Butyrates are important as food for cells lining the mammalian colon (colonocytes). Without butyrates for energy, colon cells undergo autophagy (self digestion) and die.Most of your butyrate requirement is taken care of by the butyrate-producing bacteria in your gut. All you need to do is give them the resistant starches (i.e. fiber) they need to make it. Since butyrate is made via bacterial fermentation of fiber, you can increase your butyrate level by increasing fiber in your diet. This means eating more of the following sources of soluble fiber: Whole grains – brown rice, oats, barley, rye, quinoa, buckwheat, millet, corn. Legumes – lentils, chickpeas, kidney beans, pinto beans, mung beans, adzuki beans. Fruits and vegetables – leafy green vegetables, apples, kiwifruit, berry fruits, bananas, citrus fruit. Butyrate is also naturally occurring in dairy products. It’s not a good idea to eat too much dairy, though, because it has a very high saturated fat content. Most people already have too much saturated fat in their diets. Butter is around 3%-4% butyrate, so you’d need to eat 10 grams daily to get your dose of 300 mg butyrate. This is the equivalent of around two teaspoons of butter each day.

Butyrate ameliorates allergic airway inflammation by limiting eosinophil trafficking and survival

Journal of Allergy and Clinical Immunolo.. - 4d ago Preview

 
 
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Publication date: Available online 11 May 2019

Source: Journal of Allergy and Clinical Immunology

Author(s): Anna Theiler, Thomas Bärnthaler, Wolfgang Platzer, Georg Richtig, Miriam Peinhaupt, Sonja Rittchen, Julia Kargl, Trond Ulven, Leigh M. Marsh, Gunther Marsche, Rufina Schuligoi, Eva M. Sturm, Akos Heinemann

Abstract

Background

Lung eosinophilia is a hallmark of asthma and eosinophils are believed to play a crucial role in the pathogenesis of allergic inflammatory diseases. Short chain fatty acids (SCFA), e.g. acetate, propionate and butyrate are produced in high amounts in the gastro-intestinal tract by commensal bacteria and can be absorbed into the blood stream. Although, there is recent evidence that SCFA are beneficial in allergic asthma models, the effect on eosinophils has remained elusive.

Objective

The role of SCFA was investigated in human eosinophil function and a mouse model of allergic asthma.

Methods

Eosinophils were purified from self-reported allergic or healthy donors. Migration, adhesion to endothelium and survival of eosinophils was studied in vitro. Ca2+ flux, apoptosis, mitochondrial membrane potential and expression of surface markers was determined by flow cytometry and in part by real time PCR. Allergic airway inflammation was assessed in vivo in an ovalbumin-induced asthma model using invasive spirometry.

Results

We observed for the first time that SCFA were able to attenuate human eosinophils at several functional levels including (i) adhesion to the endothelium, (ii) migration and (iii) survival. These effects were independent from GPR41 and GPR43, but were accompanied by histone acetylation and mimicked by TSA, a pan-HDAC inhibitor. In vivo, butyrate ameliorated allergen-induced airway and lung eosinophilia, reduced type 2 cytokines in the bronchial fluid and improved airway hyperresponsiveness in mice.

Conclusion

These in vitro and in vivo findings highlight the importance of SCFA, especially butyrate as a promising therapeutic agent in allergic inflammatory diseases.

Graphical abstract