Correlation between Drug Resistance of Klebsiella Pneumonia and Antimicrobial Drug Usage.

Objective. To assess the correlation between the drug resistance of Klebsiella pneumoniae and antimicrobial drug usage. Methods. The drug resistance rate of Klebsiella pneumoniae and the antimicrobial drug dosage of inpatients admitted to The Second Affiliated Hospital of Wannan Medical College from January 2016 to December 2020 were retrospectively recorded, and their correlation was analyzed using the Pearson method. Results. There are 6493 strains of Gram-negative bacteria, including 1272 strains of Klebsiella pneumoniae, ranking first in respiratory medicine. Klebsiella pneumoniae showed an overall increasing trend in resistance to piperacillin/tazobactam and ampicillin/sulbactam and a high resistance to aztreonam, ceftazidime, and ciprofloxacin (all P < 0.05). The top 3 antimicrobial drugs used in 2016-2020 were ß-lactams, quinolones, and macrolides. The rates of resistance to piperacillin/tazobactam, cefoperazone/sulbactam, and ampicillin/sulbactam were highly positively correlated with the use of ß-lactams. The use of carbapenems and glycopeptides was negatively correlated with the resistance to ciprofloxacin, and the resistance to ceftazidime had a high positive correlation with the use of glycopeptides and carbapenems. Conclusion. The use of antimicrobial drugs is correlated with the resistance rate of Klebsiella pneumoniae. To reduce bacterial drug resistance, the rational use of antimicrobial drugs requires joint control through multiple departments to improve the clinical use of antimicrobial drugs and improve in-hospital control.

α-Mangostin Treats Early-Stage Adjuvant-Induced Arthritis of Rat by Regulating the CAP-SIRT1 Pathway in Macrophages.

BACKGROUND: Studies have found that α-mangostin (MG) can relieve experimental arthritis by activating cholinergic anti-inflammatory pathway (CAP). It affects the polarization of macrophages and the balance of related immune cell subpopulations, but the specific mechanism is still unclear. It has been found that silent information regulator 1 (SIRT1) is closely related to macrophage activity. The purpose of this study is to explore the mechanism of MG intervening in macrophage polarization during treatment of early adjuvant-induced (AIA) rats through the CAP-SIRT1 pathway. METHODS: We investigated the polarization of M1 macrophages and the differentiation of Th1 in AIA rats by flow cytometry. Activity of acetylcholinesterase (AChE) and the level of nicotinic adenine dinucleotide (NAD+) in serum were also detected, and immunohistochemical was used to detect the levels of α7 nicotinic cholinergic receptor (α7nAChR) and SIRT1. Then in macrophages, the molecular mechanism of MG regulating the abnormal activation of macrophages in rats with early AIA through the CAP-SIRT1 pathway was studied. RESULTS: MG can significantly inhibit the polarization of M1 macrophages and the differentiation of Th1 in AIA rats in the acute phase of inflammation. MG can significantly inhibit the activity of AChE and increase the level of NAD+, thereby further up-regulated the expression levels of α7nAChR and SIRT1. Meanwhile, MG inhibited nuclear factor-κB (NF-κB)-mediated inflammation by activating the CAP-SIRT1 pathway in macrophages. CONCLUSION: In summary, the stimulation of MG induced CAP activation, which up-regulated SIRT1 signal, and thereby inhibited M1 polarization through the NF-κB pathway, and improved the pathological immune environment of early-stage AIA rats.