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Cachexia is a common pathological condition in cancer patients, affecting prognosis and treatment outcomes. The relationship between cachexia and gut microbiota and short-chain fatty acids (SCFAs) remains understudied. This research aimed to establish a cachexia mouse model and explore the gut microbiota-SCFAs connection. The study provides fundamental insights into the regulatory mechanisms of cancer cachexia and potential therapeutic strategies. A cachexia mouse model was created using C26 cells, with relevant indicators measured. Histological and immunohistochemical analyses assessed muscle structure and protein expression. ELISA was performed to detect the levels of IL-1β, IL-6, TNF-α, and LPS in serum to evaluate inflammation.16S rDNA sequencing and GC-MS quantified gut microbiota and SCFAs. Bioinformatics analysis identified indicator species and explored microbiota-SCFAs correlations.ROC analysis was performed to assess the potential of gut microbiota and SCFAs in identifying cachexia. The cachexia mouse model exhibited weight loss, muscle atrophy, and elevated inflammatory factors. Gut microbiota in cachexia mice showed decreased diversity and imbalance. Fourteen bacterial genera were identified as potential cachexia indicators. Functional prediction indicated alterations in the functional composition of gut microbial communities in cachexia mice, particularly in carbohydrate and lipid metabolism pathways. Four SCFAs showed significant changes, potentially serving as diagnostic factors. Specific microbial taxa were positively or negatively correlated with changes in SCFAs, and these microbial taxa and differential SCFAs were also correlated with inflammatory cytokines. Our study uncovers the gut microbiota and SCFAs features in a cachexia mouse model, revealing novel correlations between them. These newfound insights into the interplay between cachexia, gut microbiota, and SCFAs provide a crucial foundation for understanding the mechanisms behind cancer cachexia development and potential therapeutic approaches. • Diminished and disrupted gut microbial diversity observed in cachectic mice, accompanied by alterations in the functional composition of gut microbial communities. • Disturbed levels of SCFAs detected in the fecal samples of cachectic mice. • Potential utilization of intestinal microbiota and SCFAs as discerning markers for assessing cachexia in mice. • There is a potential correlation among the gut microbiota composition, SCFAs, and inflammatory factors in cachexic mice. [ABSTRACT FROM AUTHOR]

Nutritional intervention using probiotic fermented dairy product has emerged as a promising prophylactic strategy to curb inflammatory bowel diseases. Under present investigation, the potential of fermented whey prepared with probiotic Lactobacillus fermentum (LF:MTCC-5898) was investigated on dextran sodium sulfate (DSS) induced impaired intestinal barrier function in mice. Probiotic fermented whey (PFW) consumption improved the symptoms of colitis-associated with intestinal inflammation by significantly (p < 0.01) diminishing the percent loss in body weight, disease activity index and spleen index with improved colon length besides hematological and histopathological score. Likewise, pre-treatment with PFW improved the barrier integrity (p < 0.01) in contrast to leaky condition induced by DSS administration which increased the FITC-dextran permeability across gut epithelium. PFW consumption also provided the gut immune protection through significantly increased (p < 0.05) TLR-2 expression and stimulated T-regulatory response by producing TGF-β (p < 0.01) and, potently suppressed (p < 0.01) inflammatory response (TNF-α, IL-4 and C-reactive protein). Further, PFW intake significantly enhanced (p < 0.05) immunoglobulin (sIgA) secretion and concomitantly restored the Occludin, ZO-1 (p < 0.01) and Claudin -1(p < 0.05) transcriptional expression as compared to colitis mice. Additionally, immune-fluorescence further established the presence of intact actin cytoskeleton and tight junction proteins (claudin-1, occludin and ZO-1) after PFW consumption. Thus, PFW rectified the impaired and leaky barrier junctions not only through modulation of transcriptional expression of tight junction genes but also with reduced secretion of inflammatory mediators and helped in ameliorating the colitis. Hence, probiotic fermented whey prepared with L.fermentum (MTCC-5898) could be used as potential prophylactic functional food in the prevention of gut ailments. • Fermented foods have many nutritional components, bioactive molecules with vital effects on gut health. • Probiotic fermented whey (PFW) enhanced intestinal barrier integrity in colitis condition. • PFW provided gut immune protection by inhibiting inflammatory markers secretions. • PFW could be used as potential prophylactic functional food in prevention of gut disorders. [ABSTRACT FROM AUTHOR]

Ulcerative colitis (UC) is a chronic inflammatory disease of the intestine. It is characterized with recurrent. The pathogenesis is mainly associated with environmental factors, genetic susceptibility, dysbiosis of the intestinal flora and autoimmunity. The role of intestinal flora disorders in the pathogenesis and progression of UC is becoming increasingly prominent. More and more studies have confirmed that fecal microbiota transplantation (FMT) could reshape the composition of UC intestinal flora and it is expected to be a new strategy for UC treatment. In this study, we used 2% Dextran sulfate sodium (DSS) for 7 days to induce acute colitis model in mice, and interfere with FMT and Enterotoxigenic Escherichia coli (ETEC). ELISA and immunohistochemistry were applied to detect the concentration and expression of NF-κB p65, STAT3 and IL-6. 16SrRNA high-throughput sequencing was performed to explore the composition of intestinal flora. The aim was to study the treatment effect of FMT on UC mice and explore its potential mechanism by observing the changes of intestinal flora composition and diversity, and its relationship with NF-κB p65, STAT3 and IL-6 expression. We conclude that FMT could improve intestinal flora disorder in mice with ulcerative colitis, regulate NF-κB signaling pathway, and significantly reduce intestinal inflammation in UC mice. • FMT regulate the abundance of pathogenic bacteria and beneficial bacteria in mice with UC. • FMT could modulate NF-κB signaling pathway, and significantly reduce the inflammatory response. • FMT has shown tremendous potential in the treatment of UC and provided new insights for future research. [ABSTRACT FROM AUTHOR]

Under normal conditions, the intestinal flora and the body are in dynamic equilibrium. When the barrier function of the intestinal tract is damaged due to various reasons, changes in the number and proportion of bacteria or spatial displacement result in bacterial translocation (BT), which ultimately leads to multiple organ dysfunction syndrome (MODS). Endogenous infections and endotoxemia caused by intestinal flora and endotoxin translocation are the origins of inflammatory responses, and the intestinal tract is the organ in which MODS both initiates and targets. Only by ensuring the integrity of the intestinal mucosal barrier can intestinal BT be effectively prevented. Elimination of the primary disease and maintaining blood and oxygen supply to the intestine is the most basic treatment. Early initiation of the intestinal tract, establishment of enteral nutrition, and selective digestive decontamination are also highly effective treatments. Early diagnosis, intervention, or prevention of BT may be a new avenue or important connection in the treatment of various diseases. The mechanism of BT, detection techniques, prevention and treatment, and its interaction with parenteral diseases were reviewed. • Intestinal bacterial translocation plays an important role in the development of extraintestinal diseases. • Endogenous infections and endotoxemia caused by intestinal flora and endotoxin translocation are the origins of inflammatory responses. • Early diagnosis, intervention, or prevention of BT may be a new avenue or important connection in the treatment of various diseases. [ABSTRACT FROM AUTHOR]

The human intestinal microbiota coevolves with its host through a symbiotic relationship and exerts great influence on substantial functions including aspects of physiology, metabolism, nutrition and regulation of immune responses leading to physiological homeostasis. Over the last years, several studies have been conducted toward the assessment of the host–gut microbiota interaction, aiming to elucidate the mechanisms underlying the pathogenesis of several diseases. A defect on the microbiota–host crosstalk and the concomitant dysregulation of immune responses combined with genetic and environmental factors have been implicated in the pathogenesis of inflammatory bowel diseases (IBD). To this end, novel therapeutic options based on the gut microbiota modulation have been an area of extensive research interest. In this review we present the recent findings on the association of dysbiosis with IBD pathogenesis, we focus on the role of gut microbiota on the treatment of IBD and discuss the novel and currently available therapeutic strategies in manipulating the composition and function of gut microbiota in IBD patients. Applicable and emerging microbiota treatment modalities, such as the use of antibiotics, prebiotics, probiotics, postbiotics, synbiotics and fecal microbiota transplantation (FMT) constitute promising therapeutic options. However, the therapeutic potential of the aforementioned approaches is a topic of investigation and further studies are needed to elucidate their position in the present treatment algorithms of IBD. • Microbes are key players for maintaining the homeostasis of immune system. • Gut microbiota imbalance and immunity defects have been implicated in gut inflammation. • Novel therapeutic advances for IBD management involve gut microbiota regulation. • Fecal microbiota transplantation is very promising for ulcerative colitis' treatment. [ABSTRACT FROM AUTHOR]