Journal
MUCOSAL IMMUNOLOGY
Volume 15, Issue 5, Pages 1000-1011Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/s41385-022-00544-5
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Funding
- National Institutes of Health [TL1TR001447, T32ES007324, T32AI007180]
- NIH [R01HL125816, U01AI22285]
- Leducq and Sergei Zlinkoff foundations
- Swiss National Science Foundation [BSCGIO 462 157841/1]
- National Institutes of Health/National Cancer Institute [P30CA016087]
- German Research Foundation (DFG) [RE 3652/4-1, Ta 275/7-1]
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Antibiotics, commonly used in children, can alter gut microbiome communities and metabolic functions, which in turn affects host immunity. This study shows that early-life microbiome alterations due to antibiotic exposure can lead to increased susceptibility to allergy and asthma.
Antibiotics, among the most used medications in children, affect gut microbiome communities and metabolic functions. These changes in microbiota structure can impact host immunity. We hypothesized that early-life microbiome alterations would lead to increased susceptibility to allergy and asthma. To test this, mouse pups between postnatal days 5-9 were orally exposed to water (control) or to therapeutic doses of azithromycin or amoxicillin. Later in life, these mice were sensitized and challenged with a model allergen, house dust mite (HDM), or saline. Mice with early-life azithromycin exposure that were challenged with HDM had increased IgE and IL-13 production by CD4(+) T cells compared to unexposed mice; early-life amoxicillin exposure led to fewer abnormalities. To test that the microbiota contained the immunological cues to alter IgE and cytokine production after HDM challenge, germ-free mice were gavaged with fecal samples of the antibiotic-perturbed microbiota. Gavage of adult germ-free mice did not result in altered HDM responses, however, their offspring, which acquired the antibiotic-perturbed microbiota at birth showed elevated IgE levels and CD4(+) cytokines in response to HDM, and altered airway reactivity. These studies indicate that early-life microbiota composition can heighten allergen-driven Th2/Th17 immune pathways and airway responses in an age-dependent manner.
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