Background/Objectives: Small Intestinal Bacterial Overgrowth (SIBO) and Small Intestinal Fungal Overgrowth (SIFO) are distinct yet often overlapping conditions characterized by an abnormal increase in microbial populations within the small intestine. SIBO results from an overgrowth of colonic bacteria, while SIFO is driven by fungal overgrowth, primarily involving Candida species. Both conditions present with nonspecific gastrointestinal (GI) symptoms such as bloating, abdominal pain, diarrhea, and malabsorption, making differentiation between SIBO and SIFO challenging. This review aims to elucidate the underlying mechanisms, risk factors, diagnostic challenges, and management strategies associated with SIBO and SIFO. Methods: A comprehensive review of current literature was conducted, focusing on the pathophysiology, diagnostic modalities, and therapeutic approaches for SIBO and SIFO. Results: SIBO is commonly associated with factors such as reduced gastric acid secretion, impaired gut motility, and structural abnormalities like bowel obstruction and diverticula. It is frequently diagnosed using jejunal aspirates (≥105 colony forming units (CFUs)/mL) or breath tests. In contrast, SIFO is linked to prolonged antibiotic use, immunosuppression, and gut microbiome dysbiosis, with diagnosis relying on fungal cultures from small intestinal aspirates due to the absence of standardized protocols. Conclusion: The clinical overlap and frequent misdiagnosis of SIBO and SIFO highlight the need for improved diagnostic tools and a multidisciplinary approach to management. This review emphasizes the importance of understanding the mechanisms behind SIBO and SIFO, how they relate to other health outcomes, and potential management strategies to optimize patient care and therapeutic outcomes.
Mesenchymal stem cell (MSC)-seeded polymeric perivascular wraps have been shown to enhance arteriovenous fistula (AVF) maturation. However, the wraps’ radiolucency makes their placement and integrity difficult to monitor. Through electrospinning, we infused gold nanoparticles (AuNPs) into polycaprolactone (PCL) wraps to improve their radiopacity and tested whether infusion affects the previously reported beneficial effects of the wraps on the AVF’s outflow vein. Sprague Dawley rat MSCs were seeded on the surface of the wraps. We then compared the effects of five AVF treatments—no perivascular wrap (i.e., control), PCL wrap, PCL + MSC wrap, PCL-Au wrap, and PCL-Au + MSC wrap—on AVF maturation in a Sprague Dawley rat model of chronic kidney disease (n = 3 per group). Via micro-CT, AuNP-infused wraps demonstrated a significantly higher radiopacity compared to that of the wraps without AuNPs. Wraps with and without AuNPs equally reduced vascular stenoses, as seen via ultrasonography and histomorphometry. In the immunofluorescence analysis, representative MSC-seeded wraps demonstrated reduced neointimal staining for markers of infiltration with smooth muscle cells (α-SMA), inflammatory cells (CD45), and fibroblasts (vimentin) compared to that of the control and wraps without MSCs. In conclusion, AuNP infusion allows in vivo monitoring via micro-CT of MSC-seeded polymeric wraps over time, without compromising the benefits of the wrap for AVF maturation.
Oral mucositis (OM) is a common and clinically impactful side effect of cytotoxic cancer treatment, particularly in patients with head and neck squamous cell carcinoma (HNSCC) who undergo radiotherapy with or without concomitant chemotherapy. The etiology and pathogenic mechanisms of OM are complex, multifaceted and elicit both direct and indirect damage to the mucosa. In this narrative review, we describe studies that use various omics methodologies (genomics, transcriptomics, microbiomics and metabolomics) in attempts to elucidate the biological pathways associated with the development or severity of OM. Integrating different omics into multi-omics approaches carries the potential to discover links among host factors (genomics), host responses (transcriptomics, metabolomics), and the local environment (microbiomics).
The ability of probiotics, comprising live microbiota, to modulate the composition of intestinal microbiomes has been connected to modulation of the central nervous system (Gut–Brain axis), neuroendocrine system (Gut–Skin axis), and immune response (Gut–Immune axis). Less information is known regarding the ability of postbiotics (cell wall components and secreted metabolites derived from live organisms) to regulate host immunity. In the present study, we tested postbiotics comprising single strains of bacteria and yeast (Lactobacillus acidophilus 16axg, Lacticaseibacillus rhamnosus 18fx, Saccharomyces cerevisiae var. boulardii 16mxg) as well as combinations of multiple strains for their ability to stimulate cytokine production by human CD14+ monocytes. We quantified cytokine gene and protein expression levels in monocytes following stimulation with postbiotics. Both heat-killed L. acidophilus and L. rhamnosus stimulated naïve monocytes without significant differences between them. Heat-killed S. boulardii stimulated less cytokine production compared to postbiotic bacteria at the same concentration. Interestingly, the addition of heat-killed yeast to heat-killed L. acidophilus and L. rhamnosus resulted in an enhancement of immune stimulation. Thus, heat-killed postbiotics have immune-modulating potential, particularly when bacteria and yeast are combined. This approach may hold promise for developing targeted interventions that can be fine-tuned to modulate host immune response with beneficial health impact.