Aluminum Is a Potential Environmental Factor for Crohn's Disease Induction

Abstract

Aluminum (Al) is a common environmental compound with immune-adjuvant activity and granulomatous inflammation inducer. Al exposure in food, additives, air, pharmaceuticals, and water pollution is ubiquitous in Western culture. Crohn's disease (CD) is a chronic relapsing intestinal inflammation in genetically susceptible individuals and is influenced by yet unidentified environmental factors. It is hypothesized, in the present review, that Al is a potential factor for induction or maintaining the inflammation in CD. Epidemiologically, CD incidence is higher in urban areas, where microparticle pollution is prevalent. Al immune activities share many characteristics with the immune pathology of CD: increased antigen presentation and APCs activation, many luminal bacterial or dietary compounds can be adsorbed to the metal and induce Th1 profile activity, promotion of humoral and cellular immune responses, proinflammatory, apoptotic, oxidative activity, and stress-related molecule expression enhancement, affecting intestinal bacterial composition and virulence, granuloma formation, colitis induction in an animal model of CD, and terminal ileum uptake. The Al-bacterial interaction, the microparticles homing the intestine together with the extensive immune activity, put Al as a potential environmental candidate for CD induction and maintenance.

Melatonin is a potent modulator of antioxidative defense and cellular proliferation against aluminum toxicity in rats

“…Lerner (2007) suggested that aluminum might play a role in Crohn's disease. It is considered that the effect causing inflammation in Crohn's disease might be the interaction between aluminum and bacteria.…”

Dietary management of IBD—insights and advice

“…Dietary ideas can start with hypotheses supported by various observations that might be epidemiological or biological, some of which are displayed in Figure 2. These hypotheses have been directed towards several factors: alteration of bacterial exposure in childhood (the so-called cold-chain hypothesis); 37 impairment of the epithelial barrier by multiple food components that have included emulsifiers, 38 fermentable oligosaccharides, disaccharides, mono saccharides and polyols (FODMAPs) in Crohn's disease, 39 and foods that induce excessive nitric oxide and sulphide production in the lumen of the large bowel in ulcerative colitis; 40 and direct modulation of the control of mucosal inflammatory processes by, for example, indigestible particles [41][42][43] or exposure to various combination or individual lipids. 44,45 Many of these ideas are potentially amenable to dietary design and clinical trials.…”

“…Ingestion of food might drive IBD via three broad mechanisms: by enabling exposure to specific microbiota in early life; 37 by enabling greater bacterial penetration of the epithelial barrier to induce inflammatory events;38,39,127 and by directly altering immune responsiveness 41,45. Abbreviations: FODMAP, fermentable oligosaccharide, disaccharide, monosaccharide and polypol; NO, nitric oxide.…”

Smoking, Physical Activity, Nutrition and Lifestyle: Environmental Factors and Their Impact on IBD

“…Dietary fats, high protein intake and low vitamin D may be the most important determinants. By contrast, there is no clear association of IBD and the intake of refined sugars [58] , and the effect of alimentary microparticles, such as natural contaminants (soil and dust), food additives and anti-caking agents, remains unclear [59] . Currently, the most consistent data are from the European Prospective Investigation into Cancer and Nutrition (EPIC) and concern linoleic acid.…”