What you eat determines how you breathe whether or not you have asthma. Wood et al. (J Allergy Clin Immunol 2011;127:1133-1140) present first-ever findings on the local inflammatory effects of high fat food, in this month’s issue.
The authors examine the effect of single high-fat or low-fat meals on non-obese subjects with asthma. Then, healthy, non-obese subjects and obese subjects with asthma were administered a single high-fat meal. All groups that consumed a high fat meal showed increased neutrophilic airway inflammation as measured by sputum induction and IL-6 levels, decreased % predicted FEV1 post-bronchodilator, and increased TLR4 expression and TNF-α levels. Wood et al. report that increased total plasma fatty acid levels were correlated significantly to increases in TNF-α and neutrophil percentage in sputum. Additionally, increased fatty acid levels were inversely correlated to change in % FEV1, %FVC, and FEV1/FVC.
They also examined the effect of meals containing trans-fatty acids as compared to meals with no trans-fatty acids. Subjects consuming trans-fatty acids demonstrated increased sputum neutrophilia compared to those that consumed no trans-fatty acids, which is consistent with other research reporting the pro-inflammatory properties of trans-fat.
Wood et al. state in conclusion that consumption of a high fat meal causes local airway inflammation and asthma worsening through activation of the innate immune response. They recommend that future research on this subject should focus on the effects of chronic consumption of high fat food in patients with asthma.
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Friday, May 6, 2011
A look at commensal gut bacteria, probiotics and atopy and obesity
In a clinical review in this month’s issue, Ly et al. (J Allergy Clin Immunol 2011;127:1087-1094) pull together what is known currently about gut microbiota influence on immunity, the association of abnormal microflora with eczema, asthma and obesity, the usefulness of probiotics for normalizing commensal gut bacteria, and newer information about vitamin D interactions with intestinal flora.
The authors begin commenting on how infants achieve gut colonization peri- and post-natally and note that vaginal delivery results in different gut flora in the infant than cesarean delivery. In particular, infants delivered by cesarean establish gut flora dominated by Klebsiella and Clostridum species, and enterobacteria other than E. coli, with later and less colonization by Bacteroides sp. and Bifidobacterium sp. Ly et al. point out that hospitalized neonates have gut flora similar to infants delivered by cesarean, suggesting that standard of care antibiotic use could be related to the decreased colonization by healthy bacteria.
They continue with a review of current knowledge of differential gut microbial populations between atopic and non-atopic infants, noting that atopic infants have lower fractions of lactobacilli, bifidobacteria, and Bacteroides sp. than their non-atopic counterparts. Ly et al. comment that current studies on neonatal gut commensalism and atopy are inconclusive, then discuss the design variability and limitations that result in contradictory findings.
The authors move to the evidence supporting a relationship between disturbance of the gut microflora and diet-related obesity, linking it to inflammation and impaired energy metabolism. They further note that gut flora composition shifts toward healthier bacteria dominance in obese subjects on dietary restriction for weight loss.
Ly et al. wrap up with a discussion of the equivocal findings from studies employing probiotics as prevention or mitigation of atopic diseases and a short note on the requirement of vitamin D for healthy gut microbial effects on inflammation. They conclude stating that evidence suggests early diversity of microbiota is pivotal to healthy gut-immune dynamics and that future research must comprise data on maternal flora-neonate flora interactions, vitamin D’s role and dietary confounders.
Have a comment? Tell us what you think. Please feel free to post your own comments and/or predictions below.
The authors begin commenting on how infants achieve gut colonization peri- and post-natally and note that vaginal delivery results in different gut flora in the infant than cesarean delivery. In particular, infants delivered by cesarean establish gut flora dominated by Klebsiella and Clostridum species, and enterobacteria other than E. coli, with later and less colonization by Bacteroides sp. and Bifidobacterium sp. Ly et al. point out that hospitalized neonates have gut flora similar to infants delivered by cesarean, suggesting that standard of care antibiotic use could be related to the decreased colonization by healthy bacteria.
They continue with a review of current knowledge of differential gut microbial populations between atopic and non-atopic infants, noting that atopic infants have lower fractions of lactobacilli, bifidobacteria, and Bacteroides sp. than their non-atopic counterparts. Ly et al. comment that current studies on neonatal gut commensalism and atopy are inconclusive, then discuss the design variability and limitations that result in contradictory findings.
The authors move to the evidence supporting a relationship between disturbance of the gut microflora and diet-related obesity, linking it to inflammation and impaired energy metabolism. They further note that gut flora composition shifts toward healthier bacteria dominance in obese subjects on dietary restriction for weight loss.
Ly et al. wrap up with a discussion of the equivocal findings from studies employing probiotics as prevention or mitigation of atopic diseases and a short note on the requirement of vitamin D for healthy gut microbial effects on inflammation. They conclude stating that evidence suggests early diversity of microbiota is pivotal to healthy gut-immune dynamics and that future research must comprise data on maternal flora-neonate flora interactions, vitamin D’s role and dietary confounders.
Have a comment? Tell us what you think. Please feel free to post your own comments and/or predictions below.
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