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Effect of Sulfamethoxazole(SMZ), Trimethoprim (TMP) and Co-trimoxazole (CTX) on gene expression of human placental BeWo cell lines

ABSTRACT: Cell–cell junctions, including tight and adherens junctions, are critical for maintaining placental barrier integrity and ensuring proper maternal–fetal exchange. To investigate the impact of co-trimoxazole (CTX) as well as sulfamethoxazole (SMA) and trimethoprim (TMP) on these junctional networks, RNA sequencing was performed on BeWo placental cells exposed to non-cytotoxic concentrations of these three antibiotics for 24 h. Transcriptomic profiling revealed significant differential gene expression in sulfamethoxazole, trimethoprim and co-trimoxazole-treated cells compared to controls, with enrichment of ERK pathway that might be related to tight junctions, adherens junctions, and cell–cell adhesion. These alterations suggested disruption of placental barrier integrity. In addition, co-trimoxazole exposure was associated with activation of the ERK1/2 signaling cascade, reflected by downregulation of multiple dual-specificity phosphatase (DUSP) genes that normally suppress MAPK activity. Together, the RNA-seq findings indicate that CTX interferes with barrier-related gene networks and promotes ERK pathway activation, supporting its potential to compromise placental barrier function.

ORGANISM(S): Homo sapiens

PROVIDER: GSE307654 | GEO | 2025/10/01

REPOSITORIES: GEO

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Project description:The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. Transcriptome analysis revealed a global down-regulation of physiological AJC gene expression in the SAE of healthy smokers (n=53) compared to healthy nonsmokers (n=59), an observation associated with changes in molecular pathways regulating epithelial differentiation such as PTEN signaling and accompanied by induction of cancer-related AJC genes. Genome-wide co-expression analysis identified a smoking-sensitive AJC transcriptional network. The overall expression of AJC-associated genes was further decreased in COPD smokers (n=23). Exposure of human airway epithelial cells to cigarette smoke extract in vitro resulted in down-regulation of several AJC-related genes, accompanied by decreased transepithelial resistance. Thus, cigarette smoking alters the AJC gene expression architecture in the human airway epithelium, providing a molecular basis for the dysregulation of airway epithelial barrier function during the development of smoking-induced lung disease. The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. In this study, microarray analysis of the SAE obtained from 53 healthy nonsmokers, 59 healthy smokers, and 23 smokers with COPD was performed to determine physiological AJC gene expression architecture in the SAE and its modification by cigarette smoking and during the development of COPD.

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Effect of Sulfamethoxazole(SMZ), Trimethoprim (TMP) and Co-trimoxazole (CTX) on gene expression of human placental BeWo cell lines

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