Histamine production via mast cell-independent induction of histidine decarboxylase in response to lipopolysaccharide and interleukin-1

Xia Wu, Atsushi Yoshida, Takashi Sasano, Yoichiro Iwakura, Yasuo Endo

Research output: Contribution to journalArticlepeer-review

34 Citations (Scopus)


Histamine modulates immune responses. There are at least two ways histamine might be supplied: one is its release from cells that pool pre-formed histamine and the other is its de novo formation via induction of histidine decarboxylase (HDC). Lipopolysaccharide (LPS) and the proinflammatory cytokine interleukin (IL)-1 induce a marked elevation of HDC activity in various tissues or organs. To examine the contribution of mast cells to HDC induction in mice given LPS or IL-1, we examined the effects of LPS and IL-1 on HDC activity and/or histamine content in various organs (liver, lung, spleen or bone marrow) in mast cell-deficient mice (W/Wv), their normal littermates (+/+) and BALB/c mice deficient in IL-1α, IL-1β and tumor necrosis factor (TNF)-α (IL-1αβ/TNFαKO mice). In non-stimulated mice, the histamine in the lung and spleen was contained largely within mast cells. The LPS-stimulated increase in HDC activity in a given organ was similar between +/+ and W/Wv mice, and between IL-1αβ/TNFαKO BALB/c and control BALB/c mice, and led to increases in histamine. In W/Wv and +/+ mice, IL-1α also elevated HDC activity. These results suggest that (i) in liver, lung and spleen, either the major cells supplying histamine via HDC induction in response to LPS and IL-1 are not mast cells, or mast cells are not a prerequisite for the induction of HDC; (ii) the cells in which HDC is induced by LPS and IL-1 are similar or identical in a given organ; and (iii) neither IL-1 nor TNF-α is a prerequisite for the induction of HDC by LPS.

Original languageEnglish
Pages (from-to)513-520
Number of pages8
JournalInternational Immunopharmacology
Issue number4
Publication statusPublished - 2004 Apr
Externally publishedYes


  • Histamine
  • Histidine decarboxylase
  • Innate immunity
  • Interleukin-1
  • Lipopolysaccharide
  • Mast cells
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pharmacology


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