A new study from the University of Illinois at Chicago suggests that reprogramming macrophages - white blood cells that respond to inflammation - is more complex than scientists previously thought.
"We found that macrophage programming is driven by more than the immune system - it is also driven by the environment in which the macrophages reside," said Asrar Malik, lead author of the study and a UIC Schweppe Family Distinguished Professor and Head of Pharmacology and Regenerative Medicine at the university's College of Medicine.
The results of their study are published in the latest journal Nature Immunology on Monday, August 24.
White Blood Cell Types in Immune Responses
Macrophages are white blood cells also responsible for the detection and consumption of pathogens, microbes, and foreign cells that do not have a particular protein specific to healthy cells locally found in the body.
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Furthermore, these cells can be programmed to be pro-inflammatory, increasing inflammation, and stimulating the immune systems. It makes them helpful when fighting infections. On the other hand, they can also serve an anti-inflammatory role, decreasing inflammation through the release of cytokines.
The flexible response of the macrophage keeps the immune system's response, driven by inflammation, to remain only as needed, with the inflammation subsiding after, promoting tissue repair after.
One macrophage application studied by the UIC is the macrophage's response in the event of lung injury, using animal models in their investigation.
"We demonstrated that lung endothelial cells -- which are the cells that line blood vessels -- are essential in programming macrophages with potent tissue-reparative and anti-inflammatory functions," Dr. Jaless Rehman, co-lead author in the study and also a professor of medicine and pharmacology and regenerative medicine at the University of Illinois at Chicago.
Endothelial Cells in Macrophage Programming
The UIC research team analyzed the proteins released by blood vessel cells to see whether these signals affected the macrophage response. These proteins act as the chemical signal that triggers the required response from the macrophage.
Researchers then found that a particular protein, Rspondin3, was released at significantly higher levels in the event of an inflammatory responsibility, playing an important role in macrophage programming.
"When we removed the gene responsible for Rspondin3 from the blood vessel endothelial cells, we observed that macrophages did not decelerate inflammation. Instead, the lungs became more injured," explained Bisheng Zhou, the first author of the study and research assistant professor of pharmacology and regenerative medicine at UIC.
He also explained that they tried the same experiment in different models of inflammatory lung injury - yielding consistent results across all models, Furthermore, the study suggests that blood vessels and epithelial cells also play important roles in guiding how macrophage programming commences.
Rehman further explains that the new discovery in this immune system response might also help explain why some patients have better responses to medication, in addition to finding new avenue pharmaceutical researchers can pursue. In the UIC press release, Rehman notes that the lack of an adequate braking system to inhibit inflammation after bacteria response turns the person's own immune system to cause even greater damage - risking vulnerable organs such as the lung.
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