Frontline immune cells can call for back-up
Australian researchers have found that neutrophils - innate immune cells that swarm to sites of injury within minutes to undertake damage control and kill invaders - can in some cases enlist reinforcements in their fight against pathogens.
Most neutrophils have very short lives and self-destruct once their job is done. But if the injury is infected, neutrophils seek out accomplices from the slower-acting adaptive immune system by travelling to the nearest lymph node, sometimes carrying a sample of bacteria or other microbe. This helps prime other types of immune cell for attack.
To investigate different neutrophil responses, Garvan Institute researchers Henry Hampton and Dr Tatyana Chtanova induced either sterile or bacterial inflammation on the ears of mice. Thanks to the use of photoconvertible proteins, bright light shone on the site of inflammation changed the colour of ‘recruited’ neutrophils from green to red.
Cell-sorting technology picked up any colour-converted red neutrophils that had moved from the site of infection to lymph nodes - a journey which was undertaken within 8 h of infection. Two-photon microscopy revealed that neutrophils travelled via the lymphatic system, rather than the bloodstream. The findings were published in the journal Nature Communications.
“Neutrophils together with T cells will try to clean up infection everywhere, including in the lymph node,” said Dr Chtanova. “Microbes from infection sites can migrate to the lymph node in the lymph stream, separately from neutrophils, so T cell recruitment by neutrophils may help prevent microbial spread.
“We can see that neutrophils bring microbes to the lymph node and that T cells proliferate as a result. While we have yet to identify the exact mechanisms that neutrophils use to communicate with T cells, we did uncover molecules involved in neutrophil migration from infected lesions to lymph nodes.
“In theory, this new finding could help us prevent microbes from exploiting neutrophils as Trojan Horses to spread infection. It might also allow us to enhance neutrophil migration and so generate a faster and more effective antimicrobial response.
“At the very least, the finding helps clarify an aspect of how the innate and adaptive arms of the immune system work together in the initial stages of infection.”
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