| First Author | Wu X | Year | 2004 |
| Journal | Int Immunopharmacol | Volume | 4 |
| Issue | 4 | Pages | 513-20 |
| PubMed ID | 15099528 | Mgi Jnum | J:324623 |
| Mgi Id | MGI:6756496 | Doi | 10.1016/j.intimp.2003.10.011 |
| Citation | Wu X, et al. (2004) Histamine production via mast cell-independent induction of histidine decarboxylase in response to lipopolysaccharide and interleukin-1. Int Immunopharmacol 4(4):513-20 |
| abstractText | 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-1alpha, IL-1beta and tumor necrosis factor (TNF)-alpha (IL-1alpha beta/TNFalphaKO 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/W(v) mice, and between IL-1alpha beta/TNFalphaKO BALB/c and control BALB/c mice, and led to increases in histamine. In W/Wv and +/+ mice, IL-1alpha 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-alpha is a prerequisite for the induction of HDC by LPS. |
