In this blog post, we want to look at some key biological mechanisms connecting dysbiosis and food sensitivity. How they all connect with each other will become clear as you read on.
Dendritic cells (DCs) are antigen presenting cells (they present toxins, pathogens, food bits, etc to immune cells so they can create antibodies) that are pivotal in the balance between oral tolerance and active immunity to commensal microorganisms that is fundamental to inflammatory conditions, including Crohn’s disease and ulcerative colitis. Dendritic cells (DCs) in the lamina propria (the layer below the epithelial cells) of the gut reach their dendrites up between the epithelial cells, to sample the contents of the intestinal lumen. As Dr. Yanuck states “This means that the person does not need to have a leaky gut in order for the immune system to sample the contents of the intestine.“
Bacteria are kept away from the intestinal epithelia by “a thick, stratified mucus layer. Bacteria are abundant in the outer mucus layer, whereas the inner layer is resistant to bacterial penetration…Plasma cells secrete lgA (SIgA) that is transcytosed across the epithelial cell layer and secreted from the apical surface of epithelial cells, limiting numbers of mucosa-associated bacteria and preventing bacterial penetration of host tissues.”
Secretory IgA (SIgA) is the most abundant immunoglobulin (also known as antibodies) in the body, and it resides in all our liquid secretions. So that means it can be found in the tears in your eyes, the saliva of your oral cavity, your blood, your sweat, your urinary system, your vagina and most importantly, in your gut! All of these places have Secretory IgA and it plays an important protective role as our first line of defence in immunity. Its job is to block and protect the body from bacterial, viral, and parasitic infections, toxins and food allergens. Therefore, if you are low in SIgA you may experience an array of gut health issues. Most treatments start by eradicating the gut of the bad guys with antibiotics, the problem is, it’s also important to look at the terrain of the gut and increase SIgA levels to treat the problem at its source. Because of SIgA’s role of fighting “the bad guys” as part of our immune system, a low SIgA level means our bodies are much less capable of controlling the equilibrium in our gut and digestive systems. This inevitably leads to the overgrowth of bad bacteria and increased levels of toxins causing inflammation and hampering the body’s ability to repair the damage. The good news is, once you uncover the imbalances in your gut chemistry and ecology, the solution(s) can be rapid and effective.
Back to what we were talking about above, when the DC’s are sampling the contents of the intestinal lumen, it is still possible for them to come into contact with bacteria. If bacteria from the intestine stimulate toll like receptors (TLRs) on the dendritic cell (DC), this will signal the DC that the antigen it has sampled from the intestinal lumen is a pathogen. When the DC presents this antigen to a T or B cell in the Peyers Patches or mesenteric lymph nodes in the intestinal lining, the T and B cells will be evoked into response mechanisms suitable to killing of pathogens. There are two ways this can go:
- The antigen being presented really is a pathogen (presumably the same pathogen that stimulated the TLR on the DC, or another similar bacterium), so the anti-pathogen response of the T and B cells will be suitable. A key piece of this response is that the B cells will be stimulated into differentiating into IgA+ plasma cells that secrete dimeric IgA that migrates across the epithelial barrier and binds to bacteria in the lumen, “limiting bacterial association with the epithelium and preventing bacterial penetration of host tissue.” This reinvigorates the barrier system, in response to the bacterial antigen presentation.
- The antigen being presented is a food protein which is where the issue begins. As Hooper and Macpherson say, “when loaded with food proteins, in the absence of activating molecules (such as Toll-like receptor ligands from microorganisms), intestinal DCs promote the peripheral tolerance of B and T cells.” But, if the DC has sampled a food protein, it will present that food protein as an antigen to a T or B cell. But, if that DC has also gotten TLR stimulation from a bacterium, the DC will…
- Present the food protein as antigen,
- Provide the T or B cell with co-stimulation,
- Provide the T or B cell with instructing cytokines to evoke an anti-pathogen response.
At that point, you’ve evoked a food sensitivity response. So, when you have persistent food sensitivity responses, especially when there are lots of them, or when the person seems to develop sensitivity reactions simply by eating a food for long enough, or taking a supplement for long enough, it’s useful to look at two mechanisms: addressing dysbiosis and addressing the adequacy of Secretory IgA (SIgA) production.
How Can I address dysbosis?
You can follow the Seasonal candida and Parasite Cleanse Program!
How Can I Raise My Secretory IgA Levels?
- Lowering Chronic Stress: Evidence suggests that Secretory IgA production can be suppressed by stress and elevated cortisol levels (this includes perceived stress) . When the cortisol level is chronically elevated, SIgA production decreases, leading to an inadequate immune response which then, ultimately, increases the risk of infection.
- Clearing dysbiosis – lowers IgA
- Increasing zinc (zinc helps secrete IgA
- Increasing Protein
- Consuming fat soluble vitamins: in particular, vitamin A and vitamin D are another key element for raising SIgA levels in the gut. Studies have demonstrated a link between increased intake of fat-soluble vitamins and elevated levels of IgA, IgG, and IgM.
- Increasing prebiotic fiber: Dietary prebiotics like GOS (galacto-oligosaccharides) and FOS (fructo-oligosaccharides) have been shown to increase SIgA levels in the gut as they act as food for “good” bacteria in the intestine and colon.
- Supplementing with probiotics
The Research
Immune adaptations that maintain homeostasis with the intestinal microbiota
Nat Rev Immunol. 2010 Mar;10(3):159-69. Hooper LV, Macpherson AJ.