COMMENTARY

Inflammatory bowel disease

The role of eosinophils in inflammatory bowel disease

S Al-Haddad¹ and R H Riddell²

¹ Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada
² Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada

Correspondence to:
Correspondence to:
Dr S Al-Haddad
Department of Laboratory Medicine, St Michael’s Hospital, 30 Bond St, Cardinal Carter Wing, Room 2-091, Toronto, Ontario, Canada M5B 1W8; Al-addadS@smh.toronto.on.ca

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Numbers of activated eosinophils are higher in patients with active and inactive ulcerative colitis (UC) compared with controls, but higher in the quiescent than in the active phase, indicating that eosinophils may play diverse roles in the pathophysiology of inflammatory bowel disease (proinflammatory versus repair)

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Keywords: neutrophils; ulcerative colitis; eosinophils; inflammatory bowel disease; inflammatory cells; Crohn’s disease

The first 150 words of the full text of this article appear below.

Eosinophils are proinflammatory leucocytes that constitute a small percentage of circulating blood cells. In the healthy state, most of these cells reside in the gastrointestinal tract within the lamina propria of the stomach and intestine. They differentiate in the bone marrow from progenitor cells under the influence of interleukin (IL)-3, IL-5, and granulocyte-macrophage colony stimulating factor. IL-5 also stimulates their release into the peripheral circulation.¹ They then migrate to the gastrointestinal tract in response to eotaxin, a chemokine that is constitutively expressed throughout the gastrointestinal tract. This chemokine binds to the CCR-3 receptor on eosinophils and is required for their homing to the gastrointestinal tract.^2,3 However, constitutive expression of eotaxin is not sufficient for tissue eosinophil trafficking because some gastrointestinal segments (such as the tongue and oesophagus) express eotaxin but are normally devoid of eosinophils.¹ So this may explain why the help of other cytokines is needed . . . [Full text of this article]

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