), a non-fimbrial adhesin from Porphyromonas gingivalis strain 381. We found that HBD3 binds to immobilized rHagB and produces a significantly higher resonance unit signal in surface plasmon resonance spectroscopic analysis, than HBD2 and HBD1 that are used as control defensins. Furthermore, we found that HBD3 significantly attenuates (P<0.05) the interleukin (IL)-6, IL-10, granulocyte macrophage colony stimulating factor (GM-CSF) and tumor-necrosis factor-α (TNF-α) responses induced by rHagB in human myeloid dendritic cell culture supernatants and the extracellular signal-regulated kinases (ERK 1/2) response in human myeloid dendritic cell lysates. Thus, HBD3 binds rHagB and this interaction may be an important initial step to attenuate a pro-inflammatory cytokine response and an ERK 1/2 response.

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