Worm infection trains lung macrophages to survive lethal influenza without clearing the virus
5 October 2026
The Nature paper, published on 30 September 2026, describes disease tolerance rather than faster clearance of the pathogen.
Mice previously infected with the parasitic nematode Nippostrongylus brasiliensis survived lethal H1N1 influenza while carrying the same viral burden as control mice.
Nerve- and airway-associated macrophages were both necessary and sufficient: removing them abolished the protection, and transferring them conferred it.
The training works through IL-4-STAT6-PPAR-gamma and ARG1-dependent chromatin reprogramming that sets up pro-resolving and reparative programmes.
Protection came from reduced immunopathology, amplified type 2 immunity, more eosinophils and faster tissue repair, not from killing more virus.
In human lung tissue the same repair programme was enriched in idiopathic pulmonary fibrosis and absent in chronic obstructive pulmonary disease.
In plain words
Macrophage macrophage — A white blood cell that swallows debris and microbes and helps repair tissue.
Disease tolerance disease tolerance — Surviving an infection by limiting the damage it causes rather than by removing the pathogen.
Chromatin reprogramming chromatin reprogramming — A lasting change in how DNA is packaged, which alters which genes a cell can switch on.