Proceedings of the Nutrition Society

Meeting Report

Fine and ultrafine particles of the diet: influence on the mucosal immune response and association with Crohn’s disease

Miranda C. E. Lomera1 c1, Richard P. H. Thompsona1 and Jonathan J. Powella2

a1 Gastrointestinal Laboratory, The Rayne Institute, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK

a2 Department of Nutrition, King's College London, Franklin-Wilkins Building, Stamford Street, London SE1 8WA, UK

Abstract

Crohn’s disease is a modern Western disease characterised by transmural inflammation of the gastrointestinal tract. It is of unknown aetiology, but evidence suggests that it results from a combination of genetic predisposition and environmental factors. Bacterial-sized microparticles (0·1–1·0 µm) are potent adjuvants in model antigen-mediated immune responses and are increasingly associated with disease. Microparticles of TiO2 and aluminosilicate accumulate in macrophages of human gut-associated lymphoid tissue where the earliest signs of lesions in Crohn’s disease are observed. Dietary microparticles are of endogenous or exogenous origin. Endogenous microparticles dominate and are calcium phosphate (most probably hydroxyapatite), which precipitates in the lumen of the mid-distal gastrointestinal tract due to secretion of Ca and phosphate in the succus entericus. Exogenous dietary microparticles are contaminants (soil and/or dust) and food additives. TiO2, for example, is a food colourant, and aluminosilicates are anti-caking agents, although some aluminosilicates occur as natural contaminants. Food additives alone account for ingestion of approximately 1012 particles/person per d. Possible mechanisms for the role of exogenous and endogenous dietary microparticles in promoting toleragenic or immune responses of gastrointestinal mucosal phagocytosis are discussed. In a double-blind randomised pilot study we have shown that a diet low in Ca and exogenous microparticles appears to alleviate the symptoms of ileal Crohn’s disease, with a significant (P = 0·002) improvement in the Crohn’s disease activity index. A multi-centre trial and further mechanistic studies at the cellular level are underway.

Correspondence:

c1 *Corresponding Author: Miranda Lomer, fax +44 20 7960 5710, email miranda.lomer@kcl.ac.uk