Microbiota Composition Research Articles

Hepatic encephalopathy (HE) results from a debilitating complication of liver cirrhosis and acute liver failure, characterized by neuropsychiatric abnormalities ranging broadly from mild cognitive impairment to respiratory failure to coma. The pathogenesis of HE is multifactorial, with gut-derived toxins, particularly ammonia, playing a central role. Recent advances in understanding the gut-liver-brain axis have revealed the importance of gut microbiota and dysbiosis in the development and progression of HE. Fecal microbiota transplantation (FMT), a clinical procedure that is performed to transfer fecal microbiota from a healthy donor to a patient with HE (recipient), has emerged as a promising therapeutic strategy for modulating gut microbiota and ameliorating HE. FMT facilitates the restoration of gut microbiota composition with increased microbial alpha diversity, reestablishment of the balance between beneficial and pathogenic bacteria, reduction in the production of gut-derived toxins, and improvement of intestinal barrier function. It also modulates immune and inflammatory responses, alleviating hepatocyte and biliary injury. FMT has also demonstrated efficacy in improving cognitive function and reducing hospitalizations in HE patients and can maintain a stable donor-like microbiota profile for up to 12 months post-transplantation. FMT is generally well-tolerated, with most adverse events reported to be mild and transient, providing a desirable option for HE treatment. This review provides a comprehensive overview of the current understanding of the role of gut microbiota in the pathogenesis of HE, the mechanisms underlying the therapeutic effects of FMT, and the clinical evidence supporting its use in HE. We will also discuss the limitations, challenges, and future prospects for FMT in the treatment of HE.

Enterotoxigenic Escherichia coli (ETEC) is one of the primary pathogenic bacteria causing intestinal diseases and diarrhea in young animals. Probiotics can enhance intestinal barrier function and alleviate the occurrence of intestinal diseases and diarrhea by regulating the composition and metabolic products of the gut microbiota. In preliminary studies, we isolated a strain of Lactobacillus reuteri L81 with good probiotic properties from the rectal feces of healthy calves. This strain was found to alleviate weaning diarrhea in calves and improve immune function and antioxidant capacity. However, it remains unclear whether it can mitigate intestinal barrier damage caused by Escherichia coli K99 by regulating the composition of the gut microbiota and its metabolites. Therefore, this study selected 24 male SPF-grade ICR mice aged 4 weeks, randomly divided into 4 groups (n = 6): control group, ETEC group, low-dose Lactobacillus reuteri L81 group (L_L81 group), and high-dose Lactobacillus reuteri L81 group (H_L81 group). From days 1 to 17 of the experiment, the L_L81 and H_L81 groups were gavaged with 0.2 mL of bacterial suspensions at concentrations of 1 × 10⁸ CFU/mL and 1 × 10⁹ CFU/mL daily, respectively, while the control and ETEC groups were given an equal volume of physiological saline. From days 18 to 22, the ETEC, L_L81, and H_L81 groups were infected daily with 0.2 mL of an ETEC K99 bacterial suspension at a concentration of 5 × 10⁹ CFU/mL, whereas the control group continued to receive physiological saline. The results showed that the intervention of Lactobacillus reuteri L81 could regulate the gene expression levels of tight junction proteins in the colon tissue of mice. Moreover, the intervention with H_L81 group could increase the gene expression levels of Claudin-1 and ZO-1 ( P < 0.05) in the colon tissue of mice. The intervention with L_L81 group can inhibit the expression of IL-1β, MyD88, and TLR4 genes in the colon tissue of mice. The analysis of gut microbiota composition revealed that the intervention with Lactobacillus reuteri L81 exhibited a trend toward increasing microbial richness and diversity. It elevated the relative abundances of Lactobacillus, Prevotellaceae_UCG-001, and Gordonibacter in the mouse colon, while reducing the relative abundance of Salmonella. The non-targeted metabolomics analysis indicated that the intervention with Lactobacillus reuteri L81 has regulatory effects on multiple metabolic pathways, including bile secretion, β-alanine metabolism, glutathione metabolism, and arginine and proline metabolism. In conclusion, Lactobacillus reuteri L81 can alleviate intestinal barrier damage induced by ETEC K99 in mice by modulating the composition and metabolites of the gut microbiota.

Endometriosis is a chronic inflammatory disease significantly affecting women's health and quality of life. The recent evidence highlights the role of gut microbiota dysbiosis in endometriosis pathogenesis, suggesting that gut microbiota modulation could be a promising therapeutic strategy. This study aimed to retrospectively evaluate the therapeutic efficacy of microecological therapy, via the modulation of gut microbiota, inflammatory and immune parameters, as an adjunct treatment for patients with endometriosis undergoing laparoscopic surgery. A retrospective analysis was conducted on 187 patients diagnosed with endometriosis from January 2022 to December 2023. Patients were grouped into a surgery-only group and a surgery-plus-microecological therapy group. Clinical outcomes including gastrointestinal recovery, postoperative complications, and pain were recorded. Gut microbiota composition, systemic inflammation markers, estradiol levels, intestinal barrier function (lipopolysaccharide, LPS), and intestinal mucosal immunity were also analyzed. Patients receiving microecological therapy showed significantly improved gastrointestinal recovery, decreased postoperative pain, reduced complication rates, and enhanced quality of life compared with surgery-only controls. Microecological therapy notably reduced systemic inflammation, as evidenced by lower serum IL-6, TNF-α, and LPS levels, and decreased estradiol concentrations, and significantly increased beneficial gut microbiota abundance and improved mucosal immunity markers. Microecological therapy effectively enhances postoperative outcomes, reduces systemic inflammation, restores gut microbiota balance, and strengthens intestinal mucosal immunity in endometriosis patients.

Maladaptive host metabolic responses to infection are emerging as major determinants of infectious disease pathogenesis. However, the factors regulating these metabolic changes within tissues remain poorly understood. In this study, we used toxoplasmosis, as a prototypical example of a disease regulated by strong type I immune responses, to assess the relative roles of current local parasite burden, local tissue inflammation, and the microbiome in shaping local tissue metabolism during acute and chronic infections. Toxoplasmosis is a zoonotic disease caused by the parasite Toxoplasma gondii. This protozoan infects the small intestine and then disseminates broadly in the acute stage of infection, before establishing chronic infection in the skeletal muscle, cardiac muscle, and brain. We compared metabolism in 11 sampling sites in C57BL/6 mice during the acute and chronic stages of T. gondii infection. Strikingly, major spatial mismatches were observed between metabolic perturbation and local parasite burden at the time of sample collection for both disease stages. By contrast, a stronger association with indicators of active type I immune responses was observed, indicating a tighter relationship between metabolic perturbation and local immunity than with local parasite burden. Loss of signaling through the IL1 receptor in IL1R knockout mice was associated with reduced metabolic impact of infection. In addition, we observed significant changes in microbiota composition with infection and candidate microbial origins for multiple metabolites impacted by infection. These findings highlight the metabolic consequences of toxoplasmosis across different organs and potential regulators.IMPORTANCEInflammation is a major driver of tissue perturbation. However, the signals driving these changes on a tissue-intrinsic and molecular level are poorly understood. This study evaluated tissue-specific metabolic perturbations across 11 sampling sites following systemic murine infection with the parasite Toxoplasma gondii. Results revealed relationships between differential metabolite enrichment and variables, including inflammatory signals, pathogen burden, and commensal microbial communities. These data will inform hypotheses about the signals driving specific metabolic adaptation in acute and chronic protozoan infection, with broader implications for infection and inflammation in general.

The intestinal microbiota is shaped by fiber-rich ingredients, such as unripe banana flour (UBF), high in resistant starch (RS). We investigated the effects of RS-rich UBF and inulin on gut microbiota and intestinal function in a double-blind, randomized, placebo-controlled pilot trial. Forty-eight healthy adults consumed maltodextrin (control), inulin, or UBF three times weekly for six weeks. Microbiota composition and function were analyzed using 16S rRNA gene sequencing and PICRUSt, alongside fecal short-chain fatty acids, blood biochemistry, and gastrointestinal parameters. We observed two microbiota clusters at baseline, one Prevotella-rich (P) and one Bacteroides-rich (B), with distinct responses to the interventions. Only cluster P subjects consuming UBF showed significant global microbiota shifts (weighted Unifrac Beta diversity, PERMANOVA p = 0.007) and major functional changes (533 KEGG orthologs, FDR < 0.05). Inulin produced modest modulation (19 KOs) on cluster P, and no effects were observed on cluster B. RS-rich UBF modulated gut microbiota in a composition-dependent manner, supporting the potential of microbiota-based stratification to improve dietary fiber interventions.

Malaria parasites (Plasmodium spp.) are mosquito-borne parasites that infect humans and wildlife. Several studies support the role of mosquito microbiota as a major driver of Plasmodium transmission, although studies on wildlife malaria are typically neglected. Here, we used a 16S rRNA metabarcoding approach to assess whether the exposure to avian Plasmodium parasites affects the microbiota of their natural vector, Culex pipiens. Mosquitoes, captured in the field as larvae and grown in the laboratory, were allowed to feed on house sparrows (Passer domesticus) naturally infected with Plasmodium relictum (lineage SGS1) and uninfected birds. We analyzed the microbiota composition of the abdomens of individual mosquitoes and found 2,006 Amplicon Sequence Variants (ASVs). Culex pipiens' microbiota was dominated by bacteria of the genus Wolbachia, followed by the genera Stenotrophomonas and Faecalibacterium. We observed no difference in alpha nor beta diversity between mosquitoes that fed on Plasmodium-infected birds (exposed mosquitoes) and those that fed on uninfected birds (unexposed mosquitoes). However, exposed mosquitoes had a higher relative abundance of bacteria of the family Bacteroidaceae and the genus Bacteroides than the unexposed mosquitoes. Excluding the intracellular endosymbiont Wolbachia from the analyses, we obtained similar results, and also found a higher relative abundance of bacteria of the family Rikenellaceae in exposed mosquitoes. A pathway enrichment analysis based on KEGG annotations revealed that the bacterial community in exposed mosquitoes was enriched in pathways mainly related to biosynthesis and metabolism. Our results suggest that Cx. pipiens exposed to avian Plasmodium have slightly different microbiota composition, although further research is needed to establish the causality of these effects.

The relative abundance of some bacteria in the gut of pigs is heritable, suggesting that host genetics may recursively influence boar semen quality by affecting the composition and function of gut microbiota. Therefore, it is essential to elucidate the specific contributions of heritable versus non-heritable gut microbiota to semen quality traits. Our study aimed to identify heritable and non-heritable bacterial taxa at the genus level in the boar gut and to predict their functions and respective contributions to semen quality traits. At the genus level, 39 heritable and 91 non-heritable bacterial taxa were identified. Functional analysis revealed that predicted microbial functions in both groups were primarily enriched in carbohydrate, nucleotide, and amino acid metabolism. We further analyzed the average microbiability of heritable and non-heritable bacteria on short-chain fatty acids (SCFAs) and semen quality traits. The relative abundance of heritable bacteria was found to contribute more to SCFAs levels and semen quality than non-heritable bacteria. Mediation analysis revealed that SCFAs could mediate the influence of the relative abundance of heritable bacteria on host phenotypes, identifying 99 significant genus-SCFAs-semen quality trait mediation links. Our findings underscore the substantial role of the relative abundance of heritable gut bacteria in shaping porcine semen quality through SCFAs mediation. These results highlight the potential of targeted microbiome interventions to enhance reproductive traits in pigs.

Fructose malabsorption is characterized as the incomplete absorption of fructose in the small intestine. Fructose is one of the most common monosaccharides in the human diet. The purpose of this review is to provide an updated overview of insights into the relationship between high-fructose diet, fructose malabsorption, gut microbiota and clinical consequences. Incomplete absorption of fructose causes accumulation in the colon, which leads to fermentation by gut microbiota and abdominal symptoms such as bloating and excessive gas production. Malabsorption may result from exceeding the absorptive capacity of GLUT5 or insufficient upregulation, with incidence increasing with age and higher dietary fructose concentrations. High-fructose diets generally promote an increase in inflammatory bacterial groups such as Desulfovibrio and Deferribacteraceae, while reducing beneficial Bacteroidetes. These microbial alterations may impair intestinal barrier function, modify short-chain fatty acid profiles, and contribute to systemic inflammation, metabolic disorders, and potentially mental health issues. Animal studies using fructose malabsorption models present inconclusive results regarding the impact of fructose on the composition of gut microbiota. Additional research is essential to fully comprehend the complex relationship between diet, fructose malabsorption and gut microbiota, to develop personalized, effective dietary approaches for managing symptoms of fructose malabsorption.

The small brown planthopper (SBPH), Laodelphax striatellus, transmits rice stripe virus (RSV), a devastating pathogen that causes significant yield losses in rice. The components of the gut microbiota in SBPH and the effects of RSV infection on gut microorganisms are unclear. In this study, high-throughput sequencing of 16S rRNA was utilized to evaluate the composition of gut microorganisms in SBPH. The gut microbiota of SBPH was primarily composed of Proteobacteria, Firmicutes and Bacteroidetes at ratios of 94.79%, 3.04% and 1.39%, respectively; furthermore, the composition of bacteria in the gut microbiota was relatively conserved with differences at the genus level. To elucidate the response of the SBPH gut microbiota to RSV infection, we compared its composition and abundance in viruliferous and naïve SBPH. Interestingly, RSV infection was associated with increased diversity in the SBPH gut microbiota. Comparative analysis demonstrated that RSV infection elevated the relative abundance of Proteobacteria while reducing that of Firmicutes. Population counts demonstrated that RSV infection reduced the gut loads of Stenotrophomonas, Brevundimonas, and Brevibacillus, whereas the gut load of Staphylococcus was significantly increased. Further functional predictive assays revealed that RSV infection enhanced the functions of the SBPH gut microbiota in terms of metabolism, cellular processes, genetic and environmental information processing, and organismal systems. Our results indicate that RSV reshapes the composition, abundance, and functions of the SBPH gut microbiota, offering insights into virus–host–microbiome interactions.

A diverse community of microorganisms inhabits the gastrointestinal tract in a physiological state. While a symbiotic relationship exists between commensal bacteria and the healthy host, an imbalanced microbial population (dysbiosis) is associated with the development of colitis-associated colorectal cancers. The decline of beneficial microbes (eubionts) and the expansion of commensal-derived opportunistic pathogens (pathobionts) are widely recognized as key factors in the microbial etiology of various diseases. In particular, certain bacteria with emerging virulence elements are present in the gut microbiome and have been implicated as contributors to the development of colon cancer, such as Escherichia coli, Bacteroides fragilis, and Fusobacterium nucleatum. Bacterial virulent factors, including lipopolysaccharide, fimbriae and adhesins, and toxins, promote oncogenesis through direct or indirect mechanisms. These microbial products modify host cellular functions, resulting in DNA damage, increased epithelial proliferation, and intensified inflammation, all of which ultimately contribute to tumor formation. Although the existence of pathobionts is generally accepted nowadays, an open question remains regarding why bacteria shift from harmless commensals to disease-causing pathobionts. Accumulating evidence suggests that host epithelial functions influence the composition of the intestinal microbiota by regulating oxygen availability in the lumen, providing antimicrobial defense, activating innate immune responses, synthesizing mucin glycoproteins, and establishing a physical barrier through the organization of microvilli. This review examines the various aspects of mucosal drivers that shape microbiota and provides evidence that intraepithelial stress plays a significant role in configuring colitogenic and tumorigenic microflora. Understanding the mechanisms by which microbes transition from eubionts to pathobionts that promote cancer progression is crucial for developing bacterial precision medicine. Identifying the roles of intestinal pathobionts and the critical time point for host-microbe interactions in tumorigenesis could lead to the development of new strategies for prevention and therapy.

Cirrhosis remains a significant global health burden, causing approximately 1.4–1.5 million deaths each year and contributing to nearly 46 million disability-adjusted life years (DALYs) worldwide. Increasing evidence identifies the gut–liver axis as a central driver of disease progression, wherein intestinal dysbiosis, barrier disruption, and microbe-derived metabolites collectively exacerbate inflammation, fibrogenesis, and related complications. Across more than 40 recent studies, gut microbial α-diversity declined by 30–60%, and over 80% reported a marked depletion of short-chain fatty acid (SCFA)–producing taxa, particularly Lachnospiraceae and Ruminococcaceae. Meta-analyses indicate that fecal butyrate levels decrease by 40–70%, accompanied by a two- to fourfold increase in endotoxin concentrations. Bile acid profiling demonstrates an approximately 50% reduction in secondary bile acids and significant suppression of FXR/TGR5 signaling, whereas tryptophan metabolism shifts toward the kynurenine pathway, weakening epithelial defense and exacerbating portal hypertension. Clinically, dysbiosis and microbial translocation are associated with higher MELD scores, and patients in the lowest quartile of microbial diversity have a threefold increased risk of hepatic encephalopathy or spontaneous bacterial peritonitis. Microbiome-targeted interventions—including lactulose, rifaximin, probiotics or synbiotics, fecal microbiota transplantation, and bile acid modulators—restore community balance in 70–85% of clinical trials, although efficacy and safety vary by etiology and baseline microbiota composition. Integrated microbiome–metabolome models achieve areas under the curve (AUCs) of 0.82–0.90 for noninvasive classification and early detection of cirrhosis. Collectively, these findings underscore reproducible, quantitative microbiome–metabolite alterations and outline a roadmap for microbiome-informed precision care that connects mechanistic insight with clinical application, emphasizing the need for longitudinal and multi-ethnic validation.

The gut microbiota has emerged as a critical determinant of antitumor immunity and a potential modulator of responses to immune checkpoint inhibitors (ICIs). Although pre-clinical and clinical studies suggest that specific bacterial taxa may influence both efficacy and immune-related adverse events (irAEs). However, the magnitude and consistency of these associations remain unclear. A systematic search of PubMed, Embase, Web of Science, and the Cochrane Library was conducted through March 2025. Eligible studies evaluated baseline gut microbiota composition, fecal microbiota transplantation (FMT), probiotic/prebiotic interventions, or antibiotic exposure in cancer patients treated with ICIs. Pooled hazard ratios (HRs) for overall survival (OS) and progression-free survival (PFS), and odds ratios (ORs) for response rates and irAEs, were estimated using random-effects models. Across 38 studies involving 5,642 patients were included. Pooled analysis demonstrated that enrichment of Akkermansia muciniphila, Bifidobacterium longum and Faecalibacterium prausnitzii was significantly associated with improved OS (HR 0.62, 95% CI 0.51-0.76) and PFS (HR 0.69, 95% CI 0.55-0.83). Conversely, antibiotic exposure before or during ICI treatment was associated with worse OS (HR 1.84, 95% CI 1.45-2.34). Patients undergoing FMT from responders exhibited higher objective response rates (OR 2.91, 95% CI 1.48-5.73). Microbiota diversity indices were consistently higher in responders than in non-responders. Collectively, gut microbiota composition and its modulation significantly impact the therapeutic efficacy and toxicity profile of ICIs. These findings highlight the translational potential of microbiome-based biomarkers and interventions in optimizing immunotherapy.

Purpose Previous studies have shown that Bifidobacterium animalis subsp. lactis BB-12 plays a role in maintaining the intestinal barrier and regulating inflammation; however, its potential connection to ocular diseases has not been thoroughly explored. Diabetic retinopathy (DR) is a common ocular complication of diabetes and is closely associated with metabolic dysregulation. This study investigated whether BB-12 supplementation could affect systemic diabetic symptoms, the progression of DR, and the stability of gut microbiota. Materials and methods Diabetic db/db mice were utilized to monitor metabolic parameters, assess hepatic and lipid profiles, evaluate retinal function via ERG, and examine retinal morphology through OCT and HE staining. Treg/Th17 balance was analyzed by flow cytometry, and gut microbiota composition was profiled using 16S rRNA sequencing. Results The results showed that BB-12 reduced obesity, decreased hepatic steatosis, improved retinal blood vessel health and vision, and influenced both the Treg/Th17 balance and gut dysbiosis in diabetic mice. Conclusions These findings lay the groundwork for regulatory role of intestinal microbiota on systemic and ocular complications of diabetes, and further examination of the gut-retina axis.

Introduction: Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative disorders, causing progressive cognitive and motor decline. High rates of new diagnoses, coupled with increasing evidence linking gastrointestinal (GI) dysfunction to neurodegeneration, highlight the significance of understanding the gut-brain axis (GBA). Changes in gut microbiota composition are associated with amyloid-beta accumulation in AD and α-synuclein aggregation in PD, suggesting that gut dysbiosis and inflammation may worsen disease pathology. Methods: A systematic literature review was conducted using peer-reviewed primary research articles published between 2014 and 2025. Articles were selected based on their relevance to GI inflammation, gut microbiota dysbiosis, and neurodegenerative diseases. Studies involving human participants and relevant animal models were prioritized. Databases searched included PubMed, Google Scholar, ScienceDirect, JSTOR, and SpringerLink. Results: Gut dysbiosis was consistently associated with increased intestinal permeability, systemic inflammation, and neuroinflammatory responses in AD and PD. Specific microbial imbalances correlated with accelerated disease progression and cognitive decline. Animal studies demonstrated that fecal microbiota transplantation from diseased individuals worsened motor and mental symptoms, while interventions targeting gut health, such as probiotics and dietary modifications, reduced neuroinflammation and improved outcomes. Discussion: Findings support the GBA’s critical role in mediating neurodegeneration through immune activation and inflammatory pathways. Dysbiosis-induced changes in microbial metabolite production, including short-chain fatty acids (SCFAs) and tryptophan derivatives, further contribute to neuroinflammatory processes. Despite promising preclinical results, challenges remain in translating gut-targeted therapies to clinical use due to variability in individual microbiomes and limited longitudinal human data. Conclusion: This review emphasizes the gut microbiota as a modifiable factor in the pathogenesis of AD and PD. Targeting GI inflammation and restoring microbial balance may offer novel therapeutic strategies for slowing disease progression. Future research should focus on validating gut-derived biomarkers, personalizing microbiome-based treatments, and conducting longitudinal clinical trials to optimize gut-brain interventions in neurodegenerative diseases.

Soyasaponin intolerance is common in ancient fish species, making them susceptible to enteritis caused by dietary soybean meal. β,β-Dimethylacrylshikonin is the key active monomer found in Lithospermum erythrorhizon and is known for its multiple pharmacological activities. However, its effect on soybean meal-induced enteritis remains unknown. The administration of 2 g/kg of β,β-Dimethylacrylshikonin (LE) effectively alleviated 5 g/kg of soyasaponin-induced histopathological changes and dysfunction, as evidenced by the expression of inflammation-related genes (il-1β, il-8, and il10). Regarding the gut microbiota composition, LE therapy decreased the population of inflammation-linked Proteobacteria and concurrently elevated the proportion of Fusobacteriota, effectively sustaining the balance of the zebrafish gut microbiota. Moreover, at the genus level, LE treatment also increased the abundance of Cetobacterium. Transcriptional results suggested that LE intervention mainly regulated immune-related pathways, including cytokine–cytokine receptor interaction, the TGF-beta signaling pathway, taurine and hypotaurine metabolism, and arachidonic acid metabolism. In conclusion, 5 g/kg of soyasaponins caused intestinal injury in zebrafish, and β,β-Dimethylacrylshikonin can reduce intestinal inflammation by regulating the intestinal microbial balance and metabolic disorder, with the best effect at 2 g/kg.

Abstract Ammonia dysregulation is a common pathological feature linking hyperammonemia—a severe metabolic disorder‐ and colorectal cancer (CRC), yet current treatment options remain inadequate. Here, a first‐in‐class dual‐pathway ammonia scavenging system is introduced based on a bioengineered microalgae‐hydrogel oral formulation (SPB‐CV@ALG), designed to simultaneously treat hyperammonemia and suppress CRC progression. This multifunctional system integrates Chlorella vulgaris (CV), capable of biologically capturing intestinal ammonia via extracellular adsorption and intracellular assimilation, with sodium phenylbutyrate (SPB), a clinically approved metabolic ammonia scavenger. These agents are co‐encapsulated within a semi‐interpenetrating sodium alginate–carboxymethyl chitosan hydrogel, which enhances gastrointestinal retention, protects biological activity, and ensures colon‐targeted release. In murine hyperammonemia models, SPB‐CV@ALG significantly lowered systemic ammonia levels, rescued cognitive and behavioral deficits, and mitigated hepatic and cerebral pathology. Remarkably, the same formulation also inhibited tumor growth in both subcutaneous and orthotopic CRC models. Mechanistically, the therapy reshaped gut microbiota composition by enriching beneficial taxa such as Akkermansia muciniphila and depleting pro‐tumorigenic Pseudomonadota , supporting a microbiota‐mediated anti‐cancer mechanism. Long‐term safety studies confirmed favorable biocompatibility without systemic toxicity. This study presents a transformative therapeutic paradigm that leverages microalgae's natural metabolic functions for dual‐disease intervention. The SPB‐CV@ALG platform offers a safe, effective, and translational solution to address two major unmet clinical needs through integrated ammonia detoxification, tumor suppression, and microbiome modulation.

Background Severe obesity is associated with metabolic alterations and an increased risk of developing type 2 diabetes. Bariatric surgery, especially malabsorptive procedures, results in significant clinical improvements and induces changes in the gut microbiota composition. This study aimed to identify bacterial taxa associated with changes in body mass index (BMI) in patients undergoing bariatric surgery and to explore their relationship with nutrient intake. Methods Individuals with severe obesity were recruited prior to and following bariatric surgery. Fecal DNA was extracted and the V4 region of the 16S rRNA gene was sequenced. Quality control and taxonomic classification were performed using QIIME2 and the Greengenes database. Nutrient intake was assessed through a 7-day dietary recall. Anthropometric measurements and blood samples were collected to evaluate clinical variables. Statistical analyses were conducted using R software. Results Significant differences in gut microbiota diversity were observed post-bariatric surgery. The Shannon and Simpson diversity indices decreased significantly after surgery (p &amp;lt; 0.001). Beta diversity analysis (Bray-Curtis, Weighted and Unweighted UniFrac) also showed significant differences between pre- and post-surgery samples (p = 0.001). The abundance of a species within the genus Coprococcus was positively correlated with magnesium and thiamin intake in post-surgery patients (rho = 0.816, p FDR = 0.029 and rho = 0.812, p FDR = 0.029, respectively). Furthermore, Coprococcus sp. abundance was positive associated with BMI in pre-surgery individuals (p = 0.043) but negative associated with BMI in post-surgery individuals (p = 0.036). Several taxa within the order Clostridiales and microbial metabolic pathways involved in sugar degradation, acetate, thiamin (vitamin B1) and some amino acid production were enriched prior to surgery. Conclusions The abundance of a species of the genus Coprococcus showed an inverse relationship with BMI in pre-surgery and post-surgery individuals and correlated positively with magnesium and thiamin intake in patients who underwent a malabsorptive bariatric surgery. These findings suggest that optimizing micronutrient intake may enhance the beneficial effects of bariatric surgery on BMI by favorably modulating gut microbiota composition.

Hypertriglyceridemia-associated acute pancreatitis (HLAP) is a severe gastrointestinal condition characterized by an increased risk of multiple organ dysfunction and elevated mortality. Intestinal microbiota, often described as the second human genome, plays a key role in maintaining gastrointestinal and systemic homeostasis. Among its various metabolites, short-chain fatty acids (SCFAs) are particularly abundant and functionally significant. Current evidence indicates a strong relationship between SCFAs and the pathogenesis and progression of HLAP. SCFAs contribute to the restoration of intestinal homeostasis by modulating the composition of gut microbiota, enhancing the integrity of the intestinal epithelial barrier, and regulating mucosal immune responses. Furthermore, SCFAs attenuate systemic inflammatory responses, promote pancreatic tissue repair, and reduce the risk of multiple organ dysfunction. These protective effects indicate that SCFAs represent a promising therapeutic target for gut-centered interventions in HLAP. This review summarizes the changes in intestinal microbiota and SCFA levels following HLAP onset, elucidates the underlying mechanisms by which SCFAs exert protective effects, and evaluates their potential therapeutic applications, thereby providing a theoretical basis for the development of gut-targeted strategies in the management of HLAP.

The human intestinal microbiota plays a vital role in health. One of the most protective benefits is the bacterial nitrogen metabolism of gut bacteria, which reduces nitrate (NO3 -) and nitrite (NO2 -) to ammonia or nitric oxide, preventing the formation of carcinogenic nitrosamines. In this study, we shed light on the gut bacterial NO2 -/NO3 - degradation, its efficacy, and the effects on the steady-state NO2 - concentration in the human colon. Highly abundant gut bacteria that represent the most prominent phyla were analyzed for their potential to reduce NO2 - or NO3 -. Escherichia coli showed the greatest efficiency, which indicates a key role in the detoxification and prevention of nitrosamine formation. Species of the genera Bacteroides and Phocaeicola also contributed to NO2 - reduction due to their high abundance. The total activity of stool samples was about 620 μmol NO2 - h-1, indicating that NO2 - concentration in the human stool should be very low. We also show that bacterial NO2 - reduction is necessary to allow NO2 --sensitive microorganisms to colonize the intestine, preventing a pathological shift in the composition of the intestinal microbiota. The results illustrate that the gut microbiota plays a central role in NO2 - detoxification, ensuring microbiota integrity and potentially preventing nitrosamine formation and gut-associated cancers.

Introduction: Hypertension remains one of the leading modifiable risk factors for cardiovascular morbidity and mortality worldwide. Emerging data indicate that the gut microbiota influences vascular tone, renal sodium handling, and systemic inflammation through metabolites and immune pathways. Clarifying this relationship could open novel avenues for prevention and treatment of hypertension. Objective: The primary objective was to synthesize mechanistic and clinical evidence linking gut microbiota composition and function to blood pressure regulation. Secondary objectives included identification of key microbial taxa and metabolites, evaluation of probiotic and dietary interventions on blood pressure, comparison of human and animal data, and assessment of evidence certainty using standardized approaches. Methods: We searched PubMed, Scopus, Web of Science, Cochrane Library, LILACS, ClinicalTrials.gov, and ICTRP for studies published in the last five years, extending to ten years if fewer than ten eligible human studies were found. Inclusion criteria prioritized human studies assessing gut microbiota or microbiota-modifying interventions with blood pressure outcomes, while mechanistic animal and in vitro studies were considered for biological plausibility. Data were extracted according to PRISMA principles, and the certainty of evidence was appraised with the GRADE framework. Results and Discussion: Of 1,243 records identified, 21 studies met the inclusion criteria, comprising 12 human studies and 9 mechanistic animal or in vitro investigations. Cross-sectional human data frequently associated reduced microbial diversity and altered taxa with higher blood pressure, while mechanistic studies implicated short-chain fatty acids, salt-sensitive immune modulation, and barrier dysfunction. Probiotic and prebiotic trials demonstrated modest blood pressure reductions, though heterogeneity in strains, dosing, and duration limited firm clinical conclusions. Conclusion: Current evidence supports a biologically plausible gut microbiota–blood pressure axis with preliminary signals for benefit from microbiota-modifying strategies. Standardization of microbiome methods, adequately powered randomized trials with blood pressure as a primary endpoint, and integration of metabolomics and diet assessments are needed to define clinical utility.