“We know from previous research that macrophages are versatile, and signals at the injury site can stimulate repair or destruction–or confusingly, both,” said John Gensel Ph.D., Assistant Professor of Physiology in the Spinal Cord and Brain Injury Research Center at the University of Kentucky. “But the mechanisms through which these signals stimulate the good and/or bad functions in macrophages are not known. So the next big question to answer in the efforts to understand and treat SCI was, ‘Why?'”
Gensel and Popovich looked at more than 50 animals with spinal cord injury to try to identify which macrophage receptors promoted neuronal repair and which directed the destructive process. Various danger-associated molecular patterns released from dying cells in the injured spinal cord likely activate distinct subtypes of macrophage pattern recognition receptors, including bacterial toll-like receptors (TLRs) and fungal C-type lectin receptors (e.g., dectin-1).
“We found that activating bacterial receptors boosted the macrophage response and limited damage to the spinal cord following injury, while activating fungal receptors actually contributed to pathology,” Gensel said. Note that this simplifies the overall complex process but gives better understanding to mechanisms.
“The implications are exciting: we now can look for treatments targeted to the receptors that jump-start the macrophage’s restorative effects without activating the receptors that modulate the destructive processes in that same cell.” http://www.eurekalert.org/pub_releases/2015-07/uok-fir071015.php
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