Professor, Pathology and Laboratory Medicine, Emory University School of Medicine
Pathology
Dr. Andrew S. Neish, MD
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Andrew S. Neish, MD works in the field of Pathology. He researched medicine at University of North Carolina at Chapel Hill School of Medicine. University of North Carolina at Chapel Hill School of Medicine is a one of the best medicals schools. University of North Carolina at Chapel Hill School of Medicine has a rank of 22 in research and a 2 in primary care Andrew Neish is a published doctor as well. He has 45 publications published. The latest was: O-012The Intestinal Wound Regeneration Modulates Mucosal Microenvironment to Stimulate Expansion of a Local Pro-restitutive Microbiota. He accepts Medicare payments and is registered with Medicare.gov.
Publications
- O-012 The Intestinal Wound Regeneration Modulates Mucosal Microenvironment to Stimulate Expansion of a Local Pro-restitutive Microbiota.
- Epithelial adhesion mediated by pilin SpaC is required for Lactobacillus rhamnosus GG-induced cellular responses.
- Mucosal immunity and the microbiome.
- Symbiotic lactobacilli stimulate gut epithelial proliferation via Nox-mediated generation of reactive oxygen species.
- Redox signaling regulates commensal-mediated mucosal homeostasis and restitution and requires formyl peptide receptor 1.
- Redox signaling mediated by the gut microbiota.
- Nox Enzymes and New Thinking on Reactive Oxygen: A Double-Edged Sword Revisited.
- Annexin A1, formyl peptide receptor, and NOX1 orchestrate epithelial repair.
- Microbial-induced immunomodulation by targeting the NF-?B system.
- Enteric commensal bacteria induce ERK pathway signaling via formyl peptide receptor (FPR)-dependent redox modulation of Dual specific phosphatase 3 (DUSP3).
- The Salmonella effector AvrA mediates bacterial intracellular survival during infection in vivo.
- Enteric commensal bacteria potentiate epithelial restitution via reactive oxygen species-mediated inactivation of focal adhesion kinase phosphatases.
- The Microbiota and Colonic Neoplasia: An Emerging Link?
- Expression profiling and pathway analysis of Krüppel-like factor 4 in mouse embryonic fibroblasts.
- Commensal-epithelial signaling mediated via formyl peptide receptors.
- Lactobacillus rhamnosus blocks inflammatory signaling in vivo via reactive oxygen species generation.
- Toll-like receptor 5-dependent regulation of inflammation in systemic Salmonella enterica Serovar typhimurium infection.
- Microbes in gastrointestinal health and disease.
- The bacterial fermentation product butyrate influences epithelial signaling via reactive oxygen species-mediated changes in cullin-1 neddylation.
- The probiotic Lactobacillus GG may augment intestinal host defense by regulating apoptosis and promoting cytoprotective responses in the developing murine gut.
- Flagellin treatment protects against chemicals, bacteria, viruses, and radiation.
- Salmonella AvrA Coordinates Suppression of Host Immune and Apoptotic Defenses via JNK Pathway Blockade.
- Toll-like receptor 5-deficient mice have dysregulated intestinal gene expression and nonspecific resistance to Salmonella-induced typhoid-like disease.
- Deletion of TLR5 results in spontaneous colitis in mice.
- Activation of toll-like receptor 3 protects against DSS-induced acute colitis.
- Antiinflammatory adaptation to hypoxia through adenosine-mediated cullin-1 deneddylation.
- TLRS in the gut. II. Flagellin-induced inflammation and antiapoptosis.
- Flagellin suppresses epithelial apoptosis and limits disease during enteric infection.
- TLR5-mediated phosphoinositide 3-kinase activation negatively regulates flagellin-induced proinflammatory gene expression.
- Flagellin/TLR5 responses in epithelia reveal intertwined activation of inflammatory and apoptotic pathways.
- Cutting edge: bacterial modulation of epithelial signaling via changes in neddylation of cullin-1.
- Activation of beta-catenin by carcinogenic Helicobacter pylori.
- Protein kinase R mediates intestinal epithelial gene remodeling in response to double-stranded RNA and live rotavirus.
- STAT signaling underlies difference between flagellin-induced and tumor necrosis factor-alpha-induced epithelial gene expression.
- Bacterial activation of beta-catenin signaling in human epithelia.
- Paneth cell cryptdins act in vitro as apical paracrine regulators of the innate inflammatory response.
- Molecular aspects of intestinal epithelial cell-bacterial interactions that determine the development of intestinal inflammation.
- Bacterial inhibition of eukaryotic pro-inflammatory pathways.
- Flagellin is the major proinflammatory determinant of enteropathogenic Salmonella.
- TLR5-mediated activation of p38 MAPK regulates epithelial IL-8 expression via posttranscriptional mechanism.
- Beta defensin-1, parvalbumin, and vimentin: a panel of diagnostic immunohistochemical markers for renal tumors derived from gene expression profiling studies using cDN...
- Cutting edge: Salmonella AvrA effector inhibits the key proinflammatory, anti-apoptotic NF-kappa B pathway.
- Lipoxin a4 analogs attenuate induction of intestinal epithelial proinflammatory gene expression and reduce the severity of dextran sodium sulfate-induced colitis.
- Mechanisms of active intestinal inflammation and potential down-regulation via lipoxins.
Schools
University of North Carolina At Chapel Hill
Brigham and Women39s Hospital
Doctors Specialties
- Anatomic Pathology
- Pathology
Accepted Insurances
Education
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Brigham and Women's Hospital -
University of North Carolina at Chapel Hill School of Medicine
Hospital
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Emory University Hospital
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1316996382 |
| Last Name Of The Provider | NEISH |
| First Name Of The Provider | ANDREW |
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