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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #381638
Research Project: Intestinal Microbial Ecology and Metagenomic Strategies to Reduce Antibiotic Resistance and Foodborne Pathogens

Location: Food Safety and Enteric Pathogens Research

Title: Butyrate alters lipopolysaccharide-induced inflammatory response by porcine monocytes

Author
item BECKER, SAGE - Orise Fellow
item Byrne, Kristen
item Loving, Crystal

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/15/2021
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Continuous, low-level inflammation can have a negative impact on intestinal health. Butyrate is a short-chain fatty acid produced in the lower intestinal tract by microbial fermentation of dietary fibers and modulates immune cell responses through various mechanisms. Blood monocytes migrate into the intestine and respond to signals, including potential modulation by butyrate or in response to microbial components, such as lipopolysaccharide (LPS). To investigate the impact of butyrate on inflammatory response to LPS, porcine monocytes were either cultured with a combination of LPS and varying butyrate concentrations or pre-treated with butyrate before LPS exposure. Independent of butyrate, LPS stimulation of monocytes induced IL-1 beta and TNF production. Monocytes cultured just three hours (h) prior to LPS stimulation had reduced overall cytokine production, suggesting rapid phenotypic changes in monocytes. Butyrate had varying effects on the amount of cytokine produced in response to LPS. Specifically, low butyrate concentrations (0.25mM) limited IL-1 beta production, but did not impact TNF production. Higher butyrate concentrations (greater than 4mM) limited TNF production to LPS stimulation. Pre-treatment of monocytes with butyrate for 3 h prior to LPS stimulation altered IL-1 beta production. Pre-treatment with 0.25 mM butyrate did not limit IL-1 beta production, but concentrations greater than 4mM did. In conclusion, reduction of LPS-induced cytokine production by porcine monocytes was dependent on butyrate concentration and exposure time relative to LPS exposure. Further work is ongoing to understand the mechanism of butyrate modulation of pig monocytes and inflammatory response to LPS for potential application in vivo.