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The gut microbiota is a complex community of microorganisms inhabiting the intestinal tract, which plays a vital role in human health. It is intricately involved in the metabolism, and it also affects diverse physiological processes. The gut–lung axis is a bidirectional pathway between the gastrointestinal tract and the lungs. Recent research has shown that the gut microbiome plays a crucial role in immune response regulation in the lungs and the development of lung diseases. In this review, we present the interrelated factors concerning gut microbiota and the associated metabolites in pulmonary hypertension (PH), a lethal disease characterized by elevated pulmonary vascular pressure and resistance. Our research team explored the role of gut‐microbiota‐derived metabolites in cardiovascular diseases and established the correlation between metabolites such as putrescine, succinate, trimethylamine N‐oxide (TMAO), and N, N, N‐trimethyl‐5‐aminovaleric acid with the diseases. Furthermore, we found that specific metabolites, such as TMAO and betaine, have significant clinical value in PH, suggesting their potential as biomarkers in disease management. In detailing the interplay between the gut microbiota, their metabolites, and PH, we underscored the potential therapeutic approaches modulating this microbiota. Ultimately, we endeavor to alleviate the substantial socioeconomic burden associated with this disease. This review presents a unique exploratory analysis of the link between gut microbiota and PH, intending to propel further investigations in the gut–lung axis. Highlights: The significant development in gut microbiota has brought an unprecedented paradigm for pulmonary hypertension (PH) management in recent years, which has delighted researchers and clinicians in precise disease control.The gut–lung axis is the bidirectional interaction between the gut and lung, which occurs through circulation, the nervous system, and other physiological processes, ultimately affecting the health of both the gut and the lung.We provided a comprehensive landscape of gut microbiota and its associated metabolites in PH, emphasizing the interplay between microorganisms and hosts in modulating PH.With the rapid development of technologies, including metagenomic and metabolomics on gut microbiota, the association of microorganisms and the human body will be untangled eventually, which will bring the dawn for disease cure followed by prognosis improvement among patients with PH. [ABSTRACT FROM AUTHOR]

Wheat is a major diet from many years; apart from its nutritious value, the wheat protein gliadin is responsible for many inflammatory diseases like celiac disease (CD), and non-celiac gluten sensitivity (NCGS). In this study, the gliadin-induced inflammation and associated cellular damage along with the protective role of curcumin was evaluated using human intestinal cell lines (HCT-116 and HT-29) as a model. Cells were cultured and exposed to 160 μg/ml of gliadin, 100 μM H2O2, and 10 μM curcumin (3 h pretreatment) followed by the assessment of inflammation. Spectrophotometric methods, real-time-PCR, ELISA, Western blotting, and confocal microscopy techniques were used to assess inflammatory markers such as advanced oxidation protein products (AOPPs) level, activity of myeloperoxidase (MPO) and NADPH oxidase (NOX), cytokines, and cell damage markers. The results show that gliadin increases the AOPPs level and the activity of MPO and NOX expression. It enhances inflammation by increasing expression of pro-inflammatory cytokines, altered expression of anti-inflammatory, and regulatory cytokines. It exacerbates the cellular damage by increasing MMP-2 and 9 and decreasing integrin α and β expression. Gliadin promotes disease pathogenesis by inducing the inflammation and cellular damage which further alter the cellular homeostasis. The pretreatment of curcumin counteracts the adverse effect of gliadin and protect the cells via diminishing the inflammation and help the cell to regain the cellular morphology suggesting phytochemical-based remedial interventions against wheat allergies. [ABSTRACT FROM AUTHOR]

Background: Convalescent plasma therapy for COVID‐19 relies on transfer of anti‐viral antibody from donors to recipients via plasma transfusion. The relationship between clinical characteristics and antibody response to COVID‐19 is not well defined. We investigated predictors of convalescent antibody production and quantified recipient antibody response in a convalescent plasma therapy clinical trial. Methods: Multivariable analysis of clinical and serological parameters in 103 confirmed COVID‐19 convalescent plasma donors 28 days or more following symptom resolution was performed. Mixed‐effects regression models with piecewise linear trends were used to characterize serial antibody responses in 10 convalescent plasma recipients with severe COVID‐19. Results: Donor antibody titres ranged from 0 to 1 : 3892 (anti‐receptor binding domain (RBD)) and 0 to 1 : 3289 (anti‐spike). Higher anti‐RBD and anti‐spike titres were associated with increased age, hospitalization for COVID‐19, fever and absence of myalgia (all P < 0.05). Fatigue was significantly associated with anti‐RBD (P = 0.03). In pairwise comparison amongst ABO blood types, AB donors had higher anti‐RBD and anti‐spike than O donors (P < 0.05). No toxicity was associated with plasma transfusion. Non‐ECMO recipient anti‐RBD antibody titre increased on average 31% per day during the first three days post‐transfusion (P = 0.01) and anti‐spike antibody titre by 40.3% (P = 0.02). Conclusion: Advanced age, fever, absence of myalgia, fatigue, blood type and hospitalization were associated with higher convalescent antibody titre to COVID‐19. Despite variability in donor titre, 80% of convalescent plasma recipients showed significant increase in antibody levels post‐transfusion. A more complete understanding of the dose‐response effect of plasma transfusion amongst COVID‐19‐infected patients is needed. [ABSTRACT FROM AUTHOR]