Molecular mechanisms and pathological features of p-Cresyl sulfate (PCS)-induced uremic lung injury (ULI) in chronic kidney disease (CKD) remain unclear. We analyzed pleural effusions (PE) from CKD and non-CKD patients for uremic toxins, reactive oxygen species (ROS), and chemotactic cytokines. Correlations between PE biomarkers and serum creatinine were also studied. Cell viability and inflammatory signaling pathways were investigated in PCS-treated human alveolar cell model. To mimic human diseases, CKD-ULI mouse model was developed with quantitative comparison of immunostaining and morphometric approach. PE from CKD patients enhance expressions of uremic toxins, hydroxyl radicals, and IL-5/IL-6/IL-8/IL-10/IL-13/ENA-78/GRO α/MDC/thrombopoietin/VEGF. PE concentrations of ENA-78/VEGF/IL-8/MDC/PCS/indoxyl sulphate correlate with serum creatinine concentrations. In vitro, PCS promotes alveolar cell death, cPLA2/COX-2/aquaporin-4 expression, and NADPH oxidase/mitochondria activation-related ROS. Intracellular ROS is abrogated by non-specific ROS scavenger N-acetyl cysteine (NAC), inhibitors of NADPH oxidase and mitochondria-targeted superoxide scavenger. However, only NAC protects against PCS-induced cell death. In vivo, expressions of cPLA2/COX2/8-OHdG, resident alveolar macrophages, recruited leukocytes, alveolar space, interstitial edema and capillary leakage increase in lung tissues of CKD-ULI mice, and NAC pretreatment ameliorates alveolar–capillary injury. PCS causes alveolar–capillary injury through triggering intracellular ROS, downstream prostaglandin pathways, cell death, and activating leukocytes to release multiplex chemoattractants and extracellular ROS. Thus PCS and nonspecific ROS serve as potential therapeutic targets.

MDRAB with biofilm-formation presented significantly higher desiccation and ethanol resistances than their planktonic type. Moreover, the 2% CHG in 70% ethanol agent provided a superior antiseptic efficacy for MDRAB-Bs than that of the 70% ethanol agent.

A 50-year-old Taiwanese woman had a history of massive hemoptysis occurring every 6 months for the past 4 years. After each bout of hemoptysis, chest roentgenography would show diffuse alveolar infiltration of bilateral lungs, which would usually resolve within 7 days. Transbronchial biopsy revealed diffuse alveolar hemorrhage and hemosiderin-laden macrophage infiltration. Idiopathic pulmonary hemosiderosis was diagnosed by excluding other glomerular, cardiac and immunological disorders. An initial dose of 20 mg prednisolone daily was tapered to 10 mg daily 1 month later. The patient is currently undergoing steroid therapy, and there have been no further episodes of hemoptysis.

Lung injury caused by acid aspiration provoked secondary MDRAB pneumonia; also synergistic effects between acid aspiration and Ab396 infection resulted in a detrimental outcome in the infected mice.

TB patients with prior exposure to FQs had more favourable outcomes compared with patients who had prior exposure to third-generation cephalosporins or third-generation penicillins. This study provides new insights into the impact of previous exposure to FQs on the survival of TB patients.