Electronic Journal of Biotechnology

Analysis of drug resistance, virulence phenotype, and genetic sequences in microevolutionary strains of Pseudomonas aeruginosa MPAO1

2026-09-08T15:42:01+00:00

Background: The Pseudomonas aeruginosa PAO1 strain is a foundation of research on bacterial virulence and antibiotic resistance. However, its tendency for microevolution during laboratory culture can lead to genetic and phenotypic divergence, potentially compromising experimental reproducibility. This study aimed to systematically characterize such variations in laboratory-maintained MPAO1 sublines to assess their genetic stability and suitability for research.

Results: We identified two distinct MPAO1 sublines (MPAO1-P and MPAO1-M) with divergent phenotypes. MPAO1-M exhibited markedly increased antimicrobial susceptibility to multiple antibiotics, including ciprofloxacin, imipenem, gentamicin and chloramphenicol, while concurrently displaying enhanced production of key virulence factors, including pyocyanin, rhamnolipids, elastase, and twitching motility. Whole-genome resequencing uncovered a novel missense mutation in the mexT gene of MPAO1-M. Consistent with this finding, quantitative reverse transcription PCR analysis revealed a significant downregulation of the mexEF-oprN efflux pump operon and a marked upregulation of the quorum-sensing genes rhlI and pqsA.

Conclusions: Our findings confirm the critical impact of microevolution on MPAO1 genotype and phenotype, underscoring the necessity of strain verification in experimental design. We further identify a novel mexT mutation as a potential mechanistic driver of these changes, providing new insights into the genetic basis of adaptive evolution in laboratory P. aeruginosa strains.

Optimization of one-step enzymatic hydrolysis conditions for two large brown algae and analysis of the antioxidant activity of the hydrolysis products

2026-09-08T19:11:48+00:00

Background: The industrial production of alginate lyase provides high-quality tool enzymes for the enzymatic hydrolysis of large brown algae. Establishing a seaweed enzymatic hydrolysis process that is simple to operate while offering both high enzymatic hydrolysis efficiency and a high yield of oligosaccharides contributes to the high-value utilization of large brown algae.

Results: A one-step enzymatic hydrolysis process combining alginate lyase, pectinase and cellulase was adopted to conduct enzymatic hydrolysis experiments on Sargassum horneri and Saccharina japonica, respectively. The Box-Behnken experimental design was applied to optimize the dosage of the three enzymes, as well as the temperature, pH and reaction time of enzymatic hydrolysis. The results showed that the optimal enzymatic hydrolysis conditions for S. horneri were as follows: alginate lyase 490 U/g, pectinase 4660 U/g, cellulase 380 U/g, hydrolysis temperature 47°C, hydrolysis pH 5.5 and hydrolysis time 8 h. For S. japonica, the optimal enzymatic hydrolysis conditions were alginate lyase 360 U/g, pectinase 5000 U/g, cellulase 284 U/g, hydrolysis temperature 49.5°C, hydrolysis pH 5.2 and hydrolysis time 8.8 h. After process optimization, the solid hydrolysis rates of S. horneri powder and S. japonica powder were increased to 71.4% and 66.3%, respectively, and the proportion of low-molecular-weight alginate oligosaccharides (DP < 6) in the hydrolysates reached approximately 70%; both enzymatic hydrolysates exhibited favorable antioxidant activity according to the detection.

Conclusions: The findings of this study greatly simplify the technological process for preparing alginate oligosaccharides via brown algae enzymatic hydrolysis and significantly improve the production efficiency.

Exploration of OLFM4 as a biomarker for infantile pneumonia and underlying mechanisms via bioinformatics, machine learning algorithms, and LPS-induced models

2026-09-15T11:47:44+00:00

Background: Infantile pneumonia is a common health concern worldwide, with elevated morbidity and mortality rates among affected children. This study aims to identify key genes associated with infantile pneumonia using bioinformatics and unravel the underlying mechanisms.

Results: OLFM4 was the only biomarker identified for infantile pneumonia. Besides, OLFM4 expression was promoted in the serum of infantile pneumonia patients, and LPS-stimulated cells and mouse models. OLFM4 knockdown repressed cell apoptosis, levels of TNF-α, IL-6, IL-1β, MPO, MDA, ROS, and activation of the NF-κB pathway, and facilitated the SOD level in LPS-induced models. OLFM4 knockdown alleviated the lung injury of the LPS-induced mouse model.

Conclusions: OLFM4 knockdown alleviated cell apoptosis, inflammatory response, and oxidative stress via the NF-κB signaling pathway in LPS-induced WI-38 cells and mouse model. The findings suggest that OLFM4 may pave the way for the treatment of infantile pneumonia.

Molecular targets and mechanisms of resveratrol in alleviating arrhythmia based on network pharmacology and bioinformatics

2026-09-15T11:57:27+00:00

Background: Arrhythmia refers to a disorder in which abnormal cardiac electrical activity leads to irregular heart rhythm and conduction. Resveratrol (Res), a natural polyphenol compound extracted from medicinal plants, plays an important role in the treatment of arrhythmia, but its precise molecular mechanisms remain unclear.

Results: The intersection of Res targets and arrhythmia yielded 78 common targets, including F-box protein 32 (FBXO32). These targets were significantly enriched in cardiac conduction system development, protein-containing complex, vascular endothelial growth factor (VEGF) signaling pathway, cyclic adenosine monophosphate (cAMP) signaling pathway, and forkhead box O (FoxO) signaling pathway. Molecular docking confirmed that FBXO32 could stably bind to Res. Res treatment increased cell viability in the arrhythmia cell model. FBXO32 was highly expressed in the arrhythmia cell model, but its expression was significantly reduced under Res treatment. Knockdown of FBXO32 increased cell viability, decreased apoptosis, and increased protein levels of calcium voltage-gated channel subunit alpha1 C (CACNA1C) and human ether-à-go-go-related gene (hERG), whereas Res treatment partially modulated these effects.

Conclusions: Res inhibits the expression of FBXO32, thereby suppressing the malignant phenotypes of arrhythmia.

IGF2BP3 promotes diabetic retinopathy development by enhancing SEMA3G mRNA stability

2026-09-15T12:42:14+00:00

Background: Diabetic retinopathy is characterized by excessive microvascular proliferation that leads to vitreous hemorrhage, retinal traction, and subsequent visual impairment. Aberrant expression of IGF2BP3 is involved in the pathogenesis of multiple diseases. This study aimed to elucidate the mechanism by which IGF2BP3 mediates diabetic retinopathy by regulating semaphorin-3G (SEMA3G) expression.

Results: Elevated IGF2BP3 expression was observed in diabetic retinopathy. In vitro, IGF2BP3 overexpression promoted pathological angiogenesis, whereas its knockdown significantly attenuated wound healing, reduced inflammatory cytokine secretion, and suppressed cellular proliferation. A targeted regulatory relationship between IGF2BP3 and SEMA3G mRNA was identified, with IGF2BP3 enhancing SEMA3G mRNA stability. SEMA3G was upregulated in diabetic retinopathy, and its overexpression partially rescued the diabetic retinopathy progression suppressed by IGF2BP3 silencing. In vivo, IGF2BP3 overexpression aggravated histopathological alterations, thereby accelerating diabetic retinopathy development.

Conclusions: In summary, IGF2BP3 promotes diabetic retinopathy development by enhancing SEMA3G mRNA stability.

Oxidative stress gene signature associated with vitiligo: A multi-algorithm machine learning and Mendelian randomization validation

2026-09-15T12:53:26+00:00

Background: Vitiligo is a common depigmentation disorder that affects approximately 1–2% of the global population. Oxidative stress plays a crucial role in its pathogenesis, yet systematic identification of oxidative stress-related biomarkers remains limited. This study aimed to identify and validate oxidative stress-related biomarkers for vitiligo and to construct a risk prediction model using bioinformatics, machine learning, and Mendelian randomization approaches.

Results: Through integration of high-throughput sequencing data, 1,581 differentially expressed genes were identified, of which 42 intersected with known oxidative stress-related genes. Three machine learning algorithms converged on five candidate genes. Real-time polymerase chain reaction validation in paired vitiligo lesional and non-lesional skin tissues confirmed the significant upregulation of ATOX1, STAT1, and PDCD10 and downregulation of FXN (p < 0.05). A risk prediction nomogram based on these four genes achieved high accuracy in the training dataset (area under the curve = 1.00) and an independent validation dataset (area under the curve = 0.93). PDCD10 demonstrated the strongest individual discriminatory performance (area under the curve = 0.820) in external validation. Mendelian randomization analysis indicated that ATOX1, STAT1, and PDCD10 had odds ratios greater than 1, suggesting a potential trend toward increased vitiligo risk, although the associations did not reach statistical significance.

Conclusions: This study identified ATOX1, STAT1, FXN, and PDCD10 as oxidative stress-related biomarkers for vitiligo. The four-gene risk prediction model demonstrated promising accuracy, with potential implications for early detection and personalized treatment strategies, pending further validation in larger cohorts.

Estrogen attenuates colonic mucinous adenocarcinoma growth in a rat model by inhibiting proliferation and promoting apoptosis

2026-09-15T13:05:41+00:00

Background: Colonic mucinous adenocarcinoma is a highly aggressive subtype of colon cancer. Epidemiological evidence has linked estrogen exposure to certain gastrointestinal malignancies, yet its pathophysiological role in the pathogenesis of colonic mucinous adenocarcinoma remains unclear. This study aimed to investigate the effect of estrogen on tumor growth in a rat model of colonic mucinous adenocarcinoma and its association with intestinal mucosal epithelial proliferation-related factors and apoptosis.

Results: Compared with the normal control group, the model control group showed significantly increased tumor proliferative activity and elevated intestinal epithelial apoptosis. After estrogen intervention, tumor volume and proliferative activity were inhibited, the expressions of Ki-67 and proliferating cell nuclear antigen were downregulated, and the apoptosis rate of intestinal epithelial cells decreased; an estrogen antagonist could enhance some of the above effects.

Conclusions: Estrogen can slow the growth of colonic mucinous adenocarcinoma by inhibiting intestinal mucosal epithelial proliferation, exhibiting potential anti-tumor effects. Its mechanism may be related to regulating the proliferation-apoptosis balance of intestinal mucosal epithelium, providing experimental evidence for colon cancer therapy research.