About

Melissa D. Bailey, OD, PhD, is a professor at The Ohio State University College of Optometry. Her research interests include soft contact lens fitting strategies, preventing adverse events associated with contact lens wear, and the lifelong development of the ciliary muscle. She is also a serial inventor with multiple U.S. and international patents. Dr. Bailey received her Doctor of Optometry and PhD in vision science from The Ohio State University. She was awarded the 2022 Innovator of the Year at OSU for her work in technology commercialization. Dr. Bailey enjoys teaching students about contact lenses within the optometry curriculum and also teaches graduate seminar courses.

Research topics

• Biology
• Medicine
• Internal medicine
• Immunology
• Bioinformatics
• Endocrinology
• Microbiology
• Political Science
• Genetics
• Ecology
• Gastroenterology
• Chemistry
• Neuroscience
• Cancer research
• Environmental health
• Cell biology
• Psychology

Selected publications

• A systematic assessment of the short- and long-term effects of commonly used breast cancer chemotherapeutics on the gut microbiome‒blood‒brain axis of female mice

  Gut Microbes · 2026-04-11

  articleOpen access

  Chemotherapy affects over 300,000 U.S. breast cancer patients, which disrupts the gut microbiome and induces gut inflammation-an effect hypothesized to drive gastrointestinal side effects (e.g., diarrhea, vomiting) experienced by 50%-80% of patients. Preclinical studies have found causal links amongst chemotherapy-induced gut microbiome disruption, systemic inflammation, and brain-mediated side effects. Therefore, the gut microbiome represents a therapeutic target to attenuate chemotherapy side effects. Because clinical populations are administered multiple chemotherapeutics in combination, a comprehensive understanding of which treatments disrupt the gut microbiome‒blood‒brain axis is lacking. Here, translationally-relevant regimens of four commonly used breast cancer chemotherapies (paclitaxel, cyclophosphamide, cisplatin, and doxorubicin) were given to adult female C57BL/6 mice, and inflammatory, metabolomics and/or bacteriome outcomes were measured in the gut, gut contents, blood, and brain tissues, along with a fatigue and anxiety-like behavioral assessment. Many inter-chemotherapy differences were observed but notable findings include prolonged circulation and central proinflammatory signals by paclitaxel and sustained disruption of the gut microbiome by cisplatin. In contrast, cyclophosphamide and doxorubicin modestly disrupted the gut microbiome‒blood‒brain axis. Taken together, this study systematically identified that paclitaxel and cisplatin most robustly disrupted the gut microbiome‒blood‒brain axis, suggesting that those treated with these drugs may benefit the most from gut-targeted interventions for associated side effects.

  PublisherDOI

• Abnormal intestinal microbial colonization in prenatally stressed offspring is related to lung and intestinal cytokine expression

  Frontiers in Microbiology · 2026-04-09

  articleOpen accessSenior author

  Introduction Prenatal stress (PNS) is associated with deleterious effects on childhood health and wellbeing. Among these consequential health repercussions, PNS-exposed children are at increased risk for acquiring early-life infections, with respiratory infections frequently reported. Stress-induced perturbations in the maternal microbiome during pregnancy represent a key link between stress in utero and aberrant offspring development and can drive abnormal pioneer colonization of offspring microbiomes. Methods Using a mouse model of PNS, we aimed to understand the extent to which these early-life intestinal microbial perturbations are related to intestinal and lung cytokine gene expression. The intestinal microbiome alongside intestinal and lung tissue gene expression were assessed over the first five weeks of life in PNS-exposed offspring to characterize basal cytokine differences in relation to intestinal microbial composition. Results In addition to significant changes in microbiome diversity and differential abundance, PNS offspring exhibited significant differences in ileal and lung cytokines characterized by overall increased interferon and proinflammatory gene signatures. PNS-associated microbiome changes also correlated to gene expression in both the ileum and lung. Finally, PNS-associated cytokine differences were not observed in MyD88 −/− offspring which lack the ability to initiate inflammatory responses through microbially-stimulated toll-like receptor signaling. Conclusion These findings suggest that PNS-mediated changes in the early-life microbiome are linked to respiratory and ileal immune development and the microbe-immune interactions are MyD88 pathway-dependent.

  PublisherDOI

• Gut microbiota and metabolite disruption during breast cancer chemotherapy is associated with peripheral neuropathy sensory symptoms and pain

  Brain Behavior and Immunity · 2026-02-19

  article
  PublisherDOI

• Biofilm state Limosilactobacillus reuteri modulates aryl hydrocarbon receptor activity and suppresses experimental necrotizing enterocolitis

  Pediatric Research · 2025-08-28 · 4 citations

  articleOpen access

  BACKGROUND: Decreased Aryl Hydrocarbon Receptor (AHR) signaling pathway activation is implicated in necrotizing enterocolitis (NEC) pathogenesis. Limosilactobacillus reuteri (Lr) is a probiotic that catabolizes tryptophan into AHR ligands. We have previously shown that Lr in its biofilm state has improved efficacy against NEC. However, the importance of the physiologic state of Lr (planktonic vs. biofilm) on AHR activation remains unknown. METHODS: In vitro experiments using intestinal epithelial cells (IEC) and in vivo experiments in premature rodents were carried out to assess the impact of planktonic- vs. biofilm-state Lr on AHR ligand production, AHR activation, and protection against NEC. RESULTS: Biofilm-state Lr was found to have increased persistence in the intestine of premature rodent pups compared to planktonic-state Lr. IECs exposed to conditioned media from Lr grown with tryptophan demonstrated increased AHR activation compared to IECs exposed to tryptophan alone. Finally, biofilm-state Lr was associated with increased intestinal AHR ligand production, AHR activation, and protection against NEC in rodent pups. CONCLUSION: Biofilm-state Lr has increased persistence in the gut and protects against NEC. This protection is associated with increased AHR activation in the intestine. Through improved understanding of the interactions of Lr and AHR signaling, we may be able to further enhance Lr efficacy against NEC. IMPACT: Limosilactobacillus reuteri in its biofilm state increases AHR activation and reduces intestinal injury during NEC. This is the first study to look at the role of the AHR signaling pathway in Limosilactobacillus reuteri-mediated protection against NEC. Development of an effective therapy to prevent NEC would reduce the morbidity and mortality of this lethal disease.

  PublisherOA PDFDOI

• Prebiotic fructan chain length influences enteric microbiota-host GABAergic signaling and intestinal motility

  The Journal of Nutritional Biochemistry · 2025-12-20

  articleOpen access

  Dietary fiber ingestion serves as a critical regulator of intestinal motility and the structure and function of the enteric microbiome. Yet, the extent to which subtle structural differences among fibers modulate motility via microbiota-host interactions remains undefined. GABA is a microbial metabolite intimately related to microbial fructan fermentation and host intestinal motility. The purpose of this study was to investigate how fructan chain length influenced microbiota-host signaling underlying ileal and colonic contractions. Male and female mice were pair-fed diets containing no fiber (fiber-free diet, FFD) or the same diet containing cellulose (CELL, fiber control), short-chain fructooligosaccharides (scFOS), or inulin (INU) for 2 weeks. scFOS and INU similarly enhanced total microbial load (fluorescence in situ hybridization), relative abundances of GABA-synthesizing bacteria (16S rRNA sequencing), and luminal GABA concentrations (ELISA) in the ileum and colon versus FFD. Conversely, scFOS altered expression (Fluidigm qPCR) of more motility- and GABA-related genes than INU in the ileum, whereas INU altered expression of more motility and GABA-related genes than scFOS in the colon. Incubation of ileal segments with GABA potentiated contraction force in INU but not scFOS ex vivo. Conversely, incubation of colon segments with GABA repressed contraction force in scFOS, reducing them to levels observed in INU with or without GABA. Notably, GABA altered contraction forces only in female mice. Our study highlights dietary fructan chain length as a determinant of segment- and sex-specific GABA-mediated intestinal motility and creates a rationale and framework for investigation of how prebiotic fiber structures influence microbiota-host interactions and physiology.

  PublisherDOI

• Social stress worsens colitis through β-adrenergic–driven oxidative stress in intestinal mucosal compartments

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-07-18 · 1 citations

  preprintOpen accessCorresponding

  Abstract Psychological stress is a known risk factor for inflammatory bowel disease (IBD), but the mechanisms linking stress to worsened disease remain unclear. Because distinct stress paradigms activate different neuroimmune circuits, it is critical to investigate model-specific effects. We examined how social stress primes the gut for heightened inflammation and whether this is mediated by specific neuroendocrine pathways, including α2-/β-adrenergic (sympathetic) or glucocorticoid/ corticotropin-releasing hormone receptor (CRHR1) (HPA axis) signaling. Mice were exposed to social disruption (SDR) stress and pre- treated with pharmacological antagonists targeting α2-adrenergic receptors (idazoxan), β-adrenergic receptor (β-AR) (propranolol), glucocorticoid receptor (mifepristone), or CRHR1 (antalarmin). Intestinal epithelial cell (IEC) gene expression and microbiota composition were assessed following SDR. To determine disease impact, SDR was combined with either Citrobacter rodentium infection or dextran sulfate sodium (DSS)-induced colitis, with interventions including the β-AR inhibitor propranolol and the NADPH oxidase inhibitor apocynin. SDR significantly upregulated expression of Dual oxidase 2 (Duox2) , Dual oxidase maturation factor 2 (Duoxa2) , and inducible nitric oxide synthase 2 (Nos2) in IECs (2- to 8- fold, p < 0.0001), effects reversed by β-AR blockade but not α2-adrenergic, CRH, or glucocorticoid inhibition. SDR also induced microbial dysbiosis, characterized by reduced alpha-diversity and compositional shifts, which was rescued by propranolol. Stress exacerbated disease severity in both infectious ( C. rodentium ) and chemically induced (DSS) colitis, amplifying colonic expression of Duox2 , Nos2 , and Ccl2, especially. Apocynin mitigated stress-induced ROS/RNS production and body weight loss even prior to colitis onset, reduced colonic gene expression of key oxidative enzymes, and alleviated both chemically and infectious colitis severity. These findings provide strong evidence that social stress sensitizes the gut to inflammation through β-adrenergic and NADPH oxidase–driven oxidative stress, highlighting potential therapeutic targets for mitigating stress-exacerbated IBD. Highlights Social disruption (SDR) and restraint stress (RST) activate distinct neuroendocrine pathways, with SDR driving epithelial ROS/RNS pathways via β-adrenergic signaling. β-adrenergic blockade prevents SDR-induced epithelial priming, microbial dysbiosis, and colitis exacerbation. NADPH oxidase inhibition with apocynin mitigates stress-induced oxidative stress and disease severity across different colitis models. Findings identify β-adrenergic and redox pathways as therapeutic targets for stress-exacerbated IBD.

  PublisherDOI

• Altered microbial carbohydrate metabolism is associated with anxiety and gastrointestinal symptoms in patients with Generalized Anxiety Disorder

  medRxiv · 2025-09-18

  preprintOpen access

  Abstract Background Generalized anxiety disorder (GAD) is a common psychiatric condition, with unknown etiology and pathophysiology. Recent studies have suggested alterations in the microbiota-gut-brain axis may be involved in the development of GAD. We aimed to explore the interactions between the gut microbiota, gastrointestinal and psychiatric symptoms, neuroimmune markers and dietary patterns in patients with GAD. Methods We recruited 83 GAD patients and 98 age- and sex-matched healthy controls (HC) and assessed their psychiatric and gastrointestinal symptoms, and long-term diet using validated questionnaires. We measured serum and stool neuroimmune markers and metabolites by ELISA and LC-MS, microbiota was analyzed using 16S rRNA gene sequencing with functional predictions by PICRUSt2. Microbial carbohydrate degradation capacity was assessed ex vivo . The data was analyzed using classical statistics and machine learning (XGBoost). Results GAD patients exhibited higher BMI, gastrointestinal symptoms and inflammatory markers, while reporting reduced intake of fiber and other macro- and micronutrients compared to HC. Gastrointestinal symptoms were the most predictive feature separating GAD from HC. GAD patients had a distinct microbiota profile, dominated by Bacteroides , compared with a Prevotella -dominated microbiota in HC. Carbohydrate degradation pathways were enriched in GAD and strongly associated with Bacteroides abundance. Anxiety scores correlated with Bacteroides abundance, carbohydrate degradation pathways and gastrointestinal symptoms, while negatively correlating with dietary fiber intake. Ex vivo mucin-to-inulin degradation ratio was higher in GAD and correlated with inflammatory markers. Conclusions GAD patients exhibited marked gastrointestinal symptoms, elevated immune markers, reduced fiber intake and a Bacteroides -dominated microbiota that preferentially degrades mucin. These data suggest that their microbiota adapted to utilize host-derived carbohydrates that may affect the mucus barrier, altering immune homeostasis and leading to gastrointestinal symptoms and anxiety. Dietary interventions, such as gradually increasing fiber intake, could reprogram bacterial carbohydrate metabolism, thus ameliorating gut barrier function and alleviating anxiety and gastrointestinal symptoms.

  PublisherOA PDFDOI

• Social stress worsens colitis through β-adrenergic–driven oxidative stress in intestinal mucosal compartments

  Brain Behavior and Immunity · 2025-12-17 · 1 citations

  articleOpen access

  Psychological stress is a known risk factor for inflammatory bowel disease (IBD), but the mechanisms linking stress to worsened disease remain unclear. Because distinct stress paradigms activate different neuroimmune circuits, it is critical to investigate model-specific effects. We examined how social stress primes the gut for heightened inflammation and whether this is mediated by specific neuroendocrine pathways, including α2-/β-adrenergic (sympathetic) or glucocorticoid/ corticotropin-releasing hormone receptor (CRHR1) (HPA axis) signaling. Mice were exposed to social disruption (SDR) stress and pre-treated with pharmacological antagonists targeting α2-adrenergic receptors (idazoxan), β-adrenergic receptor (β-AR) (propranolol), glucocorticoid receptor (mifepristone), or CRHR1 (antalarmin). Intestinal epithelial cell (IEC) gene expression and microbiota composition were assessed following SDR. To determine disease impact, SDR was combined with either Citrobacter rodentium infection or dextran sulfate sodium (DSS)-induced colitis, with interventions including the β-AR inhibitors and the NADPH oxidase inhibitor apocynin. SDR significantly upregulated expression of Dual oxidase 2 (Duox2), Dual oxidase maturation factor 2 (Duoxa2), and inducible nitric oxide synthase 2 (Nos2) in IECs (2- to 8-fold, p < 0.0001), effects reversed by β-AR blockade but not α2-adrenergic, CRH, or glucocorticoid inhibition. SDR also induced microbial dysbiosis, characterized by reduced α -diversity and compositional shifts, which was rescued by propranolol. Stress exacerbated disease severity in both infectious (C. rodentium) and chemically induced (DSS) colitis, amplifying colonic expression of Duox2, Nos2, and Ccl2, especially. Apocynin mitigated stress-induced ROS/RNS production and body weight loss even prior to colitis onset, reduced colonic expression of key oxidative enzymes, especially DUOX2, and alleviated both chemically and infectious colitis severity. These findings provide strong evidence that social stress sensitizes the gut to inflammation through β-adrenergic and NADPH oxidase-driven oxidative stress, highlighting potential therapeutic targets for mitigating stress-exacerbated IBD.

  PublisherDOI

• Solvaformer: an SE(3)-equivariant graph transformer for small molecule solubility prediction

  ArXiv.org · 2025-11-12 · 1 citations

  preprintOpen access

  Accurate prediction of small molecule solubility using material-sparing approaches is critical for accelerating synthesis and process optimization, yet experimental measurement is costly and many learning approaches either depend on quantumderived descriptors or offer limited interpretability. We introduce Solvaformer, a geometry-aware graph transformer that models solutions as multiple molecules with independent SE(3) symmetries. The architecture combines intramolecular SE(3)-equivariant attention with intermolecular scalar attention, enabling cross-molecular communication without imposing spurious relative geometry. We train Solvaformer in a multi-task setting to predict both solubility (log S) and solvation free energy, using an alternating-batch regimen that trains on quantum-mechanical data (CombiSolv-QM) and on experimental measurements (BigSolDB 2.0). Solvaformer attains the strongest overall performance among the learned models and approaches a DFT-assisted gradient-boosting baseline, while outperforming an EquiformerV2 ablation and sequence-based alternatives. In addition, token-level attention produces chemically coherent attributions: case studies recover known intra- vs. inter-molecular hydrogen-bonding patterns that govern solubility differences in positional isomers. Taken together, Solvaformer provides an accurate, scalable, and interpretable approach to solution-phase property prediction by uniting geometric inductive bias with a mixed dataset training strategy on complementary computational and experimental data.

  PublisherOA PDFDOI

• Comparing and optimizing protein extraction methods with different lysis buffers for the analyses of human fecal microbiome via metaproteomics approach

  Journal of Microbiological Methods · 2025-08-29

  articleOpen access

  Metaproteomic analysis offers critical insights into gut microbiome function; however, efficient microbial protein extraction from fecal samples remains challenging due to the complexity of different types of bacterial cell walls in the microbiome. In this study, we systematically compared three representative detergent-based lysis buffers (sodium dodecyl sulfate_urea, dodecyl β-D-maltoside_urea, sodium dodecyl sulfate_ dodecyl β-D-maltoside_urea) for metaproteomics sample preparation. After multiple levels of analyses, we identified SDS_DDM_urea as the most efficient option for extracting diverse microbial proteins, peptides, and identifying microbial species. Applying this optimized method to samples from a community based dietary intervention study (Summer Harvest Adventure), we found minimal group-level microbial diversity shifts during this type of intervention, but substantial individual-specific variations reflected by metaproteomics results. Functional analyses also revealed microbial protein changes, especially proteins related to metabolic adaptations, including enhanced carbohydrate metabolism, amino acid biosynthesis, vitamin transport, and increased expression of membrane-associated proteins. Our results highlighted the personalized microbiome response to dietary interventions and underscored the importance of selecting appropriate protein extraction methods to accurately capture microbiome functional dynamics in microbiome analyses via metaproteomics.

  PublisherDOI

Recent grants

• NIH Grant F31MH012458

  NIH · $61k

• Role of stress-induced reduction in lactobacillus reuteri on colonic inflammation

  NIH · $1.9M · 2012–2018

• Tunable Native Probiotic Formulations for the Treatment of NEC.

  NIH · $1.8M · 2017–2023

• Role of Commensal Microbiota in Stressor-Induced Immunomodulation

  NIH · $425k · 2014–2017

• Impact of Social Stress on TLR4-Induced Microbicidal Activity of CD11b+ Cells

  NIH · $149k · 2007–2010

Frequent coauthors

• John F. Sheridan

  147 shared

• Jeffrey D. Galley

  The Ohio State University Wexner Medical Center

  134 shared

• Tamar Gur

  The Ohio State University Wexner Medical Center

  90 shared

• Amy R. Mackos

  The Ohio State University

  68 shared

• Brett R. Loman

  60 shared

• David A. Padgett

  55 shared

• Helen J. Chen

  The Ohio State University Wexner Medical Center

  53 shared

• Ross Maltz

  41 shared

Labs

• Melissa Bailey LabPI

Awards & honors

• 2022 Innovator of the Year at The Ohio State University