Probiotics: Treatment for Food Allergies?
I’m not doctor – my running mantra – but I am curious as all shit. And the last week has felt very depressing to me. My son is now 8 and he continues to have food allergies and asthma. Ok, we go back mid-February for blood draw & allergist so I’m keeping my hopes up. But I’ve been feeling depressed wondering if we’ve missed too many windows. Crap!
I’ve been cheering myself up – neurotic style – with more google searches that set my brain ablaze. Most studies with probiotics and allergy markers (IgE, IL-10 or the anti-allergy IL-12 or IFN-y and oral tolerance) involve administering probiotics to conventional and germ-free mice before – and this is important – BEFORE – exposure. Well what the hell. That doesn’t work for us. We’ve obviously missed the BEFORE window.
But this study is one of the first I’ve found that talks about using probiotics to generate oral tolerance AFTER exposure. This is why the post opened with my disclaimer – because I may have allowed my excitement to blur the facts in my reading. Like wishful thinking – wishful reading. But basically – oral tolerance = cure from food allergies!
In addition, the oral tolerance response in germfree mice can be restored either by administration of lipopolysaccharide from gram-negative bacteria (35) or by monocolonization of the gut with Bifidobacterium infantis (18, 31) or Escherichia coli (18) but not with Clostridium perfringens or Staphylococcus aureus (18). Contrasting results show that germfree mice can be made tolerant to ovalbumin but that the tolerance is maintained for a shorter time than in conventional mice (20, 21), for example 2 to 3 months of systemic IgG suppression after a single feeding (30) compared to 21 days in germfree mice (21). These results show that the intestinal microbiota play a major role in the induction and long-term persistence of oral tolerance, but further experiments are needed to identify which bacteria are the most effective. ***Effect of Probiotic Bacteria on Induction and Maintenance of Oral Tolerance to β-Lactoglobulin in Gnotobiotic Mice
See above “germ free mice can be made tolerant to ovalbumin…” through (and here is the part I look for in every study – what can I DO) “administration of lipopolysaccharide from gram-negative bacteria or by monocolonization of the gut with bificobacterium infantis or Escherichia coli but not with clostridium perfringens or Staphylococcus aureus.”
How do we implement this into our treatment plan for food allergies?
How do you monocolonize? Can you do that orally? (I’m guessing not unless you’re a germ free mouse.) But how does this play out for humans, who are no longer germ free. AND –
How does this feed into our fecal microbiome results?
Let’s think about this looking at my son’s results. And these results are so high level, that while they are super interesting and possibly enlightening, I wish I had the full data down to species.
Looking at my son’s results
He’s got too many firmicutes relative to his similar gender, age, bmi. He’s even got more than Michael Pollan. He’s got too little bacteroidetes (slight but noticeable). And most interesting – he’s got waaaay to little proteobacteria and NO TENERICUTES. Now what the hell does all the mean?
Well here’s where things start to fill out a bit. Let’s take the mouse study above (and of course assuming that what works in the mice in this study directly translates to humans, which of course is not necessarily true – but for arguments sake) and talk about inducing tolerance using:
lipopolysaccharide from gram-negative bacteria (35) or by monocolonization of the gut with Bifidobacterium infantis (18, 31) or Escherichia coli (18) but not with Clostridium perfringens or Staphylococcus aureus (18).
My son is low on proteobacteria. What are proteobacteria?
The Proteobacteria are a major group (phylum) of bacteria. They include a wide variety of pathogens, such as Escherichia, Salmonella, Vibrio, Helicobacter, and many other notable genera. (wikipedia)
And what else is notable about proteobacteria? Well according to wikipedia:
How about clostridium perfingens or staph aureaus (our frenemy – more of an enemy if you ask me)?
Interesting – but what high order level does it fall under?
Wait a minute! My son has too many firmicutes – according to the biome comparison above – for his age, gender, bmi. And even a little more than Michael Pollen. How about staph aureus?
The Mouse Model
A search online will reveal many reasonable sounding articles debating the value of translating human to mouse. And while the translatability is not 100%. I thought that this study was interesting – especially in light of monocolonization of the gut with Bifidobacterium infantis having a restorative effect on oral tolerance. How the hell to monocolonize a human gut without some sort of high colonic with it is beyond me?
But here is a study comparing the biome populations of children from Ghana versus England & New Zealand. And what they found is that the children from Ghana were primarily hosting Bifidobacterium infantis. Not only that, the children from England & New Zealand were hosting other Bifidobacterium strains, but not infantis.
The gut microbiota may be important in the postnatal development of the immune system and hence may influence the prevalence of atopic diseases. Bifidobacteria are the most numerous bacteria in the guts of infants, and the presence or absence of certain species could be important in determining the geographic incidence of atopic diseases. We compared the fecal populations of bifidobacteria from children aged 25 to 35 days in Ghana (which has a low prevalence of atopy), New Zealand, and the United Kingdom (high-prevalence countries). Natal origin influenced the detection of bifidobacterial species in that fecal samples from Ghana almost all contained Bifidobacterium infantis whereas those of the other children did not. Bifidobacterial Species Differentially Affect Expression of Cell Surface Markers and Cytokines of Dendritic Cells Harvested from Cord Blood
So, one could maybe hope that by taking Bifidobacterium infantis one could return to oral tolerance. But again, a monocolony in the intestines?!?!?! But if you’ve read any of my other posts, you know I also obssess about specific strains. Because most studies for the most part are strain specific. This study, however noted an interesting occurrence.
…It is noteworthy that all three B. adolescentis strains and both B. infantis strains produced the same effect on dendritic cells, suggesting that these were species-specific rather than strain-specific influences….
This is very interesting – and for the first time, enough to give me a sense of OK about trying a probiotic species without knowing the exact strain.
Another probiotic that has now become of interest to me is soil based probiotics. I have begun to read about the strains that make up this probiotic which consists of the following strains
Arthrobacter agilis, Arthrobacter citreus, Arthrobacter globiformis, Arthrobacter luteus, Arthrobacter simplex, Acinetobacter calcoaceticus, Azotobacter chroococcum, Azotobacter paspali, Azospirillum brasiliense, Azospirillum lipoferum, Bacillus brevis, Bacillus marcerans, Bacillus pumilus, Bacillus polymyxa, Bacillus subtilis, Bacteroides lipolyticum, Bacteriodes succinogenes, Brevibacterium lipolyticum, Brevibacterium stationis, Kurthia zopfii, Myrothecium verrucaria, Pseudomonas calcis, Pseudomonas dentrificans, Pseudomonas fluorescens, Pseudomonas glathei, Phanerochaete chrysosporium, Streptomyces fradiae, Streptomyces cellulosae, Streptomyces griseoflavus.