Search Results (685)

The demand for wild animal meat, popularly called “bushmeat”, serves as a driving force behind the emergence of infectious diseases, potentially transmitting a variety of pathogenic bacteria to humans through handling and consumption. This study investigated the microbial load and bacterial diversity in bushmeat sourced from a prominent bushmeat market in Kumasi, Ghana. Carcasses of 61 wild animals, including rodents (44), antelopes (14), and African civets (3), were sampled for microbiological analysis. These samples encompassed meat, intestines, and anal and oral swabs. The total aerobic bacteria plate count (TPC), Enterobacteriaceae count (EBC), and fungal counts were determined. Bacterial identification was conducted using MALDI-TOF biotyping. Fungal counts were the highest across all animal groups, with African civets having 11.8 ± 0.3 log₁₀ CFU/g and 11.9 ± 0.2 log₁₀ CFU/g in intestinal and meat samples, respectively. The highest total plate count (TPC) was observed in rodents, both in their intestines (10.9 ± 1.0 log₁₀ CFU/g) and meat (10.9 ± 1.9 log₁₀ CFU/g). In contrast, antelopes exhibited the lowest counts across all categories, particularly in EBC from intestinal samples (6.1 ± 1.5 log₁₀ CFU/g) and meat samples (5.6 ± 1.2 log₁₀ CFU/g). A comprehensive analysis yielded 524 bacterial isolates belonging to 20 genera, with Escherichia coli (18.1%) and Klebsiella spp. (15.5%) representing the most prevalent species. Notably, the detection of substantial microbial contamination in bushmeat underscores the imperative for a holistic One Health approach to enhance product quality and mitigate risks associated with its handling and consumption. Full article

Introduction: The gut microbiota is vital for human health, and its modulation through dietary and pharmaceutical compounds has gained increasing attention. Among gut microbes, Akkermansia muciniphila has been extensively researched due to its role in maintaining intestinal barrier integrity, regulating energy metabolism, and influencing inflammatory responses. Subject: To analyze and synthesize the available scientific evidence on the influence of various bioactive compounds, including prebiotics, polyphenols, antioxidants, and pharmaceutical agents, on the abundance and activity of A. muciniphila, considering underlying mechanisms, microbial context, and its therapeutic potential for improving metabolic and intestinal health. Methods: A systematic literature review was conducted in accordance with the PRISMA 2020 guidelines. Databases such as PubMed, ScienceDirect, Scopus, Web of Science, SciFinder-n, and Google Scholar were searched for publications from 2004 to 2025. Experimental studies in animal models or humans that evaluated the impact of bioactive compounds on the abundance or activity of A. muciniphila were prioritized. The selection process was managed using the Covidence platform. Results: A total of 78 studies were included in the qualitative synthesis. This review compiles and analyzes experimental evidence on the interaction between A. muciniphila and various bioactive compounds, including prebiotics, antioxidants, flavonoids, and selected pharmaceutical agents. Factors such as the chemical structure of the compounds, microbial environment, underlying mechanisms, production of short-chain fatty acids (SCFAs), and mucin interactions were considered. Compounds such as resistant starch type 2, GOS, 2′-fucosyllactose, quercetin, resveratrol, metformin, and dapagliflozin showed beneficial effects on A. muciniphila through direct or indirect pathways. Discussion: Variability across studies reflects the influence of multiple variables, including compound type, dose, intervention duration, experimental models, and analytical methods. These differences emphasize the need for a contextualized approach when designing microbiota-based interventions. Conclusions: A. muciniphila emerges as a promising therapeutic target for managing metabolic and inflammatory diseases. Further mechanistic and clinical studies are necessary to validate its role and to support the development of personalized microbiota-based treatment interventions. Full article

Transmembrane protein 43 (TMEM43 or LUMA) encodes a highly conserved protein found in the nuclear and endoplasmic reticulum membranes of many cell types and the intercalated discs and adherens junctions of cardiac myocytes. TMEM43 is involved in facilitating intra/extracellular signal transduction to the nucleus via the linker of the nucleoskeleton and cytoskeleton complex. Genetic mutations may result in reduced TMEM43 expression and altered TMEM43 protein cellular localization, resulting in impaired cell polarization, intracellular force transmission, and cell–cell connections. The p.S358L mutation causes arrhythmogenic right ventricular cardiomyopathy type-5 and is associated with increased absorption of lipids, fatty acids, and cholesterol in the mouse small intestine, which may promote fibro-fatty replacement of cardiac myocytes. Mutations (p.E85K and p.I91V) have been identified in patients with Emery–Dreifuss Muscular Dystrophy-related myopathies. Other mutations also lead to auditory neuropathy spectrum disorder-associated hearing loss and have a negative association with cancer progression and tumor cell survival. This review explores the pathogenesis of TMEM43 mutation-associated diseases in humans, highlighting animal and in vitro studies that describe the molecular details of disease processes and clinical, histologic, and molecular manifestations. Additionally, we discuss TMEM43 expression-related conditions and how each disease may progress to severe and life-threatening states. Full article

Obesity-driven inflammation disrupts gut barrier integrity and promotes inflammatory bowel disease (IBD). Emerging evidence highlights gut hormones—including glucagon-like peptide-1 (GLP-1), glucagon-like peptide-2 (GLP-2), glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), cholecystokinin (CCK), and apolipoprotein A4 (APOA4)—as key regulators of metabolism and mucosal immunity. This review outlines known mechanisms and explores therapeutic prospects in IBD. GLP-1 improves glycemic control, induces weight loss, and preserves intestinal barrier function, while GLP-2 enhances epithelial repair and reduces pro-inflammatory cytokine expression in animal models of colitis. GIP facilitates lipid clearance, enhances insulin sensitivity, and limits systemic inflammation. PYY and CCK slow gastric emptying, suppress appetite, and attenuate colonic inflammation via neural pathways. APOA4 regulates lipid transport, increases energy expenditure, and exerts antioxidant and anti-inflammatory effects that alleviate experimental colitis. Synergistic interactions—such as GLP-1/PYY co-administration, PYY-stimulated APOA4 production, and APOA4-enhanced CCK activity—suggest that multi-hormone combinations may offer amplified therapeutic benefits. While preclinical data are promising, clinical evidence supporting gut hormone therapies in IBD remains limited. Dual GIP/GLP-1 receptor agonists improve metabolic and inflammatory parameters, but in clinical use, they are associated with gastrointestinal side effects that warrant further investigation. Future research should evaluate combination therapies in preclinical IBD models, elucidate shared neural and receptor-mediated pathways, and define optimal strategies for applying gut hormone synergy in human IBD. These efforts may uncover safer, metabolically tailored treatments for IBD, particularly in patients with coexisting obesity or metabolic dysfunction. Full article

Rheumatoid arthritis (RA) is a chronic autoimmune disease that has a serious impact on both human health and animal production. The gut microbiota is a large and complex symbiotic ecosystem in animals, and the imbalance of gut microbiota is closely related to the pathogenesis of numerous diseases, including RA. The interactions among the gut microbiota, intestinal barrier, and immune system play key roles in maintaining intestinal homeostasis and affecting the development of RA. Regulating intestinal flora and metabolites provides new ideas for the prevention and treatment of RA. Probiotics can regulate the balance of intestinal flora and metabolites, improve the immune environment, and provide novel therapeutic strategies against RA. In order to summarize the role of gut microbiota and metabolite remodeling in the development and management of RA, this review will elaborate on the role of intestinal flora imbalance in the pathogenesis of RA and assess prospective therapeutic approaches that target the gut flora. Understanding the interaction among intestinal flora, metabolites, and RA will help to clarify the pathogenesis of RA and develop innovative and personalized therapeutic interventions against chronic autoimmune diseases. Full article

In dairy cattle, abomasal ulcers are a serious but sometimes disregarded ailment that can have detrimental effects on health and cause financial losses. Due to inconclusive clinical symptoms, abomasal ulcers are typically misdiagnosed and treated improperly. Specialized diagnostic methods should be considered to ensure a correct diagnosis and the well-being of cattle. This report focuses on a 4-year-old Holstein-Friesian cow which began her third lactation two weeks before she started showing general clinical signs of an elevated fat–protein ratio in the milk and was diagnosed with an abomasum displacement. The clinical signs can also be mistaken for other conditions such as traumatic reticuloperitonitis and left dislocated abomasum. The patient was brought to the LUHS Large Animal Clinic, and after a short while, sudden death occurred. The autopsy concluded that death had occurred due to hypovolemic shock caused by abomasal ulcer perforation, which caused bleeding into the abomasum and intestines. Also, the type 3 ulcer caused severe peritonitis and anemia, and feed and fibrin could be seen on the outside of organs in the abdomen. Blood clots mixed with feed had formed in the inside of the abomasum and intestinal tract. Based on the work of previous scientific studies, it has been established that the occurrence of ulcers is more frequent in dairy cows during the first four to six weeks of lactation. And the most probable cause could be intensive feeding and dietary changes. Ulcers in the abomasum are very difficult to diagnose, because they require special diagnostic equipment such as an ultrasound or surgical interventions. Due to the similarity with other diseases, this pathological condition of the abomasum is most frequently only identified in post-mortem examinations. Full article

Chronic inflammatory enteropathies (CIEs) in companion animals represent a group of idiopathic, immune-mediated gastrointestinal disorders in which the intestinal epithelium can be altered, affecting intestinal functionality, nutrient absorption, and microbiota composition. This review presents an overview of markers that could be used for the assessment of intestinal health, focusing extensively on functional biomarkers, with particular attention to fatty acids (including short-chain fatty acids, SCFAs) and amino acids. Studies have consistently shown reduced concentrations of SCFAs in companion animals with CIEs compared to healthy groups. These alterations occur with varying intensity depending on the type of enteropathy. Alterations in saturated, monounsaturated, and long-chain polyunsaturated fatty acids have also been reported in blood and feces, particularly in omega-3 and omega-6 derivatives, as well as in the elongase and desaturase indices responsible for endogenous synthesis. In addition, amino acids serve as precursors to key metabolites involved in mucosal immunity, oxidative stress regulation, and microbial homeostasis. In CIEs, alterations in systemic and fecal amino acid profiles have been observed, reflecting both host metabolic adaptation and microbial dysbiosis. Integrating fatty acid and amino acid profiles can help distinguish different types of enteropathies, providing additional discriminatory power for determining response to dietary treatment. Future research should aim to elucidate the causal relationships between metabolic alterations and disease pathogenesis, which could lead to novel dietary interventions targeting metabolic interactions between the microbiota and the host. Full article

The development of reversible animal models for the study of intestinal pathologies is essential to reduce the number of animals used in research and to better understand disease mechanisms. In this study, we present a reversible model of intestinal malabsorption through the administration of sublethal doses of ebulin-f, a ribosome-inactivating protein, and validate its usefulness by monitoring vitamin C absorption. The scientific community increasingly recognizes the importance of rationalizing experimental designs, optimizing treatment protocols, and minimizing the use of animals in research models. Thus, new methodologies are needed to minimize invasive sampling and to develop reversible animal models that recover physiologically post-study. Such models are essential for in vivo studies of human pathologies. Sublethal doses of ebulin-f (2.5 mg/kg) administered intraperitoneally to female Swiss CD1 mice (n = 6 per group) can cause reversible intestinal alterations in the small intestine, which offer the possibility of having a valuable reversible study model of malabsorption for the investigation of this syndrome. To verify whether nutrient absorption is altered, we used vitamin C as a traceable nutrient that can be quantified in the blood. Peripheral blood samples were collected through the retro-orbital area at 30, 80, 120, 180, and 1440 min post-administration, treated with DTT and MPA, and analyzed using a validated UV/Vis–HPLC method to indirectly determine vitamin C absorption by enterocytes. Pharmacokinetic analysis revealed significantly increased vitamin C absorption on days 1 and 3 post-treatment (AUC values of 3.65 × 10⁴ and 7.10 × 10⁴, respectively) compared to control (0.94 × 10⁴), with partial recovery by day 22 (3.27 × 10⁴). Blood concentration profiles indicate that intestinal damage peaks at day 3, followed by significant regeneration by day 22, establishing this as a viable reversible model for inflammatory bowel disease research. Full article

Inflammatory bowel disease (IBD) and primary sclerosing cholangitis (PSC) are related diseases with poorly understood pathophysiology. While therapy options for IBD have increased, treatment options for PSC remain limited. Galectin-3 is a multifunctional lectin expressed in intestinal epithelial cells, and is abundant in immune cells such as macrophages, with roles in cell adhesion, apoptosis, inflammation and fibrosis being associated with IBD and PSC disease development and progression. In addition, galectin-3 is also a visceral fat-derived protein whose systemic levels are increased in obese individuals, the latter correlating with a poorer prognosis in IBD and PSC patients. On the other hand, decreased galectin-3 expression in the inflamed mucosal tissues of mice and patients with IBD possibly indicate a protective role of this lectin in IBD. However, galectin-3 loss or inhibition is protective in most animal models of liver fibrosis but exacerbates the severity of autoimmune liver disease. Hence, with PSC being a slowly progressing autoimmune hepatobiliary disease closely related to IBD, further studies evaluating galectin-3 as a therapeutic target or biomarker for the severity of IBD and the occurrence of PSC are still needed. This review summarizes studies that have analyzed expression patterns and functions of galectin-3 in IBD and PSC. Current evidence suggests that strategies to block galectin-3 are not advised for patients with IBD and PSC-IBD. Full article

The Roma population is one of Europe’s largest ethnic minorities, often living in inadequate living conditions, worse than those of the majority population. They frequently lack access to essential services, even in high-income countries. This lack of basic services—particularly in combination with proximity to (stray) animals and human and solid waste—significantly increases environmental health risks, and leads to a higher rate of endoparasitic infections. Our study sheds light on the living conditions and health situation in Roma communities in Slovakia, focusing on the prevalence of intestinal endoparasitic infections across various settlement localisations. It highlights disparities and challenges in access to safe drinking water, sanitation, and hygiene (WASH) and other potentially disease-exposing factors among these marginalised populations. This study combines a comprehensive review of living conditions as per national data provided through the Atlas of Roma communities with an analysis of empirical data on parasitological infection rates in humans, animals, and the environment in settlements, applying descriptive statistical methods. It is the first study in Europe to provide detailed insights into how living conditions vary and cause health risks across Roma settlements, ranging from those integrated within villages (inside, urban), to those isolated on the outskirts (edge, sub-urban) or outside villages (natural/rural). Our study shows clear disparities in access to services, and in health outcomes, based on where people live. Our findings underscore the fact that (i) place—geographical centrality in particular—in an already challenged population group plays a major role in health inequalities and disease exposure, as well as (ii) the urgent need for more current and comprehensive data. Our study highlights persistent disparities in living conditions within high-income countries and stresses the need for greater attention and more sensitive targeted health-promoting approaches with marginalised communities in Europe that take into consideration any and all of the humans, ecology, and animals affected (=One Health). Full article

The main aspects of brucellosis have been studied in animal models to better understand the pathogenesis of the disease. Mice are the most common animal model of brucellosis. To verify that the infection has been successfully induced, it is necessary to assess the presence of Brucella in experimentally infected mice. Traditionally, high doses of Brucella have been used to establish detectable infection in oral murine models but prevent the emulation of natural pathogenesis. We propose the use of a low dose (1 × 10⁶ CFUs) to establish a more realistic oral infection model. Using a two-step procedure consisting of selective broth enrichment followed by agar isolation, we were able to recover bacteria from gut-associated lymphoid tissues (mesenteric lymph nodes and Peyer’s patches), the spleen, and feces during the early and late stages of infection (1 h and up to 5 weeks). This technique promotes the study of early infection stages and systemic dissemination without the need for high doses to induce infection orally. It also demonstrates that Brucella remains in the intestinal-associated lymphoid tissues at time points when the infection is already systemically established. Full article

The gut serves as the main site for nutrient digestion and absorption. Simultaneously, it functions as the body’s largest immune organ, playing a dual role in sustaining physiological equilibrium and offering immunological defense against intestinal ailments. Maintaining the structural and functional integrity of the intestine is paramount for ensuring animal health and productivity. Puerarin, a naturally derived isoflavonoid from the Pueraria species, exhibits multifaceted bioactivities, such as antioxidant, anti-inflammatory, antimicrobial, and immunomodulatory properties. Emerging evidence highlights puerarin’s capacity to enhance gut health in farm animals through four pivotal mechanisms: (1) optimization of intestinal morphology via crypt-villus architecture remodeling, (2) augmentation of systemic and mucosal antioxidant defenses through Nrf2/ARE pathway activation, and (3) reinforcement of intestinal barrier function by regulating tight junction proteins (e.g., ZO-1, occludin), mucin secretion, intestinal mucosal immune barrier, the composition of microbiota, and the derived beneficial metabolites; (4) regulating the function of the intestinal nervous system via reshaping the distribution of intestinal neurons and neurotransmitter secretion function. This review synthesizes current knowledge on puerarin’s protective effects on intestinal physiology in farm animals, systematically elucidates its underlying molecular targets (including TLR4/NF-κB, MAPK, and PI3K/Akt signaling pathways), and critically evaluates its translational potential in mitigating enteric disorders such as post-weaning diarrhea and inflammatory bowel disease in agricultural practices. Full article

Paratuberculosis, caused by Mycobacterium avium subspecies paratuberculosis (MAP), is a chronic granulomatous enteritis with significant implications for ruminant health, economic productivity, and potential zoonotic risk. This study investigated the expression of biomarkers of oxidative stress and apoptosis in goats naturally infected with MAP, focusing on three biological matrices: serum, intestinal mucosa, and mesenteric lymph nodes. Twenty MAP-positive goats and ten healthy controls were included. Serum and tissue levels of malondialdehyde (MDA), glutathione S-transferase (GST), glutathione peroxidase (GPX), superoxide dismutase (SOD), glutathione reductase (GSR), and caspase-3 were quantitatively assessed using ELISA tests. Gross and histopathological analyses confirmed MAP infection. Infected animals showed significantly elevated serum levels of MDA and caspase-3 (p < 0.001), along with decreased antioxidant enzyme activities (GSR, GST, GPX, SOD). Tissue analysis revealed increased MDA and caspase-3 levels, particularly in the intestinal mucosa compared to mesenteric lymph nodes, suggesting localized oxidative damage and apoptosis. Conversely, antioxidant enzyme activity was higher in mesenteric lymph nodes, indicating a compensatory response and a pronounced involvement of the intestinal tract. These findings demonstrate that MAP infection induces marked oxidative stress and apoptotic processes, especially in the intestinal mucosa. The imbalance between pro-oxidant and antioxidant systems may play a key role in the pathogenesis and chronic progression of the disease. Caspase-3 and MDA, in particular, have been identified as promising diagnostic or prognostic biomarkers for MAP infection. This study highlights the importance of developing improved diagnostic tools and therapeutic strategies targeting oxidative stress pathways in paratuberculosis. Full article

Viral infections have been associated with multiple sclerosis (MS), an immune-mediated disease in the central nervous system (CNS). Since Theiler’s murine encephalomyelitis virus (TMEV) can induce MS-like demyelination, TMEV infection is the most widely used viral model for MS. Although the precise pathophysiology is unknown, altered fecal bacterial populations were associated with distinct immune gene expressions in the CNS. We aimed to determine the role of gut microbiota in TMEV infection by administering an antibiotic cocktail in drinking water before (prophylactic administration) or after (therapeutic administration) TMEV infection. The antibiotic administration reduced total eubacteria, including the phyla Bacillota and Bacteroidota, but increased the phylum Pseudomonadata in feces. Prophylactic administration did not alter TMEV-induced inflammatory demyelination clinically or histologically, without changes in anti-viral IgG1/IgG2c levels or lymphoproliferative responses; therapeutic administration temporarily suppressed the neurological signs. Although antibiotic treatment had minimal effects on TMEV infection, adding metronidazole and ampicillin in drinking water substantially reduced water intake in the antibiotic group of mice, resulting in significant body weight loss. Since dehydration and stress could affect immune responses and gut microbiota, caution should be exercised when planning or evaluating the oral antibiotic cocktail treatment in experimental animals. Full article

Background/Objectives: Inflammatory bowel disease (IBD), encompassing Crohn’s disease and ulcerative colitis, is characterized by cycles of inflammation and tissue remodeling that can culminate in fibrosis. Differentiating between early inflammatory and fibrotic bowel wall changes remains a diagnostic challenge due to overlapping imaging features. This study aimed to assess the potential of elastography, specifically pixel histogram analysis, as a non-invasive method to identify acute inflammatory changes in a rat model of 2,4,6-trinitrobenzenesulfonic (TNBS)-induced colitis. Methods: Female CRL:Wi rats were randomized into control and experimental groups, with the latter receiving intracolonic TNBS to induce acute colitis. On day 7 post-induction, all animals underwent ultrasonographic and strain elastographic assessment of the distal colon using a standardized protocol. Histogram-based analysis of red, green, and blue pixel distributions was performed on elastographic video frames. Results were compared with histologic grading of inflammation and fibrosis using hematoxylin-eosin and Masson’s trichrome staining. Results: Rats with TNBS-induced colitis exhibited significant weight loss, increased bowel wall thickness (31.5% vs. controls, p < 0.01), and elevated elastographic pixel intensity across all color channels (p < 0.05). Histologically, experimental animals showed severe inflammation and early submucosal fibrosis. A strong positive correlation was found between elastographic histogram values and histologic fibrosis scores (r = 0.86, p < 0.01), confirming the technique’s diagnostic relevance. Conclusions: Elastographic pixel histogram analysis is a reproducible, non-invasive approach capable of distinguishing acute inflammatory changes and early fibrotic remodeling in experimental colitis. These findings support its potential application as a diagnostic adjunct in the early assessment and monitoring of IBD-related bowel wall changes. Full article