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- W2030728478 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." @default.
- W2030728478 created "2016-06-24" @default.
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- W2030728478 date "2008-08-19" @default.
- W2030728478 modified "2023-10-15" @default.
- W2030728478 title "Human β‐defensin 3 binds to hemagglutinin B (rHagB), a non‐fimbrial adhesin from <i>Porphyromonas gingivalis</i>, and attenuates a pro‐inflammatory cytokine response" @default.
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- W2030728478 doi "https://doi.org/10.1038/icb.2008.56" @default.
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