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Just how inflamed is the normal gut?
  1. Education and Research Centre,
  2. St Vincent’s Hospital,
  3. Elm Park,
  4. Dublin 4,
  5. Ireland

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That the science of cartography is limited - and not simply by the fact that this shading of forest cannot show the fragrance of balsam, the gloom of cypresses, is what I wish to prove Eavan Boland

The mammalian intestine has evolved as a tightly regulated and intricate environment concerned with manipulating vast quantities of complex substances. Ingested matter must be processed, transported and appropriately disposed of without stimulating adverse local reactions while contaminating microorganisms with pathogenic potential must be dispatched. Cytokines are of fundamental importance in all of these processes, yet the pleiotropy, interdependence and redundancy of cytokine networks has made this a difficult and often confusing area to chart.


Cytokine studies in the intestine have, in the past, focused on the possible role of these factors as immunological mediators of inflammatory disease states and it has generally been assumed that activation, as a result of some pathogenic process, was required for their secretion. Thus, inflammatory cytokines, including interleukin (IL) 1, IL-2, tumour necrosis factor (TNF) α and interferon (IFN) γ, have all been claimed to be the primary pathogenic mediators in diseases of the intestine such as Crohn’s disease, ulcerative colitis and coeliac disease.1 However, the paper by Lambrechtset al (see page 643) clearly demonstrates that in the absence of stimulation, the healthy intestine contains significant numbers of IL-4 and IFN-γ elaborating intestinal lymphocytes. Using intracytoplasmic staining followed by flow cytometric analysis, this proportion was found to increase dramatically in response to stimulation with almost two thirds …

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