Probiotics for Autoimmunity: How They Can Help

Probiotics for autoimmunity are one of the tools to decrease your susceptibility as well as disease progression. Since each autoimmune disease has its unique presentations, probiotics are being investigated at the disease level with research focused on the ones that show efficacy for each particular autoimmune (AI) disease. Those individual AI results are discussed elsewhere on this website in articles and trainings about the various AI diseases. In this article, the focus is on how probiotics, and which probiotics, help with reducing the risk of the initiation and progression of AI diseases from a broader view. 

AI diseases affect approximately 8.5% of the worldwide population and are characterized by tissue damage and loss of function from an abnormal immune response directed at specific organs or various tissues throughout the body. More than 80-100 (depending on the source) AI diseases (such as the more familiar celiac disease, Crohn’s disease, lupus, Type 1 diabetes, rheumatoid arthritis, and MS) and AI-associated diseases are known to exist. In many cases there are preclinical clues, such as circulating autoantibodies, in years prior to obvious manifestations of disease.

According to the American Autoimmune-Related Diseases Association, these diseases are related to autoimmunity:

  • Achalasia
  • Addison’s disease
  • Adult Still's disease
  • Agammaglobulinemia
  • Alopecia areata
  • Amyloidosis
  • Ankylosing spondylitis
  • Anti-GBM/Anti-TBM nephritis
  • Antiphospholipid syndrome
  • Autoimmune angioedema
  • Autoimmune dysautonomia
  • Autoimmune encephalomyelitis
  • Autoimmune hepatitis
  • Autoimmune inner ear disease (AIED)
  • Autoimmune myocarditis
  • Autoimmune oophoritis
  • Autoimmune orchitis
  • Autoimmune pancreatitis
  • Autoimmune retinopathy
  • Autoimmune urticaria
  • Axonal & neuronal neuropathy (AMAN)
  • Baló disease
  • Behcet’s disease
  • Benign mucosal pemphigoid
  • Bullous pemphigoid
  • Castleman disease (CD)
  • Celiac disease
  • Chagas disease
  • Chronic inflammatory demyelinating polyneuropathy (CIDP)
  • Chronic recurrent multifocal osteomyelitis (CRMO)
  • Churg-Strauss Syndrome (CSS) or Eosinophilic Granulomatosis (EGPA)
  • Cicatricial pemphigoid
  • Cogan’s syndrome
  • Cold agglutinin disease
  • Congenital heart block
  • Coxsackie myocarditis
  • CREST syndrome
  • Crohn’s disease
  • Dermatitis herpetiformis
  • Dermatomyositis
  • Devic’s disease (neuromyelitis optica)
  • Discoid lupus
  • Dressler’s syndrome
  • Endometriosis
  • Eosinophilic esophagitis (EoE)
  • Eosinophilic fasciitis
  • Erythema nodosum
  • Essential mixed cryoglobulinemia
  • Evans syndrome
  • Fibromyalgia
  • Fibrosing alveolitis
  • Giant cell arteritis (temporal arteritis)
  • Giant cell myocarditis
  • Glomerulonephritis
  • Goodpasture’s syndrome
  • Granulomatosis with Polyangiitis
  • Graves’ disease
  • Guillain-Barre syndrome
  • Hashimoto’s thyroiditis
  • Hemolytic anemia
  • Henoch-Schonlein purpura (HSP)
  • Herpes gestationis or pemphigoid gestationis (PG)
  • Hidradenitis Suppurativa (HS) (Acne Inversa)
  • Hypogammalglobulinemia
  • IgA Nephropathy
  • IgG4-related sclerosing disease
  • Immune thrombocytopenic purpura (ITP)
  • Inclusion body myositis (IBM)
  • Interstitial cystitis (IC)
  • Juvenile arthritis
  • Juvenile diabetes (Type 1 diabetes)
  • Juvenile myositis (JM)
  • Kawasaki disease
  • Lambert-Eaton syndrome
  • Leukocytoclastic vasculitis
  • Lichen planus
  • Lichen sclerosus
  • Ligneous conjunctivitis
  • Linear IgA disease (LAD)
  • Lupus
  • Lyme disease chronic
  • Meniere’s disease
  • Microscopic polyangiitis (MPA)
  • Mixed connective tissue disease (MCTD)
  • Mooren’s ulcer
  • Mucha-Habermann disease
  • Multifocal Motor Neuropathy (MMN) or MMNCB
  • Multiple sclerosis
  • Myasthenia gravis
  • Myositis
  • Narcolepsy
  • Neonatal Lupus
  • Neuromyelitis optica
  • Neutropenia
  • Ocular cicatricial pemphigoid
  • Optic neuritis
  • Palindromic rheumatism (PR)
  • PANDAS
  • Paraneoplastic cerebellar degeneration (PCD)
  • Paroxysmal nocturnal hemoglobinuria (PNH)
  • Parry Romberg syndrome
  • Pars planitis (peripheral uveitis)
  • Parsonnage-Turner syndrome,
  • Pemphigus
  • Peripheral neuropathy
  • Perivenous encephalomyelitis
  • Pernicious anemia (PA)
  • POEMS syndrome
  • Polyarteritis nodosa
  • Polyglandular syndromes type I, II, III
  • Polymyalgia rheumatica
  • Polymyositis
  • Postmyocardial infarction syndrome
  • Postpericardiotomy syndrome
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
  • Progesterone dermatitis
  • Psoriasis
  • Psoriatic arthritis
  • Pure red cell aplasia (PRCA)
  • Pyoderma gangrenosum
  • Raynaud’s phenomenon
  • Reactive Arthritis
  • Reflex sympathetic dystrophy
  • Relapsing polychondritis
  • Restless legs syndrome (RLS)
  • Retroperitoneal fibrosis
  • Rheumatic fever
  • Rheumatoid arthritis
  • Sarcoidosis
  • Schmidt syndrome
  • Scleritis
  • Scleroderma
  • Sjögren’s syndrome
  • Sperm & testicular autoimmunity
  • Stiff person syndrome (SPS)
  • Subacute bacterial endocarditis (SBE)
  • Susac’s syndrome
  • Sympathetic ophthalmia (SO)
  • Takayasu’s arteritis
  • Temporal arteritis/Giant cell arteritis
  • Thrombocytopenic purpura (TTP)
  • Tolosa-Hunt syndrome (THS)
  • Transverse myelitis
  • Type 1 diabetes
  • Ulcerative colitis (UC)
  • Undifferentiated connective tissue disease (UCTD)
  • Uveitis
  • Vasculitis
  • Vitiligo
  • Vogt-Koyanagi-Harada Disease
  • Wegener’s granulomatosis (or Granulomatosis with Polyangiitis (GPA))


The Triad of Autoimmunity

From the brilliance of Dr. Alessio Fasano, a physician and researcher at the University of Maryland, and other researchers came the realization that gut health plays an important role in AI initiation. Dr. Fasano discovered that zonulin, a protein involved in intestinal permeability, was upregulated in autoimmune disease. Thus, the current generally-accepted theory for AI disease is that autoimmunity is the result of the interactions between genetics, triggers in the environment and intestinal permeability (also known as leaky gut). This is known as the autoimmune triad. The leaky gut leg of the triad involves anything that causes leaky gut.

Many people are surprised by the triad, as they assume that their genetics definitely determines their fate with autoimmunity. However, there are genetic variants that raise the risk of developing multiple autoimmune diseases, and multiple genes that predispose people to each disease. There is usually not one solitary gene that is associated with AI diseases. 

The most common genetic variants are known as SNP’s (single-nucleotide polymorphisms), and some of these, such as methylation SNP’s, are associated with autoimmune disease as well as countless other conditions. Inherited genes, such as HLA-DQ2, which is associated with predisposition to celiac disease, may be fixed in your genetic code, but you can influence your epigenetic SNP’s, your environmental triggers and your intestinal permeability/gut health that set the stage for inflammatory genes to activate.

Probiotics for Autoimmunity: The Leaky Gut Connection

The intestinal epithelial lining is a layer of cells that separates the luminal (inside) contents of the intestines from the inner body. It has tight junctions which keep the cells close together so that unwanted substances do not pass through. Unwanted substances, such as food particles complexed with immune cells, toxins, and bacteria can translocate, or move from the intestines to other tissues, causing immune reactions, inflammation and disease.

Although intestinal permeability is only one of several factors involved in intestinal barrier function and gut health, it has significant associations with autoimmunity as the following examples show.

In a rodent study (1), Type 1 diabetes was induced in genetically-susceptible mice. Evaluation of the pancreatic lymph nodes (PLN’s) showed that some of the commensal gut bacteria had translocated to the PLN’s. The activation of a NOD2 receptor that is involved in the inflammatory processes that initiate autoimmunity inside the PLN’s was upregulated, suggesting that the bacterial translocation upregulated the receptor and contributed to the development of Type 1 diabetes in the mice.

In systemic lupus erythematosus (SLE), or lupus, a toxin is suspected to be a contributor to the onset of the disease. LPS (lipopolysaccharide) is a bacterial toxin produced by Gram-negative bacteria, which includes many pathogens, and this toxin can cause intestinal permeability. LPS is known to cause intestinal inflammation as well as septic shock and potentially multiple organ failure.

One of the LPS-lupus connections is that a chemical, sCD14, which is released by monocyte immune cells in response to LPS, was elevated in human blood in a study of lupus patients (2). The LPS and/or associated Gram-negative bacteria slipped through the gaps between the intestinal cells. The higher the level of sCD14, the higher the disease activity. Other mechanisms involving LPS and various immune cells and receptors, such as TLR4, point to the capability of LPS to contribute to the onset and exacerbation of lupus in genetically-susceptible animals and humans.

In another example of intestinal permeability and autoimmunity (3), the translocation of a gut microbe with pathogenic potential, Enterococcus gallinarum, was demonstrated to drive autoimmunity in mice and humans. Specifically, this microbe was found to trigger systemic lupus and autoimmune liver disease in genetically-susceptible mice and was recovered from liver biopsies of many autoimmune disease patients. While the researchers who discovered this are investigating antibiotics and vaccination as promising treatments to blunt the immune response, a simpler idea may be to prevent the ability of microbes like E. gallinarum to translocate out of the GI tract by preventing intestinal permeability.

Taming the Triad with Probiotics for Autoimmunity

Probiotics for autoimmunity aim at all three arms of the triad. This section of the article is going to focus on their effects on the intestinal permeability arm. Future sections will relate to probiotics and the other aspects of AI, environmental triggers and genetics.

Probiotics are one of the tools to prevent leaky gut, both directly and indirectly. Many probiotics are able to directly positively interact with the human intestinal epithelial cells that line the GI tract to maintain barrier function and/or to prevent bacterial translocation. In other words, there are probiotics that directly interact with your intestinal-lining cells to help keep those cells healthy and the tight junctions close together. Some of the research showing positive effects on tight junctions are discussed below. Note that the species/strains named are not all-inclusive, as not every probiotic has been screened for direct-cell, tight-junction influences.

Research in vitro on intestinal tight junctions shows that live probiotics generally are necessary for effects. Bifidobacterium infantis as a species is known to promote intestinal barrier function. Research with other Bifidobacterium, and with Lactobacillus plantarum, Lactobacillus reuteri, and Lactobacillus acidophilus have noted the same effects.  

You can see that many probiotics for autoimmunity are in direct communication with intestinal epithelial cells to prevent leaky gut. Direct probiotic effects on the tight junction proteins by probiotics are not always required, however, to maintain barrier function in autoimmunity prevention and reaction inhibition. It is well known that pathogens, their constituents and their metabolic products can cause intestinal permeability. Probiotics also indirectly maintain barrier function and prevent bacterial translocation by inhibiting the ability of pathogens to establish themselves and cause intestinal permeability. Different probiotics have different capabilities as to how they achieve that objective, which is one of the reasons that the consistent intake of various probiotics and beneficial microbes is so important for health.

Prevention of intestinal permeability, one of the components involved in the initiation of autoimmunity, can disable one of the arms of autoimmunity. Probiotics, via various mechanisms, enhance the body’s efforts to maintain the intestinal-integrity aspect of the autoimmune triad. If you are predisposed to autoimmune diseases based on your genetics, it is of supreme importance that you maintain your intestinal barrier function with probiotics for autoimmunity, as well as make other healthy lifestyle choices.

To learn more about using probiotics to improve your health, check out "Probiotics: How to Use Them to Your Advantage" and my other books.

(1) F.R.C. Costa et al. “Gut Microbiota Translocation to the Pancreatic Lymph Nodes Triggers NOD2 Activation and Contributes to T1D Onset,” JEM 213.7 (2016): 1223-1239.

(2) Q Mu et al. “SLE: Another Autoimmune Disorder Influenced by Microbes and Diet?” Frontiers in Immunology 6 (2015).

(3) V.S. Manfredo et al. “Translocation of a Gut Pathobiont Drives Autoimmunity in Mice and Humans,” Science 359.6380 (2018): 1156-1161.


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