The recent renaissance of interest in innate immunity – a nonspecific form of defence common across the animal kingdom – has yielded a number of interesting findings. Now, research has highlighted the potential significance of innate immunity in two areas: Crohn's disease and breast milk.

Currently, it is thought that Crohn's disease results from an overactive immune system, which treatments are designed to 'damp down'. But Professor Tony Segal and colleagues at University College London have put forward a different hypothesis – that impaired innate immunity is responsible for the disorder.

The team showed that the immune response of people with Crohn's disease was much lower than that of healthy people when challenged by exposure to weakened E. coli or trauma to the rectum, ileum or skin.

They suggest that bowel contents that breach the mucosal barrier may not be cleared as effectively in people with an impaired immune response, which could lead to the chronic inflammation characteristic of Crohn's disease.

In separate work, Dr Mario Labéta and colleagues at Cardiff University have shown that breast milk can regulate the activity of the innate immune system in babies.

The team has been investigating the mechanisms controlling the activity of Toll-like receptors (TLRs), which recognise parts of microbial pathogens and activate the innate immune response. They found that as yet unidentified proteins present in early breast milk (but not formula milk) boosted the immune responses triggered by some TLRs, while inhibiting those triggered by others.

As well as demonstrating a novel activity of human milk, the work has also identified a possible new target for modulating innate immune responses.

Image credit: Surface of the gut; Professor Alan Boyde

External links

Marks DJ et al. Defective acute inflammation in Crohn's disease: a clinical investigation. Lancet 2006;367(9511):668–78.

• LeBouder E et al. Modulation of neonatal microbial recognition: TLR mediated innate immune responses are specifically and differentially modulated by human milk. J Immunol 2006;176(6):3742–52.