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Human β‐defensin 3 binds to hemagglutinin B (rHagB), a non‐fimbrial adhesin from Porphyromonas gingivalis , and attenuates a pro‐inflammatory cytokine response
Author(s) -
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,
ProgulskeFox Ann,
Cavanaugh Joseph E,
Guthmiller Janet M,
Johnson Georgia K,
Joly Sophie,
Kurago Zoya B,
Dawson Deborah V,
Brogden Kim A
Publication year - 2008
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2008.56
Subject(s) - cytokine , porphyromonas gingivalis , tumor necrosis factor alpha , bacterial adhesin , biology , mapk/erk pathway , immunology , microbiology and biotechnology , chemistry , signal transduction , biochemistry , genetics , escherichia coli , bacteria , gene
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.