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Staphylococcus aureus (S. aureus) is associated with recalcitrant chronic infection, especially in chronic rhinosinusitis (CRS). S. aureus infection and biofilms cause poorer postsurgical outcomes. We developed isosorbide mononitrate (ISMN) loaded nanoparticles conjugated with an anti-Staphylococcus aureus alpha-toxin (anti-S. aureus α-toxin) antibody that could target biofilms and investigated their anti-biofilm effect. Anti-S. aureus α-toxin antibody coupled immunoliposomes were generated. The effect of ISMN immunoliposomes on S. aureus biofilm formation and their anti-biofilm efficacy were examined using the crystal violet method and confocal laser scanning microscopy, respectively. Relative biofilm viability at 24 h was tested using the alamarBlue assay. The biofilm formation inhibitory effect on all concentrations of ISMN immunoliposomes was stronger than that of ISMN liposomes and free ISMN (P<0.05). At concentrations of 45 and 23 mg/ml, the inhibitory effect of ISMN liposomes was stronger than that of free ISMN (P<0.05), while at 11 mg/ml, the inhibitory effect of ISMN liposomes was the same as that of ISMN (P>0.05). At 45 and 23 mg/ml, the inhibitory effect of ISMN immunoliposomes on formed biofilms was greater than that of ISMN liposomes and free ISMN (P<0.05) and the inhibitory effect of ISMN liposomes was stronger than that of free ISMN (P<0.05). At 11 mg/ml, ISMN immunoliposomes, ISMN liposomes, and ISMN had the same effect on formed biofilms (P>0.05). In conclusion, ISMN immunoliposomes nearly completely destroy biofilm structure. ISMN immunoliposomes provide a promising approach for treating infectious diseases caused by S. aureus biofilms, including refractory CRS, chronic skin infection, sepsis, and osteomyelitis. [ABSTRACT FROM AUTHOR]

The current study aimed to determine the expression of carnitine palmitoyltransferase 1A (Cpt1a) in the lung tissue of chronic obstructive pulmonary disease (COPD) patients and its correlation with lung function. An increase in Cpt1a expression improved lung function in patients with COPD by inhibiting apoptosis and the inflammatory response of lung endothelial cells. Lung tissues of 20 patients with COPD and 10 control patients were collected, their Cpt1a expression was determined by western blotting and apoptosis and inflammation were assessed by haematoxylin-eosin staining, TUNEL assay and ELISA. Mice with knockout or overexpression of Cpt1a were constructed by lentivirus in vivo. A COPD model was induced by cigarette smoke and the role of Cpt1a in COPD was determined in vivo and in vitro. Cpt1a expression was positively correlated with lung function and negatively correlated with apoptosis and inflammation. Patients with COPD with higher expression of Cpt1a in lung tissues had improved lung function indices and lung tissue morphology with less apoptosis and decreased inflammatory response. Compared with the control group, COPD mice with Cpt1a knockdown had aggravated lung dysfunction and increased lung inflammation and apoptosis. Overexpression of Cpt1a alleviated lung dysfunction and reduced inflammatory response and apoptosis of lung tissues in COPD mice. Pulmonary microvascular endothelial cells of mice were isolated in vitro and the results were consistent with the findings obtained in vivo. In conclusion, the clinical, in vivo and in vitro data confirmed for the first time that Cpt1a alleviated lung dysfunction of patients with COPD by inhibiting apoptosis of endothelial cells and inflammatory responses. [ABSTRACT FROM AUTHOR]