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Intravascular Crawling of Patrolling Monocytes: A Lèvy-Like Motility for Unique Search Functions?
Rocío Moreno-Cañadas1, Laura Luque-Martín1, Alicia G Arroyo1
1Molecular Biomedicine Department, Centro de Investigaciones Biológicas Margarita Salas (CIB-CSIC), Madrid, Spain.
Abstract:
Patrolling monocytes (PMo) are the organism's preeminent intravascular guardians by their continuous search of damaged endothelial cells and harmful microparticles for their removal and to restore homeostasis. This surveillance is accomplished by PMo crawling on the apical side of the endothelium through regulated interactions of integrins and chemokine receptors with their endothelial ligands. We propose that the search mode governs the intravascular motility of PMo in vivo in a similar way to T cells looking for antigen in tissues. Signs of damage to the luminal side of the endothelium (local death, oxidized LDL, amyloid deposits, tumor cells, pathogens, abnormal red cells, etc.) will change the diffusive random towards a Lèvy-like crawling enhancing their recognition and clearance by PMo damage receptors as the integrin αMβ2 and CD36. This new perspective can help identify new actors to promote unique PMo intravascular actions aimed at maintaining endothelial fitness and combating harmful microparticles involved in diseases as lung metastasis, Alzheimer's angiopathy, vaso-occlusive disorders, and sepsis.
Insights
Patrolling monocytes (PMo) act as intravascular guardians, crawling along blood vessels. Damage signals shift their movement to a Lèvy-like crawl, enhancing pathogen and debris clearance.
Area of Science:
- Immunology
- Cell Biology
- Vascular Biology
Background:
- Patrolling monocytes (PMo) are crucial for maintaining vascular integrity and homeostasis.
- PMo surveillance involves crawling on the endothelium via integrin and chemokine receptor interactions.
- Current understanding of PMo motility in vivo is limited.
Purpose of the Study:
- To propose a novel model for PMo intravascular motility based on their search behavior.
- To investigate how endothelial damage influences PMo crawling patterns.
- To identify potential therapeutic targets for diseases involving PMo dysfunction.
Main Methods:
- Conceptual model integrating T cell antigen search with PMo intravascular crawling.
- Hypothesized shift from random to Lèvy-like crawling upon detection of endothelial damage signals.
- Identification of key PMo damage receptors (e.g., integrin αMβ2, CD36).
Main Results:
- PMo movement is proposed to transition from random to Lèvy-like crawling in response to endothelial damage.
- This altered motility enhances recognition and clearance of harmful microparticles and damaged cells.
- Specific damage signals (e.g., oxidized LDL, pathogens) are implicated in triggering this response.
Conclusions:
- PMo intravascular motility is governed by a search-dependent mode, analogous to T cell surveillance.
- Endothelial damage induces a Lèvy-like crawling behavior in PMo for efficient clearance.
- This framework offers new avenues for therapeutic strategies in vascular diseases.
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