We initially discovered that RSV significantly improved cardiac function and suppressed the expression of fibrosis markers, such as collagen-I, collagen-III, and fibronectin, and pro-inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α).
The enzyme-linked immunosorbent assay showed that JOL reduced the release of inflammatory factors, including interleukin-1β(IL-1β), interleukin-18(IL-18) and interleukin-33(IL-33), in the serum and lung homogenate of RSV-infected mice.
In the present study, truncated G protein was successfully expressed both in prokaryotic and eukaryotic system, and high levels of serum IgG in response to truncated G protein were observed both in GD-protein group (intramuscularly with purified GD protein) and GD-VNP20009 group (challenged via the oral route with 1 × 10<sup>9</sup> CFU of pLIVE-RSV-GD-VNP20009 strains) since 21th day, and GD-VNP20009 significantly reduced the productions of IL-1β, IL-6, and TNF-α, histamine and pathological features caused by the RSV Long strain (P < .01).
These mediators include classical pro-inflammatory cytokines such as TGF-β, TNF-α, interferons, or IL-1β that are released upon bacterial challenge with <i>Streptococcus pneumoniae, Klebsiella pneumoniae</i>, or <i>Mycoplasma pneumoniae</i> as well as in viral infection with influenza A virus, pathogenic coronaviruses, or respiratory syncytial virus.
RSV-infected MSCs showed differentially altered expression of cytokines and chemokines such as IL-1β, IL6, IL-8 and SDF-1 compared to epithelial cells.
In this study, we describe an increased IL-1β response to RSV ΔSH, which may explain the attenuation in vivo and supports targeting the SH gene in live attenuated vaccines.