Macrophage Invasion
Macrophage Invasion - Related Videos
09:23
Coculture Assays to Study Macrophage and Microglia Stimulation of Glioblastoma Invasion
0 Views •
Cited by 19 •
2016
Understanding the malignant behavior of cancer requires creating accurate models of how tumor cells interact with components of the tumor microenvironment, such as macrophages. Here we describe two methods to study glioblastoma cell interaction with tumor associated macrophages and microglia where the effect on glioblastoma invasion is assessed.
09:01
A Macrophage-Tumor Spheroid Co-Invasion Assay
0 Views •
2025
Here, we present a protocol to investigate the interaction of primary human monocyte-derived macrophages with a tumor spheroid in a three-dimensional (3D) collagen I matrix, with the possibility to compare the impact of soluble and physical properties of the microenvironment on cell invasion.
10:07
Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
0 Views •
Cited by 326 •
2013
The article describes a readily easy adaptive in vitro model to investigate macrophage polarization. In the presence of GM-CSF/M-CSF, hematopoietic stem/progenitor cells from the bone marrow are directed into monocytic differentiation, followed by M1 or M2 stimulation. The activation status can be tracked by changes in cell surface antigens, gene expression and cell signaling pathways.
06:46
Culture of Macrophage Colony-stimulating Factor Differentiated Human Monocyte-derived Macrophages
0 Views •
Cited by 58 •
2016
A protocol is presented for cell culture of macrophage colony-stimulating factor (M-CSF) differentiated human monocyte-derived macrophages. The protocol utilizes cryopreservation of monocytes coupled with their bulk differentiation into macrophages. Then harvested macrophages can then be seeded into culture wells at required cell densities for carrying out experiments.
08:50
Depletion and Reconstitution of Macrophages in Mice
0 Views •
Cited by 118 •
2012
Macrophages play a central role in homeostasis and pathology in many tissues. The protocol presented here describes methods for depleting macrophages in vivo, deriving polarized macrophages from bone marrow aspirates, and adoptively transferring macrophages into mice. These techniques allow determination of the role that polarized macrophages play in health and disease.
FAQs
After a macrophage engulfs an infectious agent, the surrounding phagosome normally matures and fuses with lysosomes. This delivery of lysosomal activity helps create conditions that promote microbial destruction. Invasion becomes more successful when a pathogen disrupts maturation or prevents phagosome-lysosome fusion, allowing it to remain protected inside the cell rather than encountering the macrophage’s full degradative response.
Oxidative and nitrosative stresses are part of the macrophage’s intracellular antimicrobial environment. Infectious agents that resist these stresses can persist even after engulfment, turning a normally hostile compartment into a site of survival. This resistance helps explain why intracellular infection may continue despite macrophage uptake and provides a mechanism for evading innate immune killing.
Cytoplasmic escape changes the location and conditions of intracellular survival. Instead of remaining within the phagosome, an infectious agent can reach the macrophage cytoplasm, where it may avoid some compartment-specific defenses and interact differently with the host cell. Studying this transition helps researchers distinguish persistence based on phagosome disruption from persistence based on escape into the cytoplasm.
Intracellular persistence can alter how infected macrophages respond and how infectious agents are maintained within host tissues. These interactions may contribute to inflammation while also providing a protected reservoir that supports continued infection and spread. Examining both outcomes is important because macrophage responses can reflect an attempt to control the pathogen while simultaneously shaping tissue-level disease.
A useful analysis follows the infection from phagocytic uptake through intracellular persistence. Key events include phagosome maturation, fusion with lysosomes, disruption of that pathway, resistance to oxidative and nitrosative stress, and possible cytoplasmic escape. Linking these events to inflammatory responses and tissue spread allows investigators to connect cellular mechanisms with broader host-pathogen outcomes.
These studies identify points at which infectious agents evade innate immunity and macrophages lose effective killing activity. Such information can guide the development of antimicrobial therapies, inform vaccine research, and support strategies designed to restore macrophage function. The broader goal is to interfere with intracellular persistence while improving the host cell’s ability to control infection.