Objective To investigate the effect of non-coding RNA activated by DNA damage (NORAD) on acute lung injury (ALI) in septic rats by regulating the miR-155-5p/TLR6 molecular axis. Methods The rats were randomly divided into control group, model group, low NORAD expression no-load group (LV-sh-NC), low NORAD expression group (LV-sh-NORAD), low NORAD expression +miR-155-5p low expression no-load group (LV-sh-NORAD+NC antagomir), NORAD low expression +miR-155-5p low expression group (LV-sh-NORAD+miR-155-5p antagomir). ELISA kits were applied to detect interleukin (IL)-8, IL-1β, and tumor necrosis factor-α (TNF-α) levels; quantitative real-time polymerase chain reaction was applied to detect the expression of NORAD, miR-155-5p, and Toll-like receptor 6 (TLR6) genes in lung tissue of rats in each group. The ratio of wet weight to dry weight (W/D) of lung tissue was measured. The pathological changes of lung tissue were observed by hematoxylin-eosin staining, and apoptosis in lung tissue cells was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling. Western blot was applied to detect the expressions of TLR6, Bax, Bcl-2, and cleaved cysteinyl aspartate specific proteinase 3 caspase-3) proteins in cells. Dual luciferase reporter gene experiment was applied to verify the relationship between miR-155-5p and NORAD and TLR6. Results Compared with the control group, the lung tissue of rats in the model group and LV-sh-NC group was obviously damaged, the levels of serum IL-1β, TNF-α, IL-8, expression of NORAD and TLR6 mRNA in lung tissue, W/D ratio, apoptosis rate, expression of TLR6, Bax, and Cleaved-caspase-3 proteins were obviously increased, the expression of miR-155-5p and Bcl-2 proteins in lung tissue was obviously reduced (P<0.05). Down-regulation of NORAD expression could reduce lung tissue injury, serum IL-1β, TNF-α, IL-8 levels, mRNA expression of NORAD and TLR6 in lung tissue, W/D ratio, apoptosis rate, TLR6, Bax, Cleaved caspase-3 protein expression, and cleaved caspase-3 protein expression. The expression of miR-155-5p and Bcl-2 protein in lung tissue were significantly increased (P<0.05). Down-regulating the expression of miR-155-5p could reduce the improvement effect of negatively regulated NORAD on sepsis ALI rats (P<0.05). Conclusion Interference with NORAD can alleviate lung injury in ALI rats by regulating the miR-155-5p/TLR6 molecular axis.
ObjectiveTo investigate the clinical characteristics of severe Chlamydia abortus pneumonia complicated by acute respiratory distress syndrome (ARDS). MethodsSix cases of severe Chlamydia abortus pneumonia with ARDS admitted to the Department of Critical Care Medicine, Quanzhou First Hospital Affiliated to Fujian Medical University, from January 2021 to June 2025 were enrolled. The clinical features were analyzed based on demographic data, laboratory tests, imaging findings, and other clinical information. ResultsAll six patients were diagnosed via metagenomic next-generation sequencing (mNGS). The median age was 63.5 years (range, 42~73), and four patients had a history of exposure to poultry or animals. Initial symptoms were nonspecific, including fever and cough. All patients developed high fever and dyspnea, with a peak body temperature of 39.7°C (range, 39.2~41.1°C). The median time from symptom onset to dyspnea was 2 days (range, 1~3). Four patients presented with extrapulmonary symptoms. Elevated white blood cell count was observed in three patients; all six patients had an increased neutrophil percentage and a decreased lymphocyte percentage. Three patients had mild anemia and mild thrombocytopenia. All six patients showed markedly elevated procalcitonin, interleukin-6, and C-reactive protein. Elevated liver enzymes and creatine kinase levels were observed in all six patients to varying degrees. Four patients had mild hyponatremia, two had hypokalemia, and five had varying degrees of elevated serum creatinine. Chest CT findings included consolidation involving single or multiple lobes, with or without small pleural effusions. All patients met the diagnostic criteria for severe ARDS and received invasive mechanical ventilation via endotracheal intubation as well as prone positioning. After targeted therapy, five patients improved markedly, whereas one female patient died of secondary infection. ConclusionsSevere community-acquired pneumonia caused by Chlamydia abortus can lead to ARDS and/or multiorgan involvement. In patients with severe pneumonia and a history of exposure to sick poultry or aborted animals, Chlamydia abortus infection should be considered. mNGS plays a critical role in early diagnosis and the transition to targeted therapy. Appropriate antimicrobial therapy combined with rational respiratory support strategies may contribute to favorable patient outcomes.