Springer Seminars in Immunopathology

, Volume 27, Issue 2, pp 249–271

Role of helminths in regulating mucosal inflammation

Authors

    • Department of Internal Medicine, Division of Gastroenterology–HepatologyUniversity of Iowa
    • Division of Gastroenterology–Hepatology (4607 JCP)University of Iowa Hospital and Clinics
  • Robert W. Summers
    • Department of Internal Medicine, Division of Gastroenterology–HepatologyUniversity of Iowa
  • David E. Elliott
    • Department of Internal Medicine, Division of Gastroenterology–HepatologyUniversity of Iowa
Original Paper

DOI: 10.1007/s00281-005-0209-3

Cite this article as:
Weinstock, J.V., Summers, R.W. & Elliott, D.E. Springer Semin Immun (2005) 27: 249. doi:10.1007/s00281-005-0209-3

Abstract

The rapid rise in prevalence of ulcerative colitis (UC) and Crohn’s disease (CD) in highly developed countries suggests that environmental change engenders risk for inflammatory bowel disease (IBD). Eradication of parasitic worms (helminths) through increased hygiene may be one such change that has led to increased prevalence of these diseases. Helminths alter host mucosal and systemic immunity, inhibiting dysregulated inflammatory responses. Animals exposed to helminths are protected from experimental colitis, encephalitis, and diabetes. Patients with CD or UC improve when exposed to whipworm. Lamina propria (LP) mononuclear cells from helminth-colonized mice make less interleukin (IL)-12 p40 and IFN-γ, but more IL-4, IL-13, IL-10, TGF-β, and PGE2 compared to LP mononuclear cells from naive mice. Systemic immune responses show similar skewing toward Th2 and regulatory cytokine production in worm-colonized animal models and humans. Recent reports suggest that helminths induce regulatory T cell activity. These effects by once ubiquitous organisms may have protected individuals from many of the emerging immune-mediated illnesses like IBD, multiple sclerosis, type I diabetes, and asthma.

Copyright information

© Springer-Verlag 2005