Heba M Abostate’s research while affiliated with Egyptian Russian University and other places

Introduction Chronic obstructive pulmonary disease (COPD) is a well-known respiratory illness, and COPD patients oscillate between a stable state and an exacerbated state. which can lead to disease deterioration. Studies suggest that respiratory microbiome dysbiosis plays a vital role in COPD exacerbation. However, the exact microbial composition among different clinical states of COPD is still elusive. Objectives To determine and compare the respiratory microbiome composition in different COPD clinical states, namely, the stable state (S-COPD) and the acute exacerbated state (AE-COPD). Methods In this study, 35 sputum samples were collected from COPD patients: S-COPD patients (n = 18), and AE-COPD patients (n = 17). The sputum microbiome was analyzed via 16S rRNA gene sequencing. Bioinformatics analysis was used to determine changes in the microbiota among the comparison groups. Results The most abundant phyla among all the samples were Proteobacteria, Fusobacteria, Firmicutes, and Actinobacteria, with Paracoccus, Streptomyces Leptotrichia Fusobacterium and Ruminococcaceae being the most prevalent genera.A dissimilarity in abundance across the studied COPD states was observed, with signi cantly greater abundance of Proteobacteria and Fusobacteria in S-COPD patients and greater abundance of Firmicutes in AE-COPD patients at the phylum level. Paracoccus, Fusobacterium, Streptococcus, Haemophilus and Moraxella were signi cantly different between the two groups and were more prevalent in S-COPD, whereas Cellulosilyticum, Streptomyces, Leptotrichia, Ruminococcaceae_UCG_014 and Atopobium were more prevalent in exacerbated individuals. Alpha diversity revealed greater diversity in stable versus exacerbated patients, and a PCoA plot of Bray-Curtis and weighted UniFrac distances revealed that stable patients were highly clustered, whereas exacerbated patients were more disseminated. At the genus level, LEfSe analysis revealed the dominance of Cellulosilytic, Liptotrichia and Streptomyces in the AE-COPD group, whereas the S-COPD group microbiome was dominated by the genera Paracoccus, Fusobacterium, Streptococcus Haemophilus and Moraxella (p < 0.05). Conclusion The results of the present study suggest that COPD patients have unique microbial pro les that differ across different states, with increased abundances of Proteobacteria, chie y Paracoccus. These ndings need more research to clarify the de nite role of microbiome dysbiosis in COPD pathogenesis.

Aim: Inhibition of some quorum sensing (QS) regulated virulence factors via using non-antibiotic helping drugs to overcome antibiotic resistance problem. Introduction: P. aeruginosa is one of the major causes of. P. aeruginosa's virulence factors are highly controlled by QS systems which lead to antibiotics resistance. Targeting QS may be a promising therapeutic hope for P. aeruginosa infections. Methods: Molecular Docking was performed using the required constraints in the binding sites of the Las & Rhl receptor proteins of P. aeruginosa to estimate the expected activity of (quercetin and meloxicam) and compare them with great docking scores compounds like rosmarinic acid. PAO1 was used as reference strain with other P. aeruginosa strains (clinical samples). An antibiotic sensitivity test was performed to evaluate antibiotic resistance. The minimum inhibitory concentration (MIC) of tested drugs were also measured against the resistant strains. Virulence factors thanked for QS (protease, pyocyanine, rhamnolipids) and biofilm formation of selected strains were assessed before and after treatment with quercetin & meloxicam. Results and conclusion: In silico studies indicated that quercetin and meloxicam could act as inhibitors for the auto-inducer molecules as they have a high affinity for the regulatory proteins of the QS system lasR and rhlR. The experimental study of quercetin and meloxicam against P. aeruginosa showed that at sub-MIC, both drugs reduced biofilm formation and some tested virulence factors. Treatment of P. aeruginosa infection using QS inhibitors is expected and this approach may overcome the antibiotic resistance problem.