Immunomodulatory effect and molecular mechanism of deoxyribonucleic acid receptor toll-like receptor 9 signaling pathway on newborn babies with acute lung injury.

Abstract

This work was to demonstrate the immunomodulatory effect of toll-like receptor 9 (TLR9) signaling on newborn babies with acute lung injury (ALI) and the mechanism of TLR9 in vivo, so as to provide experimental basis for clinical treatment of newborn babies with ALI. Firstly, the expression of TLR9 in peripheral blood mononuclear cell (PBMC) was compared among ALI and healthy newborn babies. Then, PBMCs of newborn babies with ALI were extracted and divided into three groups. They were added with non-methylated cytosine purine-guanine dinucleotide sequence oligodeoxyribonucleotide (CpG ODN), ODN without non-methylated CpG, and blank nutrient solution, respectively, so as to determine the proliferation changes of PBMC. The immunohistochemistry (IHC) method was applied to detect the protein expression of TLR9-myeloid differentiation factor 88 (MyD88) signaling in lung tissue, and the number of T cell subsets (CD3+, CD4+, and CD8+) was detected by flow cytometry. Besides, enzyme-linked immunosorbent assay (ELISA) was employed to determine the concentration of interferon-α (INF-α) and INF-γ. The results revealed a neglectable difference in TLR9 expression in PBMCs among ALI and healthy newborn babies (P>0.05). Additionally, the proliferation number of PBMC cultured in CpG ODN group was greatly superior to the number of ODN and blank groups (P<0.05), and the INF-α and INF-γ of CpG ODN group increased obviously versus those of blank and ODN groups (P<0.05). In conclusion, TLR9 in PBMCs was present in both ALI and healthy newborn babies. CpG ODN could specifically recognize the TLR9 signaling, so as to activate the immune function of T lymphocyte subsets in newborn babies with ALI and promote the release of inflammatory factors from the neonatal patient's immune cells, thereby mediating the immune response of neonatal patients.