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Summary: Unlike most tissues, the retina does not summons neutrophils, the typical lifeguards of the body, when injured. Instead, microglia, the resident immune cells of the brain, handle the damage of photoreceptors without requesting a backup.
Using images of adaptive optics, the researchers observed this unique immune behavior in living mice retains. The findings suggest a “cover -up” protective mechanism that prevents excessive inflammation and can inform future treatments for vision loss.
Key facts:
Specific retina response: neutrophils do not help in the repair of photoreceptors despite being close. Microglia activation: Only brain resident immune cells respond to retinal lesion. Inflammation shield: the retina can suppress the recruitment of immune cells to avoid additional damage.
Source: Rochester University
During the majority of eye infections or injuries, neutrophils, immune cells found in the blood, are usually the first line of defense.
However, Flaum Eye Institute researchers and the Institute of Monte of Neuroscience at the University of Rochester have discovered that the retina responds differently to many other tissues in the body.
When photoreceptor cells in the retina are damaged, microglia or immune cells of the brain, they respond, and neutrophils are not recruited to help despite passing through the nearby blood vessels.
“This finding has high implications for what happens for millions of Americans who suffer the loss of vision for the loss of photoreceptors,” said Jesse Schallek, PHD, associate professor of ophthalmology and main author of a study today in Elife.
“This association between two key populations of immune cells is essential knowledge since we build new therapies that must understand the nuance of immune cell interactions.”
Using images of adaptive optics, a camera technology developed by the University of Rochester that allows the image of individual neurons and immune cells inside the living eye, the researchers studied mice retains with photoreceptor damage.
They discovered that although neutrophil and microglia cells are present in the retina, only microglia cells respond to the photoreceptor injury, and do not ask neutrophils to help repair the photoreceptor damage.
Researchers believe that this suggests that a type of cover -up occurs during retinal lesion to protect the retina from an avalanche of immune cells that could do more damage than well.
“What is remarkable here is that the neutrophils that pass are so close to reactive microglia and, nevertheless, they do not indicate that they help in the recovery of damage,” said Schallek.
“This is remarkably different from what is seen in other areas of the body where neutrophils are the first to respond to local damage and set up an early and robust response.”
Photoreceptor cells are exclusive to retina. They process light in electrical and chemical signals, they communicate that information to our brain, which allows us to see.
There are many diseases that damage and kill photoreceptor cells, including macular degeneration related to age, pigmentosa retinitis and the dystrophy of the cone bar, and currently there is no cure.
This research now shows that it is possible to visualize the dynamics of individual cells as they communicate with each other, since the retina responds to damage.
The first author Derek Power, laboratory technician at the Schallek laboratory, directed the study. Other authors include Justin Elstrott, PHD, from Genentech Inc.
Financing: The investigation was supported by the National Eye Institute, the research to prevent blindness, the Dana Foundation and a Collaborative Research subsidy of Genentech, Inc.
On this visual neuroscience research news
Author: Kelsie Smith Hayduk
Source: Rochester University
Contact: Kelsie Smith Hayduk – University of Rochester
Image: The image is accredited to Neuroscience News
Original research: open access.
“The loss of photoreceptors does not recruit neutrophils despite the strong microglial activation” of Derek Power et al. elegant
Abstract
The loss of photoreceptors does not recruit neutrophils despite the strong microglial activation
In response to the lesion of the central nervous system (CNS), immune cells residing in the tissue, such as microglia and circulating systemic neutrophils, are often first to respond.
The degree to which these cells interact in response to the damage of the CNS is understood little, and even less like this, in the neural retina, which raises a challenge for high resolution images in vivo.
In this study, we display the ophthalmoscopy of scanning scanning light of scanning fluorescence (Aoslo) to study microglia and neutrophils in mice.
Simultaneously we trace the dynamics of immune cells using Aos without a label phase to the resolution at the microns level. Retinal lesions were induced with light of 488 nm focused on external photoreceptor (PR) segments.
These lesions filed Focally PRS, with minimal collateral damage to the cells above and below the focus plane.
We use in vivo images of Aoslo and Optical Coherence Tomography (OCT) to reveal the natural history of the microglial response and neutrophils from minutes to months after the lesion.
While the microglia showed a dynamic and progressive immune response with the cells that migrate to the locus of the lesion within 1 day after the lesion, the neutrophils were not recruited despite the proximity to the vessels that transport neutrophils only microns away. Confocal microscopy Post mortem confirmed findings in vivo.
This work illustrates that microglial activation does not recruit neutrophils in response to the acute focal loss of PRS, a condition found in many retinal diseases.
