Taken together, our results indicate that RV may stimulate expression of CXCL-10 and IFN-γ via activation of ST2/IL-33 signaling axis, which in turn promote accumulation of CD11b+/CD11c+ macrophages and CD8<sup>+</sup> T cells.
Barrier integrity to cigarette smoke extract (CSE), house dust mite (HDM) extract, interferon-γ (IFN-γ) or human rhinovirus (HRV) infection alone or in combination was assessed.
We therefore examined the effects of intranasal IFN-γ administration on RV-induced ILC2 expansion and IL-13 expression in 6-day-old BALB/c and IL-13 reporter mice.
Tonsillar virus detection showed a strong negative association with age; especially rhinovirus or parainfluenza virus detection showed positive association with IFN-γ and Tbet expressions.
After RV infections were confirmed using semi-nested reverse transcription-polymerase chain reaction (RT-PCR), mRNA expression and protein secretion of the inflammatory cytokines interferon-γ (IFN-γ), interleukin-1β (IL-1β),IL-6, and IL-8, indicators of the severity of RV-induced inflammation, were measured by real-time PCR and enzyme-linked immunosorbent assays.