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 language | English (US) |
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Pages (from-to) | 643-649 |
Number of pages | 7 |
Journal | Immunology and Cell Biology |
Volume | 86 |
Issue number | 8 |
DOIs | |
State | Published - Nov 2008 |
Externally published | Yes |
Keywords
- Defensin
- HBD3
- Innate immunity
- Pro-inflammatory cytokine suppression
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Cell Biology