Abstract
Inflammation is a highly effective component of the innate response of the body to infection or injury. The inflammatory response is an important consequence of injury and one that normally leads to repair and restoration of function. Indeed, until the last two or three decades, inflammation was perceived as an entirely beneficial host response. From his experiences on the battle fields of Europe, John Hunter stated “Inflammation is itself not to be considered as a disease but as a salutary operation consequent either to some violence or to some disease” and Eli Metchnikoff (1968), the father of modern inflammatory cell biology, emphasized this concept in his work. The clear-cut implication of these observations is the close connection between the inflammatory process and repair. It has become apparent, however, that inflammation can contribute to the pathogenesis of a large number of diseases. For example, neutrophil infiltration, if not controlled, contributes to tissue injury and necrosis. A relationship between inflammation and scarring has been recognized in such disorders as adult respiratory distress syndrome, fibrosing alveolitis in the lung, hepatitic cirrhosis, glomerulonephritis, as well as infected cutaneous wounds. Extensive scarring or fibrosis of any organ can cause catastrophic loss of function of that organ.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
Similar content being viewed by others
References
Berenberg, J. L., and Ward, P. A., 1973, Chemotactic factor of inactivator in normal human serum, J. Clin. Invest. 52:1200–1207.
Chapes, S. K., and Haskill, S., 1983, Evidence for granulocyte-mediated macrophage activation after C. parvum immunization, Cell Immunol. 75:367–377.
Clark, R. J., Jones, H. A., Rhodes, C. G., and Haslett, C., 1989, Non-invasive assessment in self-limited pulmonary inflammation by external scintigraphy of 111indium-labelled neutrophil influx and by measurement of the local metabolic response with positron emission tomography, Am. Rev. Respir. Dis. 139:A58.
Colditz, I. G., and Movat, H. Z., 1984, Desensitisation of acute inflammatory lesions to chemotaxins and endotoxin, J. Immunol. 133:2163–2168.
Doherty, D. E., Downey, G. P., Worthen, G. S., Haslett, C., and Henson, P. M., 1988. Monocyte retention and migration in pulmonary inflammation, Lab. Invest. 59:200–213.
Duvall, E., Wyllie, A. H., and Morris, R. G., 1985, Macrophage recognition of cells undergoing programmed cell death, Immunology 56:351–358.
Evan, G. I., Wyllie, A. H., Gilbert, G. S., Littlewood, T. D., Land, H., Brooks, M., Waters, C. M., Penn, L. Z., and Hancock, D. C., 1992, Induction of apoptosis in fibroblasts by c-myc protein, Cell 69:119–128.
Fadok, V., Savill, J. S., Haslett, C., Bratton, D. L., Doherty, D. E., Campbell, P. A., and Henson, P. M., 1992a, Different populations of macrophages use either the vitronectin receptor or the phosphatidylserine receptor to recognise and remove apoptotic cells, J. Immunol. 149:4029–4035.
Fadok, V. A., Voelker, D. R., Campbell, P. A., Cohen, J. J., Bratton, D. L., and Henson, P. M., 1992b, Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages, J. Immunol. 148:2207–2216.
Fadok, V. A., Laszlo, D. J., Noble, P. W., Weinstein, L., Riches, D. W. H., and Henson, P. M., 1993, Particle digestibility is required for induction of the phosphatidylserine recognition mechanism used by murine macrophages to phagocytose apoptotic cells, J. Immunol. 151:4274–4285.
Fanidi, A., Harrington, E. A., and Evan, G. I., 1992, Co-operative interaction between c-myc and bcl-2 proto-oncogenes, Nature 359:554–556.
Grigg, J. M., Savill, J. S., Sarraf, C., Haslett, C., and Silverman, M., 1991, Neutrophil apoptosis and clearance from neonatal lungs, Lancet 338:720–722.
Hall, S. E., Savill, J. S., Henson, P. M., and Haslett, C., 1994, Apoptotic neutrophils are phagocytosed by fibroblasts with participation of the fibroblast vitronectin receptor and involvement of a mannose/fucose-specific lectin, J. Immunol 153:3218–3227.
Haslett, C., Jose, P. J., Giclas, P. C., Williams, T. J., and Henson, P. M., 1989a, Cessation of neutrophil influx in C5a-induced acute experimental arthritis is associated with loss of chemoattractant activity from joint spaces, J. Immunol. 142:3510–3517.
Haslett, C., Shen, A. S., Feldsien, D. C., Allen, D., Henson, P. M., and Cherniack, R. M., 1989b, 111Indium-labelled neutrophil flux into the lungs of bleomycin-treated rabbits assessed non-invasively by external scintigraphy, Am. Rev. Respir. Dis. 140:756–763.
Haudenschild, C. L., and Schwartz, S. M., 1979, Endothelial regeneration. II. Restitution of endothelial continuity, Lab. Invest. 41:407–418.
Hellewell, P. G., Henson, P. M., Downey, G. P., and Worthen, G. S., 1991, Control of local blood flow in pulmonary inflammation: Role for neutrophils, PAF, and thromboxane, J. Appl. Physiol. 70:1184–1193.
Henson, P. M., Schwartzmann, N. A., and Zanolari, B., 1981, Intracellular control of human neutrophil secretion. II. Stimulus specificity of desensitisation induced by six different soluble and particulate stimuli, J. Immunol. 127:754–759.
Henson, P. M., Henson, J. E., Fittschen, C., Kimani, G., Bratton, D. L., and Riches, D. H. W., 1988, Phagocytic cells: Degranulation and secretion, in: Inflammation, Basic Principals and Clinical Correlates (J. I. Gallin, ed.), pp. 363–390, Raven Press, New York.
Hurley, J., 1963, An electron microscopic study of leukocyte emigration and vascular permeability in rat skin, Aust. J. Exp. Biol. Med. Sci. 41:171–179.
Hurley, J. V., 1983, Termination of acute inflammation. I. Resolution, in: Acute Inflammation, 2nd ed. Churchill Livingstone, pp. 109–117, London.
Kar, S., Ren, Y., Savill, J. S., and Haslett, C., 1993, Inhibition of macrophage phagocytosis in vitro of aged neutrophils increases release of neutrophil contents, Clin Sci (Abstract). 85:27.
Kerr, J. F. R., Wyllie, A. H., and Currie, A. R., 1972, Apoptosis: A basic biological phenomenon with wide-ranging implications in tissue kinetics, Br. J. Cancer 26:239–257.
Larsen, G. L., McCarthy, K., Webster, R. O., Henson, J. E., and Henson, P. M., 1980, A differential effect of C5a and C5a des arg in the induction of pulmonary inflammation, Am. J. Pathol. 100:179–192.
Lee, A., Whyte, M. B. K., and Haslett, C., 1993, Prolonged in vitro lifespan and functional longevity of neutrophils induced by inflammatory mediators acting through inhibition of apoptosis, J. Leuk. Biol. 54:283–288.
Majno, E., and Palade, G. E., 1961, Studies on inflammation. I. The effect of histamine and serotonin on vascular permeability: An electron microscopic study, J. Biol. Phys. Biochem. Cytol. 11:571–605.
Malech, H. D., and Gallin, J. I., 1988, Neutrophils in human diseases, N. Engl. Med. J. 37:687–694.
McConkey, D. J., Nicotera, P., Hartzell, P., Bellomo, G., Wyllie, A. H., and Orrenius, S., 1989, Glucocorticoids activate a suicide process in thymocytes through an elevation of cytosolic Ca2+ concentration, Arch. Biochem. Biophys. 269:365–370.
Meagher, L. C., Savill, J. S., Baker, A., Fuller, R. W., and Haslett, C., 1993, Phagocytosis of apoptotic neutrophils does not induce macrophage release of thromboxane B2, J. Leuk. Biol. in press.
Metchnikoff, E., 1968, Lectures on the Comparative Pathology of Inflammation. Lecture VII. Delivered at the Pasteur Institute in 1891, Dover, New York.
Milks, L., and Cramer, E., 1984, Transepithelial electrical resistance studies during in vitro neutrophil migration, Fed. Proc. 43:477.
Newman, S. L., Henson, J. E., and Henson, P. M., 1982, Phagocytosis of senescent neutrophils by human monocyte-derived macrophages and rabbit inflammatory macrophages, J. Exp. Med. 156:430–442.
Noble, P. W., Henson, P. M., Lucas, C., Mora-Worms, M., Carre, P., and Riches, D. W. H., 1993, Transforming growth factor β TGFβ primes murine macrophages to express inflammatory gene products in response to particulate stimuli by an autocrine/paracrine mechanism, J. Immunol. 151:979–989.
Parsons, P. E., Sugahara, K., Cott, G. R., Mason, R. J., and Henson, P. M., 1987, The effect of neutrophil migration and prolonged neutrophil contact on epithelial permeability, Am. J. Pathol. 129:302–312.
Pekin, T., Malinin, T., and Zwaifler, R., 1967, Unusual synovial fluid findings in Reiter’s syndrome, Ann. Intern. Med. 66:677–684.
Pietsch, M. C., Polzar, B., Stephan, H., Crompton, T., MacDonald, H. R., Mannherz, H. G., and Tschopp, J., 1993, Characterisation of the endogenous deoxyribonuclease involved in nuclear DNA degradation during apoptosis (programmed cell death), EMBO J. 12:371–377.
Savill, J. S., Wyllie, A. H., Henson, J. E., Henson, P. M., and Haslett, C., 1989a, Macrophage phagocytosis of aging neutrophils in inflammation—programmed cell death leads to its recognition by macrophages, J. Clin. Invest. 83:865–875.
Savill, J. S., Henson, P. M., and Haslett, C., 1989b, Phagocytosis of aged human neutrophils by macrophages is mediated by a novel “charge sensitive” recognition mechanism, J. Clin. Invest. 84:1518–1527.
Savill, J. S., Dransfield, I., Hogg, N., and Haslett, C., 1990, Macrophage recognition of “senescent self.” The vitronectin receptor mediates phagocytosis of cells undergoing apoptosis, Nature 342:170–173.
Savill, J. S., Hogg, N., and Haslett, C, 1992a, Thrombospondin co-operates with CD36 and the vitronectin receptor macrophage in recognition of aged neutrophils, J. Clin. Invest. 90:1513–1529.
Savill, J. S., Smith, J., Sarraf, C., Ren, Y., Abbott, F., and Rees, A., 1992b, Glomerular mesangial cells and inflammatory macrophages ingest neutrophils undergoing apoptosis, Kidney Int. 42:924–936.
Savill, J. S., Fadok, V., Hersar, P. M., and Haslett, C., 1993, Phagocyte recognition of cells undergoing apoptosis, Immunol. Today 14:131–136.
Shi, Y., Glynn, J. M., Guilbert, L. J., Cotter, T. G., Bissonnette, R. P., and Green, D. R., 1992, Role for c-myc in activation-induced cell death in T cell hybridomas, Science 257:212–215.
Spitznagel, J. K., 1990, Antibiotic proteins of neutrophils, J. Clin. Invest. 86:1851–1854.
Spriggs, R. S., Boddington, M. M., and Mowat, A., 1978, Joint fluid cytology in Reiter’s syndrome, Ann. Rheum. Dis. 37:557–560.
Steinmann, R. M., Brodie, S. E., and Cohn, Z. A., 1976, Membrane flow during pinocytosis—a sterological analysis, J. Cell Biol. 68:665–687.
Stern, M., Meagher, L., Savill, J., and Haslett, C., 1992, Apoptosis in human eosinophils. Programmed cell death in the eosinophil leads to phagocytosis by macrophages and is modulated by IL-5, J. Immunol. 148:3543–3549.
Vartio, T., Seppa, H., and Vaheri, A., 1981, Susceptibility of soluble and matrix fibronectins to degraduation by tissue proteinases, mast cell chymase and cathepsin G, J. Biol. Chem. 256:471–477.
Vaux, D. L., Cory, S., and Adams, J. M., 1992, Bcl-2 gene promotes haemopoitic cell survival and cooperates with c-myc to immortalise pre-B cells, Nature 335:440–442.
Ward, P. A., and Becker, E. L., 1967, The deactivation of rabbit neutrophils by chemotactic factor and the nature of the activatable esterase, J. Exp. Med. 127:693–709.
Wedmore, C. V., and Williams, T. J., 1981, Control of vascular permeability by polymorphonuclear leukocytes in inflammation, Nature 289:646–650.
Weiss, S. J., 1989, Tissue destruction by neutrophils, N. Engl. Med. J. 320:365–376.
Whyte, M. K. B., Meagher, L. C., Hardwick, S. J., Savill, J. S., and Haslett, C., 1993a, Transient elevations of cytosolic free calcium retard subsequent apoptosis in neutrophils in vitro, J. Clin. Invest. 92:446–455.
Whyte, M. K. B., Meagher, L. C., MacDermott, J., and Haslett, C., 1993b, Down-regulation of neutrophil function by apoptosis: A mechanism for functional isolation of neutrophils from inflammatory mediator stimulation, J. Immunol. 150:5124–5134.
Wyllie, A. H., 1981, Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endo-nuclease activation, Nature 284:555–558.
Wyllie, A. H., Kerr, J. F. R., and Currie, A. R., 1980, Cell death: The significance of apoptosis, Int. Rev. Cytol. 68:251–306.
Zimmerli, W., Seligmann, B., and Gallin, J. I., 1986, Exudation primes human and guinea pig neutrophils for subsequent responsiveness to the chemotactive peptide N-formyl methionyl leucyl phenylamine and increases complement C3bi receptor expression, J. Clin. Invest. 77:925–933.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1988 Springer Science+Business Media New York
About this chapter
Cite this chapter
Haslett, C., Henson, P. (1988). Resolution of Inflammation. In: Clark, R.A.F. (eds) The Molecular and Cellular Biology of Wound Repair. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0185-9_4
Download citation
DOI: https://doi.org/10.1007/978-1-4899-0185-9_4
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4899-0187-3
Online ISBN: 978-1-4899-0185-9
eBook Packages: Springer Book Archive