Alternaria inhibits double-stranded RNA-induced cytokines productions through TLR3

Kouta Wada, Takao Kobayashi, Yoshinori Matsuwaki, Hiroshi Moriyama, Hirohito Kita

Research output: Contribution to journalArticlepeer-review


Fungi may be involved in asthma and chronic rhinosinusitis (CRS). PBMCs from CRS patients produce IL-5, IL-13 and INF-± by Alternaria. In addition, Alternaria produces potent Th2-like adjuvant effects in the airway. Therefore, we hypothesized that Alternaria may inhibit Th1-type defense mechanisms against virus infection. Dendritic cells (DCs) were generated from mouse bone marrow. The functional responses were assessed by expression of cell surface molecules by FACS (MHC Class II, CD40, CD80, CD86 and OX40L. Production of IL-6, IP-10, I-TAC and IFN-β were measured by ELISA. TLR3 mRNA and protein expression were detected by quantitative Real time-PCR and Western blot. Alternaria and poly I:C enhanced cell surface expression of MHC Class II, CD40, CD80, CD86 and OX40L, and IL-6 production in a concentration-dependent manner. However, Alternaria significantly inhibited IP-10, I-TAC and IFN-β production induced by viral double-stranded RNA (dsRNA)-mimic poly I:C. TLR3 mRNA expression and protein production by poly I:C were significantly inhibited by Alternaria. These reactions are likely caused by heat-stable factor(s) in Alternaria extract with >100 kDa molecular mass. These findings suggest that fungus, Alternaria may inhibit production of IFN-β and other cytokines by DCs by suppressing TLR3 expression. These results indicate that Alternaria may inhibit host innate immunity against virus infection.

Original languageEnglish (US)
Pages (from-to)117-126
Number of pages10
JournalPractica Otologica, Supplement
Issue number143
StatePublished - Jul 1 2015


  • Alternaria
  • Dendritic cell
  • DsRNA
  • I-TAC
  • IFN-b
  • IP-10
  • Poly I:C
  • Toll-like receptor-3

ASJC Scopus subject areas

  • Otorhinolaryngology


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