American Journal of Animal and Veterinary Sciences

Dietary β-glucan Leads to Increased TNF-α Production in the Lung

Radiah C. Minor, Melody L. Robinson-Wright, Morika Williams and Steven L. Hurley

DOI : 10.3844/ajavsp.2012.55.60

American Journal of Animal and Veterinary Sciences

Volume 7, Issue 2

Pages 55-60


Problem statement: Beta (β)-glucan is notable for its ability to stimulate the immune system and as such β-glucan and products containing β-glucan are used as dietary supplements for livestock and companion animals. β-glucan has been shown to activate macrophages and neutrophils and modulate the production of certain cytokines, including the pro-inflammatory cytokine, Tumor Necrosis Factor Alpha (TNF-α). Because TNF-α is a contributing factor in a number of chronic inflammatory diseases and is present at higher concentrations in bronchoalveolar fluid from patients with asthma a preliminary experiment was designed to determine if a diet supplemented with β-glucan leads to increased TNF-α production in response to chitin, an ubiquitous environmental antigen that is associated with airway inflammation. Approach: Mice were divided into two groups. One group was given normal rodent chow and water while the other group was given normal rodent chow and water containing β-glucan (1 mg mL-1) for 14 days. After 14 days, two experimental protocols were conducted to evaluate TNF-α production. In experimental protocol 1, mice were injected intraperitoneally with 4% thioglycollate broth and TNF-α production from the immune cells elicited into the peritoneal cavity was evaluated. In experimental protocol 2, mice were exposed to either chitin or PBS (as a control) via intranasal administration for two consecutive days. Six hours post secondary exposure, Bronchoalveolar Lavage Fluid (BALF) was collected and ELISA for TNF-α performed. Results: TNF-α expression by thioglycollate-elicited cells isolated from animals that consumed β-glucan was greater (27 fold) than controls. Similarly, dietary β-glucan was also associated with increased TNF-α expression (four fold) in the lung, after chitin exposure in vivo. Conclusion: These preliminary results suggest that dietary β-glucan may promote inflammatory responses after exposure to chitin and therefore could be contributing factor to lung inflammation particularly in animals prone to airway inflammatory diseases.


© 2012 Radiah C. Minor, Melody L. Robinson-Wright, Morika Williams and Steven L. Hurley. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.