To investigate the effect and mechanism of polydatin on bleomycin (BLM)‐induced pulmonary fibrosis in a mouse model. The lung fibrosis model was induced by BLM. The contents of TNF‐α, LPS, IL‐6 and IL‐1β in lung tissue, intestine and serum were detected by ELISA. Gut microbiota diversity was detected by 16S rDNA sequencing; R language was used to analyse species composition, α‐diversity, β‐diversity, species differences and marker species. Mice were fed drinking water mixed with four antibiotics (ampicillin, neomycin, metronidazole, vancomycin; antibiotics, ABx) to build a mouse model of ABx‐induced bacterial depletion; and faecal microbiota from different groups were transplanted into BLM‐treated or untreated ABx mice. The histopathological changes and collagen I and α‐SMA expression were determined. Polydatin effectively reduced the degree of fibrosis in a BLM‐induced pulmonary fibrosis mouse model; BLM and/or polydatin affected the abundance of the dominant gut microbiota in mice. Moreover, faecal microbiota transplantation (FMT) from polydatin‐treated BLM mice effectively alleviated lung fibrosis in BLM‐treated ABx mice compared with FMT from BLM mice. Polydatin can reduce fibrosis and inflammation in a BLM‐induced mouse pulmonary fibrosis model. The alteration of gut microbiota by polydatin may be involved in the therapeutic effect.

Adult-onset Still’s disease (AOSD) is a rare systemic autoinflammatory disorder without universally accepted disease-specific biomarkers, although serum ferritin and glycosylated ferritin may provide supportive diagnostic value. Therefore, diagnosis relies on a combination of clinical manifestations, laboratory abnormalities, and exclusion of alternative diagnoses, commonly using criteria such as Yamaguchi or Fautrel. Although serosal involvement has been reported, presentation with massive hemorrhagic pericardial effusion in the absence of the characteristic rash is extremely rare and may mimic tuberculosis, malignancy, or other rheumatic diseases. We report a 67-year-old Asian man who was referred to our department from a local hospital because of persistent cough, fever, and polyserositis predominantly characterized by massive hemorrhagic pericardial effusion. Laboratory evaluation revealed marked systemic inflammation, elevated ferritin levels, a positive interferon-gamma release assay, elevated adenosine deaminase in pericardial fluid, increased tumor markers, and anti-SAE1 positivity, initially raising suspicion for tuberculous pericarditis, malignancy, or autoimmune myopathy. However, comprehensive microbiological, cytological, imaging, and neuromuscular assessments found no evidence supporting these conditions, and the patient did not develop the typical evanescent rash of AOSD. After initiation of diagnostic glucocorticoid therapy, rapid defervescence and marked resolution of serous effusions were observed, supporting the diagnosis. This case highlights an atypical presentation of AOSD and emphasizes that AOSD should be considered in patients with unexplained serositis, particularly hemorrhagic pericardial effusion accompanied by systemic inflammation.