Inflammatory bowel disease and pregnancy: overlapping pathways

Transl Res. 2012 Jul;160(1):65-83. doi: 10.1016/j.trsl.2011.12.002. Epub 2011 Dec 23.

Abstract

Several studies have reported on the association between inflammatory bowel disease (IBD) and adverse pregnancy outcomes, such as preterm birth. The exact mechanisms of action are unclear; however, several pathways and processes are involved in both IBD and pregnancy that may help explain this. In this review, we discuss the immune system's T helper cells and human leukocyte antigens, inflammation, its function, and the role of Toll-like receptors (TLRs), NOD-like receptors (NLRs), and prostaglandins in the inflammatory response. For each of these topics, we consider their involvement in IBD and pregnancy, and we speculate as to how they can lead to preterm birth. Finally, we review briefly corticosteroids, biologic therapies, and immunosuppressants for the treatment of IBD, as well as their safety in use during pregnancy, with special focus on preterm birth.

Publication types

  • Review

MeSH terms

  • Adrenal Cortex Hormones / therapeutic use
  • Female
  • HLA Antigens / genetics
  • Humans
  • Immunosuppressive Agents / therapeutic use
  • Infant, Newborn
  • Inflammation / complications
  • Inflammation / immunology
  • Inflammatory Bowel Diseases / complications*
  • Inflammatory Bowel Diseases / immunology*
  • Inflammatory Bowel Diseases / therapy
  • Models, Immunological
  • Nod Signaling Adaptor Proteins / metabolism
  • Pregnancy
  • Pregnancy Complications / etiology
  • Pregnancy Complications / immunology*
  • Pregnancy Complications / therapy
  • Premature Birth / etiology
  • Prostaglandins / metabolism
  • Risk Factors
  • T-Lymphocytes, Helper-Inducer / immunology
  • Toll-Like Receptors / metabolism
  • Translational Research, Biomedical
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors

Substances

  • Adrenal Cortex Hormones
  • HLA Antigens
  • Immunosuppressive Agents
  • Nod Signaling Adaptor Proteins
  • Prostaglandins
  • Toll-Like Receptors
  • Tumor Necrosis Factor-alpha