Effects of adjuvant pidotimod therapy on levels of inflammatory factors and expressions of serum GM-CSF and KL-6 in elderly patients with mycoplasma pneumonia.

OBJECTIVE: To observe the intervention effects of adjuvant pidotimod therapy on the serum inflammatory factor and GM-CSF and KL-6 expression levels in elderly mycoplasma pneumonia patients. METHODS: Elderly patients (n=104) diagnosed with mycoplasma pneumonia were divided into a control group (52 cases, given conventional anti-infective therapy combined with ambroxol) and a research group (52 cases, given conventional anti-infective therapy combined with ambroxol + pidotimod) according to the different treatment methods each patient was administered. The pulmonary function indexes (FVC, FEV1, FEV1/FVC), the serum inflammatory factor levels (interleukin (IL)-6, IL-8, the tumor necrosis factor α), the serum granulocyte-macrophage colony-stimulating factor (GM-CSF), and the Krebs von den Lungen-6 (KL-6) expression levels were measured before and after the treatment. The cough stopping times, the rale disappearance times, the hospital stay durations, the overall response rates, the incidences of adverse reactions during the administration, and the recurrence rates at 3, 6, and 12 months after the treatment were recorded. RESULTS: The research group had shorter cough stopping times, rale disappearance times, and hospital stays than the control group (all P<0.05). After the treatment, the FVC, FVE1, and FVE1/FVC levels in both groups were increased, and the research group had higher levels than the control group (all P<0.05). After the treatment, the serum tumor necrosis factor α, IL-6, IL-8, GM-CSF, and KL-6 levels in the two groups were significantly decreased, and the levels of these indicators in the research group were significantly lower than they were in the control group (all P<0.05). The total overall treatment response rate was higher, and the recurrence rate at 12 months after the treatment was significantly lower in the research group than they were in the control group (P<0.05). CONCLUSION: Adjuvant pidotimod therapy in the treatment of elderly patients with mycoplasma pneumonia can ameliorate patients' inflammatory responses and pulmonary functions, and reduce the serum GM-CSF and KL-6 factor levels, as well as the recurrence rate. Moreover, the combined medication is safe, and no significant increase in toxicity was found.

let7f­5p attenuates inflammatory injury in in vitro pneumonia models by targeting MAPK6.

Pneumonia accounts for ~1.3 million mortalities in children per year worldwide. MicroRNAs are implicated in several diseases, including cancer and pneumonia; however, the role of let7f­5p in pneumonia is not completely understood. In the present study, lipopolysaccharide (LPS) was used to establish an in vitro pneumonia model in A549 and WI­38 cells. The reverse transcription­quantitative PCR (RT­qPCR) and western blotting results demonstrated that let7f­5p expression levels were significantly decreased, whereas MAPK6 expression levels were significantly increased in the peripheral venous blood of patients with pneumonia and in LPS­induced A549 and WI­38 cells compared with healthy volunteers and control cells, respectively. Furthermore, the dual­luciferase reporter assay demonstrated that let7f­5p targeted the 3'­untranslated region of MAPK6. The ELISA and RT­qPCR results demonstrated that let7f­5p mimic ameliorated LPS­induced inflammatory injury in A549 and WI­38 cells, as demonstrated by decreased expression levels of proinflammatory cytokines, including TNF­α and IL­6. In addition, the Cell Counting Kit­8 assay results indicated that let7f­5p mimic ameliorated LPS­induced reductions in cell viability, and the western blotting results demonstrated that let7f­5p mimic reversed LPS­induced activation of the STAT3 signaling pathway. Notably, the aforementioned let7f­5p­mediated effects were reversed by MAPK6 overexpression. Collectively, the results of the present study suggested that let7f­5p inhibited inflammation by targeting MAPK6 in the in vitro pneumonia model, thus let7f­5p may serve as a potential novel therapeutic target for pneumonia.