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Inflammatory response phases and their hypothetical trophic meaning

¹ Surgery Chair, Surgery I Dept, Complutense University of Madrid, and ² Psychobiology Dept, Psychology School, University of Oviedo, Principality of Asturias, Spain

CORRESPONDENCE:

To the Editor:

A recent review by WOOD et al. 1 emphasises the role of oxidative stress, specifically lipid peroxidation, in the pathophysiology of asthma.

We have also found that oxidative stress is involved in the pathophysiology of post­traumatic inflammation 2–4. In order to integrate the different alterations that are produced after injury by mechanical energy, we consider that a response based on the successive functional predominance of the nervous, immune and endocrine systems would be produced. This hypothesis implies that the final and prevalent functions of these systems may represent the consecutive phases of the response to stress and all of them could have a trophic meaning.

Considering that these functions are expressed by the endothelium and, thus, by extension, by the vascular wall, the post­traumatic local inflammatory response could be divided into three phases. The first one is a nervous or immediate phase, with vasoconstriction and vasodilation that lead to the ischemia­reperfusion phenomenon. This, in turn, causes cellular oedema (ischemia) and interstitial oedema (reperfusion). The second phase is an immune or intermediate one, which is the cause of diapedesis or cell migration, especially of neutrophils and macrophages, and which is associated with coagulation and bacterial infiltration of the injured tissue. Finally, there is an endocrine or late phase characterised by proliferation with endothelium and vascular wall modelling (angiogenesis), which, in the case of healing, involves tissular regeneration or wound healing by scar formation 2–4.

Therefore, in an early or nervous phase, the nutrition of the injured tissue would be produced by diffusion (oedema), a mechanism with low energetic requirement that does not require oxygen (ischemia) or that is not correctly used (synthesis of reactive oxygen species (ROS)). Products derived from the degradation of macromolecules by the ROS action can constitute substrates that reach the cells by diffusion. In the intermediate or immune phase, the nutrition could be mediated by the inflammatory cells because both the neutrophils, as well as the macrophages, have a large capacity for intracellular (phagocytosis of debris) and extracellular (release of enzymes) digestion 5, 6. Complex proteins, such as enzymes and debris, can be important sources of fermentation 7. These inflammatory cells respond with respiratory burst and release high concentrations of superoxide anion radical, hydroxyl radical, hypochlorus acid, hypobromite and hydrogen peroxide 1. The lymphatic circulation could predominate in these phases of the inflammation in detriment of the blood circulation. Finally, in the late or endocrine phase, blood circulation is involved in the nutrition 5, 6. Angiogenesis makes it possible to acquire a capillary network that is specialised in supplying oxygen and substrates to cells, which, in turn, use them through oxidative metabolism 6, 8, thus producing regeneration. However, the wounds heal by scar formation, a process in which the fibroblasts, due to their phenotypic plasticity 9, could become intermediary cells of the epithelial nutrition. The deficient capacity of the fibroblasts for this trophic function could explain the defective quality of the epithelium obtained.

Phases that are similar to the above­mentioned ones are commonly described in airway asthmatic inflammation 1, 9. In this way, reactive oxygen species hyperproduction, whether by revascularisation or by reactive oxygen species release by the inflammatory cells during the respiratory burst, could represent primitive trophic mechanisms, which are used by the injured tissue when the use of oxygen by oxidative phosphorylation is not possible. More useful energy (adenosine triphosphate) can be generated through this latter pathway and it is a more elaborated trophic mechanism.

References

1. Wood LG, Gibson PG, Garg ML. Biomarkers of lipid peroxidation, airway inflammation and asthma. Eur Respir J 2003;21:177–186.[Abstract/Free Full Text]
2. Lorente L, Aller MA, Arias JL, Arias J. Complement: a cascade with neuro, immune and endocrine functions (letter). Transplantation 1996;61:1424–1425.[Web of Science][Medline] [Order article via Infotrieve]
3. Lorente L, Aller MA, Arias JL, Alonso MS, Arias J. Clinical biology of nitric oxide (letter). Br J Surg 1996;83:1010–1011.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
4. Aller MA, Arias JL, Lorente L, Nava MP, Durán HJ, Arias J. Neuro­immune­endocrine functional system and vascular pathology. Med Hypotheses 2001;57:561–569.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
5. Lawrence WT. Physiology of the acute wound. Clin Plastic Surg 1998;25:321–340.[Web of Science][Medline] [Order article via Infotrieve]
6. Monaco JL, Lawrence T. Acute wound healing. An overview. Clin Plastic Surg 2003;30:1–12.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
7. Bengmark S. Pre­, pro­ and symbiotics. Curr Opin Clin Nutrition Metab Care 2001;4:571–579.
8. Lingen MW. Role of leukocytes and endothelial cells in the development of angiogenesis in inflammation and wound healing. Arch Pathol Lab Med 2001;125:67–71.[Web of Science][Medline] [Order article via Infotrieve]
9. Davies DE, Wicks J, Powell RM, Puddicombe SM, Holgate ST. Airway remodelling in asthma: new insights. J Allergy Clin Immunol 2003;111:215–215.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Permissions Request Permissions Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Aller, M-A. Articles by Arias, J. Search for Related Content PubMed PubMed Citation Articles by Aller, M-A. Articles by Arias, J.