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Mechanisms of Inflammation in Lung Tissue

  • Donald L. Kreutzer
  • Usha Desai
  • William H. J. Douglas
  • Mark Blazka
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 134)

Abstract

Inflammation can be seen as a balance of pro-inflammatory and anti-inflammatory reactions, with pro-inflammatory reactions involved in the initiation and amplification of inflammation via mediators (chemotactic and vasopermeability factors) and tissue injury (by loss of cell function and death). Anti-inflammatory reactions, on the other hand, will suppress inflammation by inactivation of these mediators (via chemotactic factor inactivator [CFI] and anaphylatoxin inactivator), thus reducing the delivery of destructive enzymes and products of activated leukocytes (1). Although basic mechanisms of inflammatory processes are beginning to be reasonably well understood in the kidney, relatively little is known about inflammation in the lung. Insult to the lung, whether immunologic, infectious or environmental, often will activate intrinsic systems such as the complement system, which generates vasopermeability and chemotactic factors. These factors will recruit leukocytes and serum factors into the lung which will directly damage lung structure and function. In addition, these recruited leukocytes have the potential capacity to amplify inflammatory reactions and tissue injury by various mechanisms: 1. release of lysosomal enzymes; 2. production of free radicals and other factors that damage structural elements; 3. the activation or direct cleavage of complement, complement components, or other lung constituents into active chemotactic factors; 4. activation of other inflammatory pathways such as coagulation; and 5. stimulation of resident lung cells such as macrophages or type II cells to elaborate preformed (chemotactic factors) and precursor (C3 and C5) inflammatory mediators which would increase the recruitment of leukocytes (PMN’s and monocytes) into the lung. At the same time, anti-inflammatory modulators such as the CFI system (serum and cell-derived CFI’s) serve to regulate and limit the inflammatory reactions by inactivating the chemotactic factors, thus blocking the influx of leukocytes into the lung (2). When pro-inflammatory and anti-inflammatory reactions are properly balanced, inflammation will occur with minimal damage to healthy tissue. Uncontrolled, these inflammatory reactions can destroy healthy tissue with resulting loss of normal lung architecture and function.

Keywords

Lung Tissue Human Serum Albumin Idiopathic Pulmonary Fibrosis Complement Component Chemotactic Factor 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Ward, P.A. In: Granulocyte Physiology Function and Dysfunction, ed. Beckman. American Association of Blood Banks (1979) 35.Google Scholar
  2. 2.
    Kreutzer, D.L. et al. Clin Immunol Immunopathol 12 (1979) 162.PubMedCrossRefGoogle Scholar
  3. 3.
    Ward, P.A. et al. J Exp Med 122 (1965) 327.PubMedCrossRefGoogle Scholar
  4. 4.
    Showeil, H.J. et al. J Exp Med 143 (1976) 1154.CrossRefGoogle Scholar
  5. 5.
    Fernandez, H.N. et al. J Immunol 120 (1978) 109.PubMedGoogle Scholar
  6. 6.
    Schiffman, E. et al. Proc Natl Acad Sci USA 72 (1975) 1059.CrossRefGoogle Scholar
  7. 7.
    Kreutzer, D.L. et al. Immunopharmacol 1 (1979) 39.CrossRefGoogle Scholar
  8. 8.
    Tack, B.F.; Prahl, J.W. Biochemistry 15 (1976) 4513.PubMedCrossRefGoogle Scholar
  9. 9.
    Schreiber, R.D.; Müller-Eberhard, H.J. J Exp Med 140 (1974) 1324.PubMedCrossRefGoogle Scholar
  10. 10.
    Krohn, K. et al. Biochem Biophys Acta 285 (1972) 404.PubMedCrossRefGoogle Scholar
  11. 11.
    Kreutzer, D.L. et al. Chest 75 (1979) 259.PubMedGoogle Scholar
  12. 12.
    Desai, U. et al. Am J Pathol 96 (1979) 71.PubMedGoogle Scholar
  13. 13.
    Ward, P.A.; Hill, J.H. Proc Soc Exp Biol Med 141 (1972) 898.PubMedGoogle Scholar
  14. 14.
    Colten, H.R. Adv Immunol 22 (1976) 67.PubMedCrossRefGoogle Scholar
  15. 15.
    Desai, U. et al. Am J Pathol (in press).Google Scholar

Copyright information

© Plenum Press, New York 1981

Authors and Affiliations

  • Donald L. Kreutzer
    • 1
    • 2
  • Usha Desai
    • 1
    • 2
  • William H. J. Douglas
    • 1
    • 2
  • Mark Blazka
    • 1
    • 2
  1. 1.Department of PathologyUniversity of Connecticut Health CenterFarmingtonUSA
  2. 2.Department of AnatomyTufts Medical CenterBostonUSA

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