Irritable Bowel Syndrome (IBS) is a symptom-based disorder with diverse causes. Growing evidence implicates the gut microbiome—bacteria, fungi, and their metabolites—as influential in symptom emergence and subtype differences. Researchers have identified multiple microbial markers that correlate with IBS risk, severity, or subtype, though no single pathogen explains all cases. For a detailed reference on markers, see [IBS Gut Microbiome Markers](https://www.innerbuddies.com/blogs/irritable-bowel-syndrome-ibs/ibs-gut-microbiome-markers). Common markers observed in comparative sequencing studies include fragments of Bacteroides fragilis enterotoxin genes, reduced levels of Bifidobacterium and Lactobacillus, overrepresentation of Proteobacteria (including Escherichia coli), altered short‑chain fatty acid (SCFA) profiles, microbial genes affecting serotonin pathways, and increased fungal abundance such as Candida. Each of these can influence barrier function, immune signaling, gas production, and motility. Bacteroides fragilis enterotoxins have been linked to increased intestinal permeability. When tight junctions are disrupted, bacterial products can access immune cells and amplify low‑grade inflammation—mechanisms that may underlie diarrhea‑predominant IBS (IBS‑D) in some patients. Restoring barrier integrity is therefore a research priority. Beneficial genera such as Bifidobacterium and Lactobacillus contribute to SCFA production (notably butyrate), limit opportunistic overgrowth, and support digestion of fermentable carbohydrates. Reductions in these taxa are commonly reported in IBS cohorts and may relate to constipation, bloating, and pain. Clinical trials suggest certain strains (for example, B. infantis 35624 or L. plantarum 299v) can provide symptom relief in subsets of patients. An increase in Proteobacteria and specific E. coli strains can promote endotoxin exposure (e.g., LPS), low‑grade inflammation, and gas production—factors associated with bloating and visceral hypersensitivity. Small intestinal bacterial overgrowth (SIBO) testing is sometimes used to detect pathogenic overgrowths that affect symptoms. SCFA imbalances also matter: lower butyrate is often noted in constipation‑predominant IBS (IBS‑C), slowing transit and impacting stool consistency, while different SCFA patterns may accelerate transit in IBS‑D. Diets that support SCFA production—resistant starches and varied plant fibers—can help rebalance metabolite profiles. Microbial modulation of tryptophan and serotonin pathways affects motility, secretion, and gut sensation; altered microbial enzymatic activity has been linked with symptom variability. Fungal dysbiosis (notably Candida) is less well characterized but may interact with bacterial communities to influence symptoms, particularly after antibiotic exposure. Markers interact: loss of beneficial bacteria can permit Proteobacteria expansion; toxin‑induced permeability can intensify immune responses to fungi and bacteria; motility changes reshape microbial communities. Because of these interdependencies, multi‑modal strategies—dietary adjustments, targeted probiotics and prebiotics, stress management, and selective antimicrobials when appropriate—are often more effective than single interventions. Lab tools include stool microbiome sequencing and metabolome analysis, SIBO breath testing, and inflammatory markers such as fecal calprotectin. For practical context on how individual microbiomes affect probiotic needs, see How Your Unique Microbiome Dictates Your Probiotic Needs and an overview at Gut Microbiome — The Good, The Bad, and The Ugly. Additional diagnostic options include stool tests such as Microbiome test. Ongoing research aims to define subtype‑specific signatures and develop precision interventions. For clinicians and patients, microbiome markers offer a promising avenue for more personalized, mechanism‑based IBS care.