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. 2021 Dec 28;11(1):67. doi: 10.3390/antiox11010067

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Proinflammatory mediator response in IFN I receptor knockout. IFNAR KO and WT mice were infected with RSV and sacrificed at different timepoints of infection to collect BAL for measurements of cytokines (a), chemokines (b), TGF-β (c), and type I and III IFN (d). Data are shown as means ± SD. Significance was determined using repeated-measures ANOVA for (a), (b), and (c), and Student’s t-test for (d); * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to WT RSV with the exception of 2c, where it indicates a difference between RSV and PBS mice. # p < 0.05 compared to WT RSV. Data are representative of one of two independent experiments, with 4–6 animals/group.

Proinflammatory mediator response in IFN I receptor knockout. IFNAR KO and WT mice were infected with RSV and sacrificed at different timepoints of infection to collect BAL for measurements of cytokines (a), chemokines (b), TGF-β (c), and type I and III IFN (d). Data are shown as means ± SD. Significance was determined using repeated-measures ANOVA for (a), (b), and (c), and Student’s t-test for (d); * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to WT RSV with the exception of 2c, where it indicates a difference between RSV and PBS mice. # p < 0.05 compared to WT RSV. Data are representative of one of two independent experiments, with 4–6 animals/group.