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Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
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Acidosis differently modulates the inflammatory program in monocytes and macrophages
Anne Riemann1, Hanna Wußling1, Harald Loppnow2
1Julius-Bernstein-Institute of Physiology, University Halle-Wittenberg, Germany.
Biochimica Et Biophysica Acta
|October 27, 2015
Summary
Extracellular acidosis, common in tumors, alters immune cell responses. While it may hinder immune cell recruitment, it can promote inflammation by increasing macrophage phagocytosis and specific inflammatory markers like COX-2 and iNOS.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Extracellular pH reduction (acidosis) occurs in inflammatory conditions, ischemia, and solid tumors.
- Acidosis impacts cellular signaling, transcription, and function.
- Understanding acidosis effects on immune cells is crucial for disease insight.
Purpose of the Study:
- To investigate the impact of acidosis on inflammatory marker expression in monocytic cells and macrophages.
- To assess functional changes in immune cells, including migration and phagocytosis, under acidic conditions.
- To identify signaling pathways modulated by acidosis in immune cells.
Main Methods:
- Monocytic cell lines (e.g., RAW264.7) and primary human monocytes/macrophages were exposed to acidic extracellular pH.
- Expression levels of inflammatory mediators (e.g., IL-1ß, IL-6, TNF-α, MCP-1, COX-2, iNOS) were measured.
- Functional assays for phagocytic activity and cell migration were performed.
- Analysis of key signaling pathways (e.g., p38, ERK1/2, CREB) was conducted.
Main Results:
- Acidosis differentially affected inflammatory marker expression across cell types; generally reducing some in monocytes but increasing IL-1ß, COX-2, and iNOS in macrophages.
- Monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) were downregulated by acidosis in most tested cells.
- Phagocytic activity of immune cells was enhanced in a time-dependent manner under acidosis, while cellular motility remained unchanged.
- p38 MAPK activation by acidosis was identified as critical for the induction of IL-1ß, COX-2, and iNOS in RAW264.7 macrophages.
Conclusions:
- Acidosis may impair immune cell infiltration into tissues.
- In the presence of macrophages, acidosis can exacerbate inflammation by upregulating COX-2 and iNOS and enhancing phagocytic capacity.
- These findings highlight a complex role for acidosis in modulating immune responses within the tumor microenvironment.
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