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Expression of intercellular adhesion molecule-1 by murine macrophages is up-regulated during differentiation and
1Institute of Experimental Dermatology, University of Münster, Germany.
Insights
Intercellular adhesion molecule-1 (ICAM-1) expression increases with murine monocyte/macrophage maturation. Inflammatory signals and cytokines further modulate ICAM-1, highlighting its role in immune cell interactions during inflammation.
Area of Science:
- Immunology
- Cell Biology
Background:
- Intercellular adhesion molecule-1 (ICAM-1, CD54) is a key glycoprotein in cell-cell interactions.
- Limited information exists regarding ICAM-1 expression in the murine monocyte/macrophage (M phi) lineage.
Purpose of the Study:
- To analyze ICAM-1 expression across M phi maturation stages.
- To investigate ICAM-1 regulation during inflammatory activation in murine models.
Main Methods:
- Flow cytometry was used to assess ICAM-1 expression on bone marrow-derived M phi, peritoneal M phi, and myeloblasts.
- Analysis included M phi cell lines and experimental murine inflammation models (contact hypersensitivity, cutaneous leishmaniasis).
Main Results:
- ICAM-1 expression progressively increased with monocytic maturation.
- Tumor necrosis factor-alpha, interferon-gamma, and lipopolysaccharide (LPS) upregulated ICAM-1 on M phi.
- M phi expressing ICAM-1 were abundant in inflammation models, and Leishmania major parasites upregulated ICAM-1 on M phi.
Conclusions:
- ICAM-1 expression is integral to murine M phi maturation.
- Inflammatory stimuli and cytokines significantly modulate M phi ICAM-1 levels.
- ICAM-1 plays a crucial role in inflammatory processes, potentially by providing co-stimulatory signals for T cell activation.
Abstract:
Intercellular adhesion molecule-1 (ICAM-1, CD54) is a cell-surface glycoprotein which has been shown to play an important role for cell/cell interaction. Little is known about its occurrence in the murine monocyte/macrophage (M phi) lineage; hence, we analyzed ICAM-1 expression in cells and cell lines representing different stages of M phi maturation and studied its regulation during inflammatory activation. Flow cytometric analysis of bone marrow-derived M phi cultured in the presence of M-CSF, of thioglycollate-elicited peritoneal M phi and of M1 myeloblasts differentiated by lipopolysaccharide (LPS) treatment revealed that ICAM-1 is increasingly expressed during monocytic maturation. Accordingly, the myelomonocytic cell lines RMB.TG, WEHI.TG, J774A and P388D, which can be ordered in a linear differentiation sequence, showed increasing levels of ICAM-1 expression. Furthermore, ICAM-1 expression by bone marrow-derived M phi could be up-regulated by tumor necrosis factor-alpha, interferon-gamma and LPS. In two models of murine experimental inflammation, i.e. induction phase of contact hypersensitivity and cutaneous leishmaniasis, which are both dependent on M phi/T cell interaction, M phi expressing ICAM-1 were found to be highly abundant. In addition, it was demonstrated that co-culture of Leishmania maior parasites with bone marrow M phi led to up-regulation of ICAM-1 on these cells. In conclusion, our data clearly demonstrate that ICAM-1 is increasingly being expressed during maturation of murine M phi. Cytokines and inflammatory stimuli modulate M phi ICAM-1 expression as well thus referring to its considerable role during inflammation, e.g. providing accessory or costimulatory signals for T cell activation.