Detection of trichomonads in patients with lung cancer and transcription analysis on the response of human pulmonary epithelial cells to Trichomonas tenax invasion.

INTRODUCTION: Lung cancer is one of the most prevalent malignancies worldwide. Substantial research has illuminated the intricate interplay between microorganisms and human health, revealing their role in disease regulation. Trichomonads is a flagellated protozoan in the human cavity and have been previously identified as a pathogen associated with pneumonia, contributing to tissue chronic inflammation and carcinogenesis. METHODS: Nested polymerase chain reaction methods were employed to scrutinize the prevalence of trichomonads in the bronchovesicular fluid of patients diagnosed with lung cancer. Subsequently, the influence of Trichomonas tenax invasion on lung cancer cells was elucidated through proliferation assays, migration assays, and transcription analysis. RESULTS: Bronchoalveolar fluid samples from lung cancer patients yielded positive nested PCR results for eight out of twenty-seven samples. Seven of these samples were identified as Trichomonas tenax, while one was identified as Tetratrichomonas spp. Our findings revealed a significant upregulation of pathways associated with carcinogenesis, including cellular proliferation, migration, and drug resistance, in response to T. tenax invasion. CONCLUSIONS: This study underscores the importance of recognizing the presence of trichomonads and the influence of T. tenax invasion on host responses to respiratory diseases. The identified pathways implicated in cancer development may pave the way for developing targeted treatment strategies for pulmonary diseases. These findings hold promise for informing and improving the precision of therapeutic interventions in the context of pulmonary ailments.

Trichomonas tenax induces barrier defects and modulates the inflammatory cytotoxicity of gingival and pulmonary epithelial cells.

BACKGROUND: Trichomonas tenax is a single-cell flagellated anaerobic organism, commensal in the human oral cavity. Although a previous study indicated that T. tenax could cause cell damage and phagocytose host epithelial cells, its pathological effects on gum cells remain unknown. Furthermore, several case reports have detected T. tenax in several patients with empyema and/or pleural effusion, which may have been aspirated from the oral cavity. However, the cytotoxic effects and immune responses of alveolar cells are unknown. Therefore, we aimed to determine the cytotoxic and immune effects of T. tenax on gums and pulmonary cell lines. The cytopathic effect and lactate dehydrogenase (LDH) cytotoxicity assays were used to determine the level of cell damage in gum and lung epithelial cells. Western blot was used to determine the disruption of cell junctions. Finally, epithelial cell cytokines were measured using ELISA to elucidate the immune response to T. tenax. RESULTS: We found that T. tenax induced a cytotoxic effect on gum epithelial cells by disrupting cell junctions; however, it hardly triggered cellular damage in alveolar A549 cells and mucoepidermoid NCI-H292 cells. Furthermore, T. tenax induced the production of IL-6 at a low multiplicity of infection (MOI) in gum, A549, and NCI-H292 cells. CONCLUSIONS: Our results suggest that T. tenax can trigger gingival cell cytotoxicity, disrupt cell junctions, and induce IL-6 production in gingival and pulmonary cell lines.

Title: Trichomonas tenax induit des défauts de barrière et module la cytotoxicité inflammatoire des cellules épithéliales gingivales et pulmonaires. Abstract: Contexte : Trichomonas tenax est un organisme anaérobie unicellulaire flagellé, commensal dans la cavité buccale humaine. Bien qu'une étude précédente ait indiqué que T. tenax pouvait endommager les cellules et phagocyter les cellules épithéliales de l'hôte, ses effets pathogènes sur les cellules gingivales restent inconnus. En outre, plusieurs rapports ont détecté T. tenax chez des patients présentant un empyème et/ou un épanchement pleural, qui peut avoir été aspiré de la cavité buccale. Cependant, les effets cytotoxiques et les réponses immunitaires des cellules alvéolaires sont inconnus. Par conséquent, nous avons cherché à déterminer les effets cytotoxiques et immunitaires de T. tenax sur des lignées cellulaires de gencives et de poumons. Les tests d'effet cytopathique et de cytotoxicité de la lactate déshydrogénase (LDH) ont été utilisés pour déterminer le niveau de dommages cellulaires dans les cellules. Le Western Blot a été utilisé pour déterminer la perturbation des jonctions cellulaires. Enfin, les cytokines des cellules épithéliales ont été mesurées par ELISA pour élucider la réponse immunitaire à T. tenax. Résultats : Nous avons constaté que T. tenax induisait un effet cytotoxique sur les cellules épithéliales gingivales en perturbant les jonctions cellulaires. Cependant, T. tenax a déclenché des dommages cellulaires seulement mineurs dans les cellules alvéolaires A549 et les cellules mucoépidermoïdes NCI-H292. De plus, T. tenax a induit la production d'IL-6 à une faible multiplicité d'infection (MOI) dans les cellules de gencives, A549 et NCI-H292. Conclusions : Nos résultats suggèrent que T. tenax peut déclencher la cytotoxicité des cellules gingivales, perturber les jonctions cellulaires et induire la production d'IL-6 dans les lignées cellulaires gingivales et pulmonaires.

Potential role of Acanthamoeba Rab7.

Acanthamoeba castellanii is a free-living protozoan that causes several severe human parasitic diseases such as Acanthamoeba keratitis and granulomatous encephalitis. A. castellanii feeds on bacteria, yeasts, and other organic particles as food sources, but the mechanisms of digestion in acanthamoebal cells are unclear. Rab GTPases participate in endosomal delivery in eukaryotes after phagocytosis. This study aimed to determine the potential functions of A. castellanii Rab7 (AcRab7), which is involved in phagocytosis, and the relationship between AcRab7 and further cellular physiological phenomena. In this study, the inhibitor CID1067700 (CID) was used to specifically inhibit the binding of nucleotides to confirm the potential functions of AcRab7. Cellular proliferation and ATP assays were also used to detect underlying cellular physiological functions after blocking the phagocytosis pathway. We found that AcRab7 expression increased as the co-culture time with Escherichia coli increased. Immunofluorescence staining showed that AcRab7 colocalized with lysosomes in its GTP-activating form. In addition, AcRab7 inhibition resulted in a reduction in cell proliferation and ATP levels. Our results suggest that AcRab7 participates in endosomal delivery and dominates energy production and cell growth.