PEMF AND INFLAMATORY BOWEL DISEASE
Disclaimer: Please note that these pages are for general information purposes only. The opinions and information have not been evaluated by the FDA. They should not be considered complete in terms of the physical conditions discussed, or construed as healthcare advice
Inflammatory bowel disease (IBD) is a term for two conditions (Crohn’s disease and ulcerative colitis) that are characterized by chronic inflammation of the gastrointestinal (GI) tract. The GI tract extends from the mouth to the anus and includes the organs that digest food, absorb nutrients, and process wastes. Long-term inflammation results in damage to the GI tract. IBD is usually characterized by diarrhea, rectal bleeding, abdominal pain, fatigue, and weight loss.
We do not yet know the exact cause of IBD, but it seems to be the result of an improper immune response. The treatment of IBD involves the use of medicines and sometimes surgery, depending upon the type and course of the inflammatory bowel disease.
Therapies of inflammatory bowel disease are stemming from the exponential advancement in understanding the human intestinal immune system . However, despite an array of biological mechanisms (antibodies against proinflammatory cytokines, T-cell antibodies, anti-inflammatory cytokines) involved in gastrointestinal chronic disease with autoimmune pathogenesis like Crohn’s disease, current treatment remains difficult and individually inefficient .
Pulsed electromagnetic field (PEMF) is emerging as an innovative treatment for regulation of the inflammation/immune response pathways of different cell types which could have significant effects on tissue regeneration [3,4]. Successful regeneration requires a balanced immune cell response, with the recruitment of accurately polarized immune cells in an appropriate quantity . It is in this way that PEMF could have an influential role in the inflammatory process and thereby support tissue regeneration.
In studies the human peripheral blood mononuclear cells (PBMC) population is 90% composed of lymphocytes and 70-80% of the lymphocytes are T-helper (Th) cells. The Subpopulation Th1 is engaged in the pathogenetic mechanism of a great number of the inflammatory chronic diseases of the gastrointestinal tract like Crohn’s or ulcerative colitis by producing proinflammatory cytokines . Inflammatory bowel diseases are characterized by the production of proinflammatory cytokines like Interferon gamma (IFN-γ), interleukin-12, interleukin-1β (IL-1β) and Tumor necrosis factor-α (TNF-α). Cytokine IL-1β is proinflammatory and causes a number of autoinflammatory conditions including Crohn’s disease.
After PEMF exposure and activation with lipopolysaccharide (LPS), Data showed a significant decrease in cytokine IL-1β secretion in both the human mesenchymal stem/stromal cells (MSCs) and THP-1 macrophages (a human monocytic cell line derived from an acute monocytic leukemia) [7,8]. Tumor necrosis factor alpha (TNF- α) and its signaling receptor have also been associated with the pathogenesis of several diseases including Crohn’s. Due to its pivotal role in orchestrating the cytokine cascade in many inflammatory diseases, TNF- α has been called the master-regulator of inflammatory cytokine production . Data show that PEMF significantly decreased the production of tumor necrosis factor-α (TNF-α) in the THP-1 cells .
The Inflammatory process in IBD may also result from an innate alteration in the anti-inflammatory cytokine Interluken-10 (IL-10) production pathway [10, 11]. Studies on knockout mice that demonstrate a deficiency of IL-10 have shown that chronic enterocolitis (intestine inflammation) developed [10, 12, 13]. Anti-inflammatory effects of PEMF also comes from hypothesis that it decreases the number of free radicals and reduces the severity of inflammation by inhibiting the production of reactive oxygen intermediates .
PEMF modulates inflammatory processes through the regulation of pro- and anti-inflammatory cytokine secretion during different stages of inflammatory response. Consistent outcomes in studies involving animal and human tissue have shown promise for the use of PEMF as an alternative or complementary treatment to pharmaceutical therapies for IBD. Thus, PEMF treatment could provide a novel nonpharmaceutical means of modulating inflammation in injured tissues resulting in enhanced functional recovery .
Dr. Amanda Myers, MD, MSPH
Aura Medical Director
1 Baumgart DC, Wiedenmann B, Dignass AU. Biologic therapy of inflammatory bowel disease. Z Gastroenterol 2003; 41: 1017-1032.
2 Bamias G, Sugawara K, Pagnini C, et al. The Th1 immune pathway as a therapeutic target in Crohns disease. Curr Opin Investig Drugs 2003; 4: 1279-1286.
3 Rosado M, Simkó M, Mattsson M-O, et al. Immune-modulating perspectives for low frequency electromagnetic fields in innate immunity. Front Public Health 2018;6:85.
4 Jasti A, Wetzel B, Aviles H, et al. Effect of a wound healing electromagnetic field on inflammatory cytokine gene expression in rats. Biomed Sci Instrum 2001;37:209–214.
5 Abnave P, Ghigo E. Role of the immune system in regeneration and its dynamic interplay with adult stem cells. Semin Cell Dev Biol 2019;87:160–168.
6 Pallone F, Blanco Gdel V, et al. Genetic and pathogenetic insights into inflammatory bowel disease. Curr Gastroenterol Rep 2003; 5: 487-492.
7 Christina L. Ross, Yu Zhou, Charles E. McCall, et al. The Use of Pulsed Electromagnetic Field to Modulate Inflammation and Improve Tissue Regeneration: A Review.Bioelectricity.Dec 2019.247-259.
8 Masters S, Simon A, Aksentijevich I, et al. Horror autoinflammaticus: The molecular pathophysiology of autoinflammatory disease. Annu Rev Immunol 2009;27:621–668.
9 Parameswaran N, Sonika Patial S. Tumor necrosis factor-α signaling in macrophages. Crit Rev Eukaryot Gene Expr 2010;20:87–103.
10 Bamias G, Sugawara K, Pagnini C, et al. The Th1 immune pathway as a therapeutic target in Crohns disease. Curr Opin Investig Drugs 2003; 4: 1279-1286.
11 Gasche C, Bakos S, Dejaco C, et al. IL-10 secretion and sensitivity in normal human intestine and inflammatory bowel disease. J Clin Immunol 2000; 20: 362-370.
12 Stallmach A, Marth T, Weiss B, et al. An interleukin 12 p40-IgG2b fusion protein abrogates T cell mediated inflammation: anti-inflammatory activity in Crohns disease and experimental colitis in vivo. Gut 2004; 53: 339-345.
13 Stio M, Treves C, Martinesi M, et al. Effect of anti-TNF therapy and vitamin D derivatives on the proliferation of peripheral blood mononuclear cells in Crohns disease. Dig Dis Sci 2004; 49: 328-335.
14 Lushnikov KV, Shumilina YV, Yakushina VS, et al. Effects of low-intensity ultrahigh frequency electromagnetic radiation on inflammatory processes. Bull Exp Biol Med 2004; 137: 364-366.
15 J. Kaszuba-Zwoinska, I. Cieaeko-Michalska, D. Mydroszkiewicz, et al. Magnetic field anti-Inflammatory effects in Crohns Disease depends upon viability and cytokine profile of the Immune competent cells. JournalofPhysioloyandpharmacology 2008; 59(1): 177-187.