Abstract:
:Regulatory mechanisms in mucosal secretions and tissues recognize antigens and attenuate pro-inflammatory cytokine responses. Here, we asked whether human beta-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-alpha (TNF-alpha) 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.
journal_name
Immunol Cell Bioljournal_title
Immunology and cell biologyauthors
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 KAdoi
10.1038/icb.2008.56subject
Has Abstractpub_date
2008-11-01 00:00:00pages
643-9issue
8eissn
0818-9641issn
1440-1711pii
icb200856journal_volume
86pub_type
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