miR-143-3p impacts on pulmonary inflammatory factors and cell apoptosis in mice with mycoplasmal pneumonia by regulating TLR4/MyD88/NF-κB pathway

Abstract

<jats:title>Abstract</jats:title> <jats:p>miR-143-3p is correlated with inflammatory pain responses, such as hsa-miR-143-3p expression reduction in fibromyalgia. The present study aimed to explore the effects of miR-143-3p and Toll-like receptor (TLR) 4/myeloid differentiation factor 88 (MyD88)/NF-κB signaling pathway on pulmonary inflammatory factors levels and alveolar epithelial cell apoptosis in mycoplasmal pneumonia mice. Twenty mice were selected as normal group. The 120 successfully modeled Mycoplasma pneumoniae (MP) infection mice were randomly divided into model group (without any treatment), negative control (NC) group (injected with NC mimic), miR-143-3p mimic group (injected with miR-143-3p mimic), miR-143-3p inhibitor group (injected with miR-143-3p inhibitor), TAK-242 group (treatment with TAK-242), and miR-143-3p inhibitor + TAK-242 group (treatment with miR-143-3p inhibitor + TAK-242). Compared with model group, model mice had up-regulated miR-143-3p expression and decreased MyD88 and p-NF-κB p50 protein expressions (all P&amp;lt;0.05); Model mice treated with miR-143-3p mimic and TAK-242 had reduced interleukin (IL)-2 and tumor necrosis factor (TNF)-α contents and protein expressions of MyD88, p-NF-κB p50, increased IL-10 content, fewer alveolar epithelial cell apoptosis, lower Bax expression and higher Bcl-2 expression (all P&amp;lt;0.05); however, mice with miR-143-3p inhibitor treatment showed opposite trends in terms of above indicators. The exacerbation of mycoplasmal pneumonia caused by miR-143-3p inhibitor was partly improved by miR-143-3p inhibitor + TAK-242 combination treatment (all P&amp;lt;0.05). Therefore, up-regulation of miR-143-3p expression may ameliorate pulmonary inflammatory factors levels and reduce alveolar epithelial cell apoptosis in mycoplasmal pneumonia mice by inhibiting TLR4/MyD88/NF-κB signaling pathway.</jats:p>

Integrated Analysis of Transcriptome mRNA and miRNA Profiles Reveals Self-Protective Mechanism of Bovine MECs Induced by LPS

“…Correspondingly, the expression level of the mRNA p65 ( RELA ) was increased after LPS induction in bMECs ( Figure 9A ). Upregulation of miR-143-3p expression reduced TNFα, MyD88, p50, and alveolar epithelial cell apoptosis in mycoplasma pneumonia mice by inhibiting TLR4/MyD88/NF-κB axis ( 43 ). The bta-miR-143_1ss22GT is predicted to target OAS1Z ( Figure 6A ).…”

LncRNA UCA1 remits LPS‐engendered inflammatory damage through deactivation of miR‐499b‐5p/TLR4 axis

“…Activated NF‐κB deteriorates the inflammatory injury of lung by inhibiting apoptosis of macrophages, lymphocyte, neutrophils, and other inflammatory cells, which results in large production and secretion of pro‐inflammatory cytokines 26 . More importantly, NF‐κB signaling has been implicated in pneumonia 27 . Emerging lines of research attested that TLR4 involved in acute pneumonia 22,28 .…”

“…26 More importantly, NF-κB signaling has been implicated in pneumonia. 27 Emerging lines of research attested that TLR4 involved in acute pneumonia. 22,28 Thus, we next screened the possible interacted genes of miR-499b-5p via bioinformatics methods.…”

Panax quinquefolius L. Saponins Protect Myocardial Ischemia Reperfusion No-Reflow Through Inhibiting the Activation of NLRP3 Inflammasome via TLR4/MyD88/NF-κB Signaling Pathway

“…NLRP3 inflammasome is formed by MI/R, and its subsequent activation leads to the production of IL-1β and IL-18, leading to inflammatory reactions such as inflammatory cell infiltration, adhesion, and aggregation in the heart. TLR4/MyD88/NF-κB is a classic inflammatory signaling pathway ( Wang et al, 2020c ; Gao et al, 2020 ). During MI/R, the heart released endogenous danger signals and activated related signaling pathways represented by TLR4/MyD88/NF-κB via DAMP, and the TLR4/NF-kb/NLRP3 signaling pathway plays an important role in MI/R injury ( Zhang et al, 2017 ), but there is no evidence that the occurrence of NR phenomenon after reperfusion is related to it.…”