11. Fibroblasts

  1. Kenji Izuhara MD, PhD3,
  2. Stephen T. Holgate MD, DSc, FMedSci4 and
  3. Marsha Wills-Karp PhD5
  1. Alastair G. Stewart PhD1,
  2. Lilian Soon PhD2 and
  3. Michael Schuliga PhD1

Published Online: 27 JUL 2011

DOI: 10.1002/9781444346688.ch11

Inflammation and Allergy Drug Design

Inflammation and Allergy Drug Design

How to Cite

Stewart, A. G., Soon, L. and Schuliga, M. (2011) Fibroblasts, in Inflammation and Allergy Drug Design (eds K. Izuhara, S. T. Holgate and M. Wills-Karp), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781444346688.ch11

Editor Information

  1. 3

    Department of Biomolecular Sciences, Division of Medical Biochemistry, Saga Medical School, Nabeshima, Saga, Japan

  2. 4

    School of Medicine, Allergy and Inflammation Research, Southampton General Hospital, University Medicine, Southampton, UK

  3. 5

    Division of Immunology, Cincinnati Children's Medical Center, Cincinnati, OH, USA

Author Information

  1. 1

    Department of Pharmacology, University of Melbourne, Parkville, VIC, Australia

  2. 2

    Australian Centre for Microscopy and Microanalysis, University of Sydney, Sydney, NSW, Australia

Publication History

  1. Published Online: 27 JUL 2011
  2. Published Print: 13 AUG 2011

ISBN Information

Print ISBN: 9781444330144

Online ISBN: 9781444346688



  • fibroblasts, and structural changes - chronic asthma and goblet cell increase;
  • smooth muscle, close to epithelium - and larger airway smooth muscle (ASM) cells;
  • Holgate and colleagues, and idea - that remodeling, by defect in response to injury of epithelial mesenchymal trophic unit (EMTU);
  • allergen challenge, increasing activity - of subepithelial myofibroblasts;
  • dynamic equilibrium, in remodeled asthmatic airway - flux of cell division/apoptosis, and structural change;
  • impediments to target validation - in airway remodeling, uncertainties of remodeling process;
  • remodelling activities of airway fibroblasts - fibroblasts and myofibroblasts in airway wall;
  • drug targets - processes mediators and receptors;
  • urokinase plasminogen activator - plasminogen activation system, and fibroblast function;
  • functional antagonists, of fibroblast function - case, for multivalent treatments in asthma


Attempts to ameliorate the contribution of fibroblast remodeling and inflammation in allergy and asthma requires a thorough understanding of proliferation, survival, migration, differentiation, contraction, extracellular matrix synthesis and remodeling, and mediator production. Pharmacologic approaches that have a breadth of impact will need to be targeted to dominant causative cytokines or their common signaling pathways, or be pleiotropic in functionally antagonizing the fibrogenic activities of the fibroblast.