Ammonia (
NH
3
), a toxic gas, has deleterious effects on chicken health in intensive poultry houses. MicroRNA can mediate inflammation. The complex molecular mechanisms underlying NH
3
inhalation–caused inflammation in animal kidneys are still unknown. To explore the mechanisms, a broiler model of NH
3
exposure was established. Kidney samples were collected on day 14, 28, and 42, and meat yield was evaluated on day 42. We performed histopathological examination, detected miR-6615-5p and mothers against decapentaplegic homolog 7 (
Smad7
), and determined inflammatory factors and cytokines in kidneys. The results showed that excess NH
3
reduced breast weight and thigh weight, which indicated that excess NH
3
impaired meat yield of broilers. Besides, kidney tissues displayed histopathological changes after NH
3
exposure. Meanwhile, the increases of inducible nitric oxide synthase (
iNOS
) activity and nitric oxide content were obtained. The mRNA and protein expression of inflammatory factors, including nuclear factor-κB (
NF-κB
), cyclooxygenase-2, prostaglandin E synthases, and iNOS increased, indicating that NF-κB pathway was activated. T-helper (
Th
) 1 and regulatory T (
Treg
) cytokines were downregulated, whereas Th2 and Th17 cytokines were upregulated, suggesting the occurrence of Th1/Th2 and Treg/Th17 imbalances. In addition, we found that Smad7 was a target gene of miR-6615-5p in chickens. After NH
3
exposure, miR-6615-5p expression was elevated, and Smad7 mRNA and protein expression were reduced. In summary, our results suggest that NH
3
exposure negatively affected meat yield; and miR-6615/Smad7 axis and immune imbalance participated in NH
3
-induced inflammatory injury via the NF-κB pathway in broiler kidneys. This study is helpful to understand the mechanism of NH
3
-induced kidney injury and is meaningful to poultry health and breed aquatics.
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