Book contents
- Frontmatter
- Contents
- Foreword by James S. Goodwin
- Preface
- 1 A brief history and introduction
- 2 Prostaglandin/leukotriene structure and chemistry: a primer
- 3 Monocytes and macrophages
- 4 Lymphocyte response
- 5 Inflammation and the neutrophil
- 6 Malignancy and the arachidonic acid cascade
- 7 Tissue and organ transplantation
- 8 Rheumatoid arthritis and autoimmunity
- 9 Traumatic injury and surgery
- 10 Allergy
- Index
7 - Tissue and organ transplantation
Published online by Cambridge University Press: 24 November 2009
- Frontmatter
- Contents
- Foreword by James S. Goodwin
- Preface
- 1 A brief history and introduction
- 2 Prostaglandin/leukotriene structure and chemistry: a primer
- 3 Monocytes and macrophages
- 4 Lymphocyte response
- 5 Inflammation and the neutrophil
- 6 Malignancy and the arachidonic acid cascade
- 7 Tissue and organ transplantation
- 8 Rheumatoid arthritis and autoimmunity
- 9 Traumatic injury and surgery
- 10 Allergy
- Index
Summary
The role of the products of arachidonic acid metabolism in the immunological response to transplanted tissues has been very difficult to evaluate. This is primarily because a large volume of seemingly contradictory data has been generated by experiments in which cyclooxygenase and/or lipoxygenase inhibitors have been used, with quite mixed results, as an adjunct to transplant survival. For example, several investigators have reported that the presence of PGs, particularly PGE, significantly improved skin allograft survival in mice, while others have reported quite the opposite effect (1–4). In a recent paper, however, Foegh et al. have outlined an approach, which helps reconcile such opposing data (5). This is summarized in Figure 7.1. Arachidonic acid metabolites can be considered to belong to one of two groups: those products promoting tissue rejection, and those preventing it. It appears that most, if not all, of these metabolites are present in each transplant, and that survival or rejection of the tissue is dependent upon their balance and net cumulative activity. It is not surprising, therefore, that blanket pharmacological inhibition of cyclooxygenase activity might or might not be successful at prolonging transplant survival. A targeted manipulation of specific metabolites might lead to the generation of more interpretable data.
PGI2, PGE2, and PGD2 are recognized as antirejection metabolites.
- Type
- Chapter
- Information
- Prostaglandins, Leukotrienes, and the Immune Response , pp. 136 - 156Publisher: Cambridge University PressPrint publication year: 1988
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