Dr. Umar

ROS in gastrointestinal inflammation are both antimicrobial signals and drivers of tissue injury. This review links NOX/DUOX and mitochondrial ROS to IBD, showing that low ROS (oxidase variants) and high ROS (dysfunction/upregulation) can each promote pathology, with microbiome ties such as Proteobacteria expansion.

In mice lacking epithelial NOX activity, the gut microbiome adapts by enriching H2O2-producing lactobacilli. This community suppresses Citrobacter rodentium virulence by downregulating LEE genes (ler/escN), conferring transmissible protection that is lost with antibiotics or Western diet.

This review explains how NOX1/DUOX2/NOX2-derived ROS—especially H₂O₂—act as microbiome-relevant signals that regulate pathogen virulence, commensal ecology, and mucosal repair, and why ROS deficiency (not just excess) can drive severe IBD phenotypes.

This review explains how free radicals drive health and disease through oxidative and reductive stress, detailing mitochondrial and hyperglycemia-linked sources and why many antioxidants fail clinically. It proposes cold atmospheric plasma as a tunable redox therapy for both degenerative and proliferative disorders.

This mini review reframes oxidative stress as a mechanistically grounded redox imbalance affecting signaling and damage, warns against nonspecific “ROS” language and total antioxidant capacity testing, and emphasizes enzymatic antioxidant defenses. It offers no direct microbiome signatures but clarifies host redox biology relevant to disease interpretation.

EDTA is a metal-binding compound used as a blood anticoagulant and food stabilizer. By binding calcium, it can influence intestinal barrier integrity, and EDTA-based permeability tests are used in gut research. Experimental data also link EDTA exposure to worsened colitis in models.

EDTA worsened colitis and increased colitis-associated tumors in two IBD mouse models, disrupted epithelial barrier integrity, reduced microbiome diversity, and enriched Akkermansia muciniphila and Peptostreptococcaceae—supporting EDTA as a diet-linked driver of inflammatory dysbiosis and carcinogenesis risk.

Intestinal permeability to [51Cr]EDTA in asymptomatic Crohn’s disease closely reflects subclinical inflammation. Elevated urinary excretion often occurred despite normal serum markers and low CDAI, and aligned with positive Indium-111 leukocyte scans, suggesting permeability is a sensitive indirect indicator of mild–moderate active disease.

In 52Cr-EDTA intestinal permeability in Crohns disease, urinary 52Cr-EDTA excretion correlated with fecal calprotectin and showed dysbiosis-consistent trends (lower F. prausnitzii, higher Enterobacteriaceae). This non-radioactive test may support noninvasive monitoring of subclinical activity and barrier-focused phenotyping.

EDTA increases intestinal permeability in rats, boosting absorption of neutral, basic, and acidic poorly absorbed compounds and increasing reverse flux of inulin into the lumen. Findings imply calcium-chelation loosens epithelial barriers, with implications for oral drug delivery and microbiome-related biomarker interpretation.

This review explains how tight junction proteins and signaling pathways control intestinal permeability and how cytokines, pathogens, and microbiome-derived metabolites (especially SCFAs) disrupt or restore the barrier, shaping inflammatory and systemic disease risk.

EDTA anticoagulant diagnostic sample stability is strongest for hematology, nucleic acids, and protease-labile peptides, but EDTA can cause platelet clumping/pseudothrombocytopenia, interfere with some cytokine and troponin assays, and confound electrolytes via chelation or contamination.

Organophosphates are cholinesterase-inhibiting chemicals widely used as pesticides. Beyond neurotoxicity, evidence links chronic exposure to gut microbiome changes, barrier disruption, and metabolic effects. Microbiome medicine integrates exposure biomarkers and microbiome signatures to support personalized risk assessment.

Ambient long-term organophosphorus pesticide exposure gut microbiome signatures were associated with specific genus-level shifts and predicted functional changes (cell-wall/respiration pathways, reduced B1/B6 synthesis), despite no differences in overall microbiome diversity, in an older California cohort enriched for Parkinson’s disease.

This paper uses NHANES urinary dialkyl phosphate metabolites to estimate cumulative organophosphate exposure and compares results with EPA models, finding major model conservatism and key limitations of non-specific metabolites. Clinically, DAPs are best treated as screening biomarkers and exposure confounders in microbiome studies.

This mechanistic toxicology study shows that AChE inhibition explains most acute lethality from highly toxic organophosphorus agents. Steep dose–response slopes across species and strong correlations between enzyme inhibition/reactivation kinetics and survival support AChE inhibition as the dominant mechanism.

This review explains how AChE inhibition triggers respiratory failure and SE after organophosphate exposure, and how SE drives excitotoxic, oxidative, and inflammatory brain injury. Chronic low-dose effects may occur without SE. No microbiome signatures or microbial biomarkers are reported.

Calprotectin is a neutrophil-derived protein complex measured in stool to detect intestinal inflammation. It helps distinguish IBD from functional bowel disorders and reflects mucosal immune activity that can reshape microbiome composition through antimicrobial metal sequestration.

In older adults, higher fecal calprotectin tracked with fecal calprotectin gut dysbiosis: more pro-inflammatory taxa, fewer SCFA producers, increased IL-17C/CCL19, and markedly higher indoxyl sulfate (microbiome-mediated), alongside higher BMI/obesity and more heart attack history.

This meta-analysis supports fecal calprotectin relapse prediction in adult IBD remission, identifying an optimal FC threshold of 152 µg/g with pooled sensitivity 0.72 and specificity 0.74. FC helps stratify relapse risk and can complement microbiome profiling by anchoring host inflammatory activity.

This meta-analysis shows faecal calprotectin to distinguish IBD from IBS has high pooled sensitivity (85.8%) and specificity (91.7%). It performs best as a rule-out test, with NPV 99.8% at 1% IBD prevalence. Optimal sensitivity appears at cut-offs ≤50 μg/g

Calprotectin-limits-Aspergillus-hyphal-growth by chelating zinc and manganese, restricting invasive hyphae in murine fungal keratitis. Protection is restored with recombinant calprotectin and depends on intact Zn/Mn binding, while conidial killing is calprotectin-independent. Fungal ZafA-mediated zinc uptake confers resistance and virulence.

This study shows that manganese sequestration by calprotectin is essential for maximal inhibition of multiple bacterial pathogens. A unique six-histidine Mn²⁺-binding site (enabled by the S100A9 tail) explains calprotectin’s broad antimicrobial activity and its suppression of Mn-dependent oxidative stress defenses.

This review summarizes evidence that fecal calprotectin is a stable, noninvasive stool biomarker reflecting neutrophilic intestinal inflammation, reliably distinguishing IBD from IBS, correlating with endoscopic/histologic activity, predicting relapse, and detecting pouchitis—useful for inflammation phenotyping alongside microbiome signatures.