This week
Science Translational Medicine published new study that showed that
in newborn mice resistance to pneumonia is driven by neonatally acquired microbiota. It revealed how antibiotic therapy given to mothers near time of delivery could alter and weaken baby's defenses against airway pathogens.
Newborn mice derived from
germ-free or from antibiotic-exposed pregnant mice display increased susceptibility to
Streptococcus pneumoniae serotype 19A-induced
pneumonia that could be reversed by
microflora.
Application of epithelial-focused cytokine IL-22 had similar effect on reversing newborn mice susceptibility to pneumonia.
In the lungs of newborn mice,
majority of IL-22 is made by RORgt+ group 3 innate lymphoid cells (ILC3).
Antibiotic therapy of pregnant mice reduced IL-22+ ILC3 population in the newborn lungs that could be reversed by microflora.
Moreover, depletion of endogenous ILC3 increased host's susceptibility to pneumonia that could be
reversed by adoptive transfer of WT ILC3.
In summary, this study showed that antibiotic therapy of pregnant females at the time of delivery could profoundly affect newborns' ability to mount proper defense against airway pathogens by depleting microflora and disrupting microflora → ILC3 → IL-22 axis.
David Usharauli
