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Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
Published on: January 7, 2019
MTA-induced neutrophil recruitment: a mechanism dependent on IL-1beta, MIP-2, and LTB4
Alessandra Cristina Gomes1, João Eduardo Gomes Filho, Sandra Helena Penha de Oliveira
1Department of Basic Sciences, Araçatuba Dentistry School, São Paulo State University, Araçatuba, SP, Brazil.
Objective:
The objective of this study was to investigate the mediators and the resident peritoneal cells involved in the neutrophil migration (NM) induced by mineral trioxide aggregate (MTA) in mice.
Study Design:
MTA (25 mg/cavity) was injected into normal and pretreated peritoneal cavities (PC) with indomethacin (IND), dexamethasone (DEX), BWA4C, U75302, antimacrophage inflammatory protein-2 (MIP-2), and anti-interleukin-1beta (IL-1beta) antibodies and the NM was determined. The role of macrophage (MO) and mast cells (MAST) was determined by administration of thioglycollate 3% or 48/80 compound, respectively. The concentration of IL-1beta and MIP-2 exudates was measured by ELISA.
Results:
MTA induced dose- and time-dependent NM into mice PC, with the participation of MO and MAST. NM was inhibited by DEX, BWA4C, and U75302, as well as anti-MIP-2 and anti-IL-1beta antibodies. In the exudates, IL-1beta and MIP-2 were detected.
Conclusions:
This study suggests that MTA induces NM via a mechanism dependent on MAST and MO mediated by IL-1beta, MIP-2, and LTB(4).
Insights
Mineral trioxide aggregate (MTA) triggers neutrophil migration in mice through mast cells and macrophages. This process involves interleukin-1beta and macrophage inflammatory protein-2, crucial for MTA-induced inflammation.
Area of Science:
- Immunology
- Cell Biology
- Biomaterials Science
Background:
- Mineral trioxide aggregate (MTA) is widely used in dentistry.
- The inflammatory response to MTA, particularly neutrophil migration (NM), requires further elucidation.
- Understanding the cellular and molecular mechanisms of MTA-induced inflammation is critical for optimizing its clinical application.
Purpose of the Study:
- To investigate the cellular mediators involved in MTA-induced neutrophil migration (NM) in a mouse model.
- To identify the specific peritoneal cells that mediate the inflammatory response to MTA.
- To elucidate the molecular pathways, including cytokines and chemokines, triggered by MTA.
Main Methods:
- Neutrophil migration (NM) was induced by injecting MTA into the peritoneal cavities (PC) of mice.
- Mice were pretreated with inhibitors of specific pathways (indomethacin, dexamethasone, BWA4C, U75302) and antibodies against key mediators (MIP-2, IL-1beta).
- The roles of macrophage (MO) and mast cells (MAST) were assessed using specific cell activators, and cytokine/chemokine levels (IL-1beta, MIP-2) were quantified via ELISA.
Main Results:
- MTA administration induced a dose- and time-dependent NM in mouse PC.
- Neutrophil migration was significantly inhibited by dexamethasone, BWA4C, U75302, and antibodies targeting MIP-2 and IL-1beta.
- Macrophages and mast cells were identified as key cellular players in MTA-induced NM, with elevated levels of IL-1beta and MIP-2 detected in peritoneal exudates.
Conclusions:
- MTA induces neutrophil migration (NM) through a mechanism involving mast cells and macrophages.
- The inflammatory response is mediated by key signaling molecules, including interleukin-1beta (IL-1beta), macrophage inflammatory protein-2 (MIP-2), and leukotriene B4 (LTB4).
- These findings provide insights into the inflammatory potential of MTA and suggest therapeutic targets for managing MTA-induced inflammation.
