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

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

doi:10.1016/j.intimp.2003.10.011

Cited by 36 publications

(39 citation statements)

References 48 publications

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“…3). We previously reported that following administration of IL-1α or IL-1β, the induced HDC levels in various tissues are similar in normal and W/W v mice [11, 29]. These results seem to support our hypothesis that MC-derived IL-1 may mediate the HDC induction observed following OVA challenge.…”

Section: Discussionsupporting

confidence: 83%

“…Interestingly, recent in vitro studies have demonstrated that MCs produce not only Th2 cytokines, but also inflammatory cytokines (IL-1β and TNFα) [25,26,27,28]. IL-1 induces HDC fully in MC-deficient mice, which indicates that it induces HDC in non-MCs [29]. In addition, Fcε receptors have recently been found on various cell types, including non-MCs such as monocytes, eosinophils, Langerhans cells, and neutrophils [30].…”

Section: Introductionmentioning

confidence: 99%

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Inductions of Histidine Decarboxylase in Mouse Tissues following Systemic Antigen Challenge: Contributions Made by Mast Cells, Non-Mast Cells and IL-1

Xue

et al. 2007

Int Arch Allergy Immunol

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Background: Previous findings suggest that antigen challenge (AC) may induce histidine decarboxylase (HDC) in cells other than mast cells (MCs) via MC-derived IL-1. We examined this hypothesis. Methods: Mice were sensitized to ovalbumin. After the sensitization, an AC was delivered intravenously. Results: In control mice, AC markedly induced HDC at a postanaphylactic time in the liver, lung, spleen, and ears. In MC-deficient W/W^v mice, AC also induced HDC, although the effect was weaker than in control mice. AC increased IL-1 in the tissues, the pattern being similar in W/W^v and control mice. AC induced HDC similarly in IL-1-deficient and control mice. In control mice, AC decreased histamine in the tissues (except the liver) for several hours. Conclusion: (1) AC induces HDC in both MC-dependent and MC-independent ways. (2) AC induces IL-1 mostly in non-MCs, but this IL-1 is not a prerequisite for the induction of HDC by AC. (3) HDC induction may contribute to the replenishment of the reduced pool of MC histamine in the anaphylactic period. (4) In the case of MC-dependent HDC induction, AC may stimulate MCs in such a way as to induce HDC within the MCs themselves, and/or AC-stimulated MCs may stimulate HDC induction in other cells, which will need to be directly identified in future studies.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Inductions of Histidine Decarboxylase in Mouse Tissues following Systemic Antigen Challenge: Contributions Made by Mast Cells, Non-Mast Cells and IL-1

Xue

et al. 2007

Int Arch Allergy Immunol

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“…It is now well-recognized that stimulation with lipopolysaccharide (LPS) leads to a number of responses in microcirculation, such as endothelial cell damage, an increase in rolling, adhesion and emigration of leukocytes in post-capillary venules, enhanced oxygenfree radical production, mast cell degranulation and protein efflux [1][2][3][4][5][6] . Furthermore, it is demonstrated that LPS stimulation evokes an increase in the expression of adhesion molecules, including L-selectin [7] and CD11b/CD18 in leukocytes, E-selectin and intercellular adhesion molecule 1 (ICAM-1) in endothelial cells [7][8][9][10][11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Han

Horie²,

Miura³

et al. 2007

WJG

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stained with Monastral blue B, rolling and adhesion of leukocytes, production of oxygen radical in venular wall, albumin efflux and enhanced mast cell degranulation in vivo , all of which, except for the leukocyte rolling, were attenuated by the treatment with compound Danshen injection. Experiments performed in vitro further revealed that the expression of CD11b/CD18 and the production of oxygen free radical in neutrophils, and the expression of ICAM-1 in HUVECs were increased by exposure to LPS, and they were attenuated by compound Danshen injection. CONCLUSION: These results suggest that compoundDanshen injection is an efficient drug with multi-targeting potential for improving the microcirculatory disturbance. INTRODUCTIONIt is now well-recognized that stimulation with lipopolysaccharide (LPS) leads to a number of responses in microcirculation, such as endothelial cell damage, an increase in rolling, adhesion and emigration of leukocytes in post-capillary venules, enhanced oxygenfree radical production, mast cell degranulation and protein efflux [1][2][3][4][5][6] . Furthermore, it is demonstrated that LPS stimulation evokes an increase in the expression of adhesion molecules, including L-selectin [7] and CD11b/CD18 in leukocytes, E-selectin and intercellular adhesion molecule 1 (ICAM-1) in endothelial cells [7][8][9][10][11][12][13] . In addition, LPS stimulation can cause the release of proinflammatory mediators and vasoactive substances, such Abstract AIM: To investigate the effect of compound Danshen injection on lipopolysaccharide (LPS)-induced rat mesenteric microcirculatory dysfunctions and the underlying possible mechanism by an inverted intravital microscope and high-speed video camera system. METHODS:LPS was continuously infused through the jugular artery of male Wistar rats at the dose of 2 mg/kg per hour. Changes in mesenteric microcirculation, such as diameters of arterioles and venules, velocity of RBCs in venules, leukocyte rolling, adhesion and emigration, free radicals released from post-capillary venules, FITCalbumin leakage and mast cell degranulation, were observed through an inverted intravital microscope assisted with CCD camera and SIT camera. Meanwhile, the expression of adhesion molecules CD11b/CD18 and the production of free radical in neutrophils, and the expression of intercellular adhesion molecule 1 (ICAM-1) in human umbilical vein endothelial cells (HUVECs) were quantified by flow cytometry (FACS) in vitro . RESULTS:The continuous infusion with LPS resulted in a number of responses in microcirculation, including a significant increase in the positive region of venule

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“…49,50) As described in Section 4.1., N-BPs induce HDC in various tissues in mice and also augment HDC-induction by LPS, and vascular endothelial cells are supposed to be the major cells in which HDC is induced. 26,51) Thus, inhibition of FPP synthase results in toxic effects via a variety of effects on a variety of cells.…”

Section: Necrotic Effectsmentioning

confidence: 99%

Underlying Mechanisms and Therapeutic Strategies for Bisphosphonate-Related Osteonecrosis of the Jaw (BRONJ)

Endo

Kumamoto

Nakamura

et al. 2017

Biological & Pharmaceutical Bulletin

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Bisphosphonates (BPs), with a non-hydrolysable P-C-P structure, are cytotoxic analogues of pyrophosphate, bind strongly to bone, are taken into osteoclasts during bone-resorption and exhibit long-acting anti-bone-resorptive effects. Among the BPs, nitrogen-containing BPs (N-BPs) have far stronger anti-boneresorptive effects than non-N-BPs. In addition to their pyrogenic and digestive-organ-injuring side effects, BP-related osteonecrosis of jaws (BRONJ), mostly caused by N-BPs, has been a serious concern since 2003. The mechanism underlying BRONJ has proved difficult to unravel, and there are no solid strategies for treating and/or preventing BRONJ. Our mouse experiments have yielded the following results.

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

Cited by 36 publications

References 48 publications

Inductions of Histidine Decarboxylase in Mouse Tissues following Systemic Antigen Challenge: Contributions Made by Mast Cells, Non-Mast Cells and IL-1

Inductions of Histidine Decarboxylase in Mouse Tissues following Systemic Antigen Challenge: Contributions Made by Mast Cells, Non-Mast Cells and IL-1

Compound Danshen injection improves endotoxin-induced microcirculatory disturbance in rat mesentery

Underlying Mechanisms and Therapeutic Strategies for Bisphosphonate-Related Osteonecrosis of the Jaw (BRONJ)

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