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Balance the immune system with pre- and probiotics

synbiotic supplementation boosts the immune system

 

 

 

 

Synbiotic supplementation is required for optimum immune system balance.

The lining of your alimentary canal is fully equipped as your first line of defense against microbial pathogens.

However, the critical essence of the immune cell presence in the gut is its effects extending far beyond the gut, exercising control over all aspects of systemic immune responses. Do you marvel that immune cells use the gut lining as their home base, from which they are commanded by microbiota to mobilize in combat against immune system stress assaults on any tissue? Truly, it is the power of the intestinal microbiota that commands both activation and inhibition of dendritic cells, macrophages, mast cells and eosinophils in the gut lining.1,2,3,4,5

Your microbiota is the “major general” of your immune system forces

The benefits of a healthy microbiota include:

The microbiota controls the enteroendocrine cells communicating with a broad array of immuno-neuro-endocrine functions. The communication network includes the gut-liver axis, the gut-brain axis, the gut-hypothalamus axis, the gut-adipose axis and the gut-pancreas axis. However, the overarching influence of the microbiota is via the gut-immune axis.

The microbiota-gut-immune system axis

Researchers have identified a select group of probiotics that are essential, not only for gut health, but for a highly responsive yet thoroughly controlled and balanced systemic immune system. One specific component of immune system balance is the antagonism/balance between lymphocytic T-helper cell-1 (Th1) and T-helper cell-2 (Th2) function. The Th1 inflammatory cytokine family includes interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) and interleukins (IL) 1, 2, 8 and 12. Th2 inflammatory cytokines include the pro-inflammatory IL-5, 6 and 13, along with the anti-inflammatory IL-4 and 10. Deficiency in either family of Th1 or Th2 cytokines is characteristic of both acute and chronic inflammatory processes. But more significant than deficiencies of these inflammatory cytokines are uncontrolled excesses.2,4,5,8,9,10,11

Uncontrolled immune reactivity of Th1 inflammatory cytokines is typical of chronic auto-immune diseases such as rheumatoid arthritis, Crohn’s disease, Type 1 diabetes and multiple sclerosis. Dysregulated Th2 reactivity, often accompanied by a deficiency of Th1 immune system defense, is characteristic of immunoglobulin-E-mediated allergies, with elevated eosinophil and mast cell reactivity, along with other histamine-mediated reactions and asthma.2,4,5,8,9,10,11

Synbiotic supplementation, which combines probiotics and prebiotics, is required for optimum immune system balance, assuring a decreased capacity to cause deviation of inflammatory response toward systemic, Th1- and Th2-activated pathology.1,3,9,10,12

Specificity in probiotic supplementation

In patients with a proclivity toward either Th1- or Th2-dominant health problems, you must be selective in probiotic supplementation. To do otherwise is to potentially exacerbate inflammatory symptoms and intensify the processes of inflamm-aging.

The probiotic species most immune-reactive in humans can be divided into two “teams.” One team strongly inhibits excessive Th1 inflammatory cytokines, and to a certain extent helps activate the anti-inflammatory Th2 cytokines. That team includes L. reuteri, B. breve and B. longus. The probiotics controlling Th2 inflammation while strengthening a weak Th1 defense include L. rhamnoses, L. casei and L. gasseri.2,5,7

To supplement in accord with every patient’s specific needs, you must be particular in recommending probiotics suitable for the individual’s tendency to be either Th1- or Th2-dominant in immune system reactivity.

In consideration of patients with high Th1 and low Th2 reactivity

Probiotics considerations for patients with high Th2 and low Th1 reactivity

Final thoughts on synbiotic supplementation

When you consider the concept of microbiota specificity, it is imperative you offer synbiotic supplementation in accordance with all patients’ specific needs, helping them battle inflammation with a powerfully mobilized microbiota.

Guy R. Schenker, DC, a Pennsylvania doctor of chiropractic since 1978, is the developer of the Nutri-Spec System of Clinical Nutrition, which eschews symptom-based nutrition in favor of individualized metabolic therapy. Nutri-Spec offers a Stage of Life Diphasic Nutrition Plan (SOLID DNP) empowering each patient to Live Stronger Longer. Schenker can be reached at 800-736-4320 or nutrispec@nutri-spec.net.

References

  1. Wiertsema S, et al. The interplay between the gut microbiome and the immune system in the context of infectious diseases throughout life and the role of nutrition in
    optimizing treatment strategies. Nutrients. 2021;13(3):886. PubMed. https://pubmed.ncbi.nlm.nih.gov/33803407/. Accessed March 17, 2025.
  2. Huihui X, et al. The dynamic interplay between the gut microbiota and autoimmune diseases. J Immunol Res. 2019:2019:7546047. PubMed. https://pubmed.ncbi.nlm.nih.gov/31772949/. Accessed March 17, 2025.
  3. Human Microbiome Project Consortium. A Framework for Human Microbiome Research. Nature. 2012. Research Gate. https://www.researchgate.net/publication/230635491_A_framework_for_human_microbiome_resea. Accessed March 17, 2025.
  4. Traina G. The role of mast cells in the gut and brain. J. Integr Neurosci. 2021;20(1):185-196. PubMed. https://pubmed.ncbi.nlm.nih.gov/33834706/. Accessed March 17, 2025.
  5. Raffaella di Vito, et al. The cross-talk between intestinal epithelial cells and mast cells is modulated by the probiotic supplementation in co-culture models. Int J Mol Sci.2023;24(4):4157. PubMed. https://pubmed.ncbi.nlm.nih.gov/36835568/. Accessed March 17, 2025.
  6. Bonaz B, et al. The vagus nerve at the interface of the microbiota-gut-brain axis. Front Neurosci. 2018:12:49. PubMed. https://pubmed.ncbi.nlm.nih.gov/29467611/. Accessed March 17, 2025.
  7. Zhou L, et al. Innate lymphoid cells support regulatory T Cells in the intestine through interleukin-2. Nature. 2019;568(7752):405-409. PubMed. https://pubmed.ncbi.nlm.nih.gov/30944470/. Accessed March 17, 2025.
  8. Wang W, et al. Inflammatory response: A crucial way for gut microbes to regulate cardiovascular diseases. Nutrients. 2023;15(3):607. PubMed. https://pubmed.ncbi.nlm.nih.gov/36771313/. Accessed March 17, 2025.
  9. Smits HH, et al. Selective probiotic bacteria-induced IL-10-producing regulatory T cells in vitro by modulating dendritic cell function through dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin. J Allergy Clin Immunol. 2005;115(6):1260-1267. PubMed. https://pubmed.ncbi.nlm.nih.gov/15940144/. Accessed March 17, 2025.
  10. He B, et al. Resetting microbiota by Lactobacillus reuteri inhibits t reg Deficiency-induced Autoimmunity via Adenosine A2A Receptors. J Exp Med. 2017;214(1):107-123. PubMed. https://pubmed.ncbi.nlm.nih.gov/27994068/. Accessed March 17, 2025.
  11. Harata G, et al. Differential implication of lactobacillus GG and L gasseri TMC0356 to immune responses of murine peyer’s patch. Microbiol Immunol. 2009;53(8):475-480. PubMed. https://pubmed.ncbi.nlm.nih.gov/19659932/. Accessed March 17, 2025.
  12. He B, et al. Lactobacillus reuteri reduces the severity of experimental autoimmune and encephalomyelitis in mice by modulating microbiota. Front Immunol. 2019:10:385. PubMed. https://pubmed.ncbi.nlm.nih.gov/30899262/. Accessed March 17, 2025.
  13. Collins FL, et al. Beneficial effects of Lactobacillus reuteri on bone density in male mice is dependent on lymphocytes. Sci Rep. 2019;9(1):14708. PubMed. https://pubmed.ncbi.nlm.nih.gov/31605025/. Accessed March 17, 2025.
  14. Jiri H, et al. Lactobacillus reuteri and bifidobacterium animalis lactis improved colitis while differentially impacting dendritic cell maturation and antimicrobial responses. Sci Rep. 2020;10(1)5345. PubMed. https://pubmed.ncbi.nlm.nih.gov/32210304/. Accessed March 17, 2025.
  15. Hoarau C, et al. Supernatant of bifidobacterium breve induces dendritic cell maturation, activation, and survival through a toll-like receptor 2 pathway. J Allergy Clin Immunol. 2006;117(3):696-702. PubMed. https://pubmed.ncbi.nlm.nih.gov/16522473/. Accessed March 17, 2025.
  16. Spacova I, et al. Lactobacillus rhamnosus probiotic prevents airway function deterioration and promotes gut microbiome resilience in a murine asthma model. Gut Microbes. 2020;11(6):1729-1744. PubMed. https://pubmed.ncbi.nlm.nih.gov/32522072/. Accessed March 17, 2025.
  17. Li L, et al. Prophylactic effects of oral administration of Lactobacillus casei on house dust mite-induced asthma in mice. Food Funct. 2020;11(10):9272-9284. PubMed. https://pubmed.ncbi.nlm.nih.gov/33047743/. Accessed March 17, 2025.
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  19. Lin WH, et al. Induced apoptosis of Th2 lymphocytes and inhibition to airway hyperresponsiveness and inflammation by combined lactic acid bacteria treatment. Int Immunopharmacol. 2013;15(4):703-11. PubMed. https://pubmed.ncbi.nlm.nih.gov/23142092/. Accessed March 17, 2025.
  20. Alvarez V, et al. An exopolysaccharide-deficient mutant of Lactobacillus rhamnosus GG efficiently displays a protective llama antibody fragment against rotavirus on its surface. Appl Environ Microbiol. 2015;81(17):5784-5793. PubMed. https://pubmed.ncbi.nlm.nih.gov/26092449/. Accessed March 17, 2025.
  21. Chapat L, et al. Lactobacillus casei reduces CD8+ T cell-mediated skin Inflammation. Eur J Immunol. 2004;34(9):2520-2528. PubMed. https://pubmed.ncbi.nlm.nih.gov/15307184/. Accessed March 17, 2025.
  22. Kato I, et al. Antitumor activity of Lactobacillus casei in mice. Gan. 1981;72(4):517-523. PubMed. https://pubmed.ncbi.nlm.nih.gov/6796451/. Accessed March 17, 2025.
  23. Ogawa T, et al. Natural killer cell activities of synbiotic Lactobacillus casei ssp. Cassei in Conjunction with Dextran. Clin Exp Immunol. 2006;143(1):103-9. PubMed. https://pubmed.ncbi.nlm.nih.gov/16367940/. Accessed March 17, 2025.
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