Xiaolun Sun
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Associate Professor
Also affiliated: University of North Carolina at Chapel Hill (2009–2020); University of Florida Health (2013–2018); University of Florida (2013–2019); Virginia Tech (2005–2007)
Poultry Science
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Xiaolun Sun is an Assistant Professor in Poultry Science at the Arkansas Agricultural Experiment Station. His research focuses on the interplay between host-microbe interactions and immune responses, particularly concerning gastrointestinal health in poultry and its relevance to human health.
Sun's work investigates the mechanisms by which specific bacteria, such as *Clostridium perfringens* and *Salmonella Enteritidis*, influence host health. This includes studying the role of microbial metabolites, like secondary bile acids, in modulating bacterial virulence and host immune responses. He has published research examining how compounds such as sodium butyrate and natural compounds like resveratrol can impact host defense pathways, including the NF-κB signaling pathway, and affect inflammation and vascular function in models involving mice and human endothelial cells.
His research also extends to the development of strategies to prevent and control enteric diseases in poultry. This includes exploring the efficacy of vaccines based on bacterial sporulation proteins and the use of recombinant enzymes to enhance the effectiveness of antimicrobial compounds. Sun's scholarship metrics include an h-index of 21 and over 1,700 citations across 64 publications. He actively collaborates with researchers at the University of Arkansas at Fayetteville.
Metrics
- h-index: 21
- Publications: 64
- Citations: 1,810
Positions
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Associate Professor 2023–presentUniversity of Arkansas UADA | POSC | Department of Poultry Science ORCID
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Assistant Professor 2016–presentUniversity of Arkansas Fayetteville Poultry Science ORCID
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Research Assistant Professor 2013–2016University of Florida Medicine ORCID
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Postdoc 2008–2013University of North Carolina at Chapel Hill Medicine ORCID
Selected Publications
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The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid (2025)
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Identification of Salt Tolerance and Stress Response in US Department of Agriculture Tomato Germplasm at the Seedling Stage (2024)
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Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence (2024)
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Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence (2023)
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Essential Oils as an Alternative to Antibiotics to Reduce the Incidence and Severity of Necrotic Enteritis in Broiler Chickens: A Short Review (2023)
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Vaccines Using Clostridium perfringens Sporulation Proteins Reduce Necrotic Enteritis in Chickens (2022)
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Clostridium perfringens-Induced Necrotic Diseases: An Overview (2022)
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Triterpenoid CDDO-IM protects against lipopolysaccharide-induced inflammatory response and cytotoxicity in macrophages: The involvement of the NF-κB signaling pathway (2022)
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Natural Compound Resveratrol Attenuates TNF-Alpha-Induced Vascular Dysfunction in Mice and Human Endothelial Cells: The Involvement of the NF-κB Signaling Pathway (2021)
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Microbiota from Specific Pathogen-Free Mice Reduces Campylobacter jejuni Chicken Colonization (2021)
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Specific Secondary Bile Acids Control Chicken Necrotic Enteritis (2021)
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Sodium butyrate modulates chicken macrophage proteins essential for Salmonella Enteritidis invasion (2021)
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Microbiota attenuates chicken transmission-exacerbated campylobacteriosis in Il10−/− mice (2020)
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Sodium Butyrate Reduces Salmonella Enteritidis Infection of Chicken Enterocytes and Expression of Inflammatory Host Genes in vitro (2020)
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Role of Gut Microbiome in Colorectal Cancer (2020)
Collaboration Network
Top Collaborators
- A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens
- Microbial metabolite deoxycholic acid controls Clostridium perfringens-induced chicken necrotic enteritis through attenuating inflammatory cyclooxygenase signaling
- Microbial metabolite deoxycholic acid shapes microbiota against Campylobacter jejuni chicken colonization
- Sodium Butyrate Reduces Salmonella Enteritidis Infection of Chicken Enterocytes and Expression of Inflammatory Host Genes in vitro
- Specific Secondary Bile Acids Control Chicken Necrotic Enteritis
Showing 5 of 12 shared publications
- A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens
- Microbial metabolite deoxycholic acid controls Clostridium perfringens-induced chicken necrotic enteritis through attenuating inflammatory cyclooxygenase signaling
- Microbial metabolite deoxycholic acid shapes microbiota against Campylobacter jejuni chicken colonization
- Microbial metabolite deoxycholic acid shapes microbiota against Campylobacter jejuni chicken colonization
- Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence
Showing 5 of 9 shared publications
- A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens
- Microbial metabolite deoxycholic acid shapes microbiota against Campylobacter jejuni chicken colonization
- Specific Secondary Bile Acids Control Chicken Necrotic Enteritis
- Vaccines Using Clostridium perfringens Sporulation Proteins Reduce Necrotic Enteritis in Chickens
- Microbial metabolite deoxycholic acid shapes microbiota against Campylobacter jejuni chicken colonization
Showing 5 of 9 shared publications
- A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens
- Clostridium perfringens-Induced Necrotic Diseases: An Overview
- Specific Secondary Bile Acids Control Chicken Necrotic Enteritis
- Vaccines Using Clostridium perfringens Sporulation Proteins Reduce Necrotic Enteritis in Chickens
- Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence
Showing 5 of 9 shared publications
- Clostridium perfringens-Induced Necrotic Diseases: An Overview
- Specific Secondary Bile Acids Control Chicken Necrotic Enteritis
- Vaccines Using Clostridium perfringens Sporulation Proteins Reduce Necrotic Enteritis in Chickens
- Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence
- Microbiota attenuates chicken transmission-exacerbated campylobacteriosis in Il10−/− mice
Showing 5 of 8 shared publications
- A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens
- Microbial metabolite deoxycholic acid controls Clostridium perfringens-induced chicken necrotic enteritis through attenuating inflammatory cyclooxygenase signaling
- Microbial metabolite deoxycholic acid shapes microbiota against Campylobacter jejuni chicken colonization
- Specific Secondary Bile Acids Control Chicken Necrotic Enteritis
- Microbial metabolite deoxycholic acid shapes microbiota against Campylobacter jejuni chicken colonization
Showing 5 of 7 shared publications
- A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens
- Microbial metabolite deoxycholic acid controls Clostridium perfringens-induced chicken necrotic enteritis through attenuating inflammatory cyclooxygenase signaling
- Microbial metabolite deoxycholic acid shapes microbiota against Campylobacter jejuni chicken colonization
- Microbial metabolite deoxycholic acid shapes microbiota against Campylobacter jejuni chicken colonization
- Microbial metabolite deoxycholic acid controls Clostridium perfringens -induced chicken necrotic enteritis through attenuating cyclooxygenase signaling
- Microbiome modulates intestinal homeostasis against inflammatory diseases
- Natural Compound Resveratrol Attenuates TNF-Alpha-Induced Vascular Dysfunction in Mice and Human Endothelial Cells: The Involvement of the NF-κB Signaling Pathway
- NADPH-quinone oxidoreductase-1 mediates Benzo-[a]-pyrene-1,6-quinone-induced cytotoxicity and reactive oxygen species production in human EA.hy926 endothelial cells
- Targeting glutathione with the triterpenoid CDDO-Im protects against benzo-a-pyrene-1,6-quinone-induced cytotoxicity in endothelial cells
- Triterpenoid CDDO-IM protects against lipopolysaccharide-induced inflammatory response and cytotoxicity in macrophages: The involvement of the NF-κB signaling pathway
- A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens
- Sodium Butyrate Reduces Salmonella Enteritidis Infection of Chicken Enterocytes and Expression of Inflammatory Host Genes in vitro
- Specific Secondary Bile Acids Control Chicken Necrotic Enteritis
- Sodium butyrate modulates chicken macrophage proteins essential for Salmonella Enteritidis invasion
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
- A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens
- Specific Secondary Bile Acids Control Chicken Necrotic Enteritis
- Sodium butyrate modulates chicken macrophage proteins essential for Salmonella Enteritidis invasion
- Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
- A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens
- Microbial metabolite deoxycholic acid controls Clostridium perfringens-induced chicken necrotic enteritis through attenuating inflammatory cyclooxygenase signaling
- Microbiota from Specific Pathogen-Free Mice Reduces Campylobacter jejuni Chicken Colonization
- Microbial metabolite deoxycholic acid controls Clostridium perfringens -induced chicken necrotic enteritis through attenuating cyclooxygenase signaling
- Microbial metabolite deoxycholic acid controls Clostridium perfringens-induced chicken necrotic enteritis through attenuating inflammatory cyclooxygenase signaling
- Essential Oils as an Alternative to Antibiotics to Reduce the Incidence and Severity of Necrotic Enteritis in Broiler Chickens: A Short Review
- Microbial metabolite deoxycholic acid controls Clostridium perfringens -induced chicken necrotic enteritis through attenuating cyclooxygenase signaling
- Microbial metabolite deoxycholic acid controls Clostridium perfringens-induced chicken necrotic enteritis through attenuating inflammatory cyclooxygenase signaling
- Essential Oils as an Alternative to Antibiotics to Reduce the Incidence and Severity of Necrotic Enteritis in Broiler Chickens: A Short Review
- Microbial metabolite deoxycholic acid controls Clostridium perfringens -induced chicken necrotic enteritis through attenuating cyclooxygenase signaling
- NADPH-quinone oxidoreductase-1 mediates Benzo-[a]-pyrene-1,6-quinone-induced cytotoxicity and reactive oxygen species production in human EA.hy926 endothelial cells
- Targeting glutathione with the triterpenoid CDDO-Im protects against benzo-a-pyrene-1,6-quinone-induced cytotoxicity in endothelial cells
- Triterpenoid CDDO-IM protects against lipopolysaccharide-induced inflammatory response and cytotoxicity in macrophages: The involvement of the NF-κB signaling pathway
- NADPH-quinone oxidoreductase-1 mediates Benzo-[a]-pyrene-1,6-quinone-induced cytotoxicity and reactive oxygen species production in human EA.hy926 endothelial cells
- Targeting glutathione with the triterpenoid CDDO-Im protects against benzo-a-pyrene-1,6-quinone-induced cytotoxicity in endothelial cells
- Triterpenoid CDDO-IM protects against lipopolysaccharide-induced inflammatory response and cytotoxicity in macrophages: The involvement of the NF-κB signaling pathway
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