The pathophysiology of inflammation in cell injury

 

 
crossMark
 
Pathophysiology of Cell Injury Journal  Volume 3, Issue 1, pages 1-9 June 2014

Elizabeth Rispens, Amanda Bron, Julie Lee, Jimmy Fukumoto

Abstract

The purpose of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and to initiate tissue repair. The process of acute inflammation is initiated by resident immune cells already present in the involved tissue, mainly residentmacrophages, dendritic cells, histiocytes, Kupffer cells andmastocytes. These cells present on their surfaces certain receptors named pattern recognition receptors (PRRs), which recognise generic molecules that are broadly shared bypathogens but distinguishable from host molecules, collectively referred to as pathogen-associated molecular patterns (PAMPs). Inflammatory abnormalities are a large group of disorders that underlie a vast variety of human diseases. The immune system is often involved with inflammatory disorders, demonstrated in both allergic reactions and some myopathies, with many immune system disorders resulting in abnormal inflammation. Non-immune diseases with etiological origins in inflammatory processes include cancer, atherosclerosis, and ischaemic heart disease. A large variety of proteins are involved in inflammation, and any one of them is open to a genetic mutation which impairs or otherwise dysregulates the normal function and expression of that protein. The aim of this narrative review is to provide an overview of pathophysiology and treatments targeting arterial inflammation in these diseases.

Keywords: Inflammation; Immune cells; PRRs; PAMPs

PDF

References

  1. Medzhitov R. Origin and physiological roles of inflammation. Nature. 2008;454(7203):428-435.
  2. Chen GY, Nuñez G. Sterile inflammation: sensing and reacting to damage. Nat Rev Immunol. 2010;10(12):826-837.
  3. Takeuchi O, Akira S. Pattern recognition receptors and inflammation. Cell. 2010;140(6):805-820.
  4. Tschopp J, Schroder K. NLRP3 inflammasome activation: the convergence of multiple signalling pathways. Nat Rev Immunol. 2010;10(3):210-215.
  5. Nathan C, Ding A. Nonresolving inflammation. Cell. 2010;140(6):871-882.
  6. Libby P. Inflammation in atherosclerosis. Nature. 2002;420(6917):868-874.
  7. Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature. 2014;510(7503):92-101.
  8. Galluzzi L, Vitale I, Aaronson SA, et al. Molecular mechanisms of cell death. Cell. 2018;173(5):1313-1326.
  9. O’Neill LAJ, Pearce EJ. Immunometabolism governs dendritic cell and macrophage function. Nat Rev Immunol. 2016;16(9):553-565.
  10. Dinarello CA. Interleukin-1 in the pathogenesis and treatment of inflammatory diseases. Nat Rev Immunol. 2011;11(9):633-642.
  11. Rock KL, Latz E, Ontiveros F, Kono H. The sterile inflammatory response. Annu Rev Immunol. 2010;28:321-342.
  12. Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006;444(7121):860-867.
  13. Ferrero-Miliani L, Nielsen OH, Andersen PS, Girardin SE. Chronic inflammation: importance of NOD2 and NALP3 in interleukin-1β generation. Clin Exp Immunol. 2007;147(2):227-235.
  14. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. 10th ed. Elsevier; 2020.
  15. Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol. 2007;35(4):495-516.
  16. Vanden Berghe T, Linkermann A, Jouan-Lanhouet S, Walczak H, Vandenabeele P. Regulated necrosis: the expanding network of non-apoptotic cell death pathways. Nat Rev Mol Cell Biol. 2014;15(2):135-147.
  17. Dixon SJ, Stockwell BR. The role of iron and reactive oxygen species in cell death. Nat Chem Biol. 2014;10(1):9-17.
  18. Zindel J, Kubes P. DAMPs, PAMPs, and LAMPs in immunity and sterile inflammation. Annu Rev Pathol. 2020;15:493-518.
  19. Brinkmann V, Reichard U, Goosmann C, et al. Neutrophil extracellular traps kill bacteria. Science. 2004;303(5663):1532-1535.
  20. Gordon S, Martinez FO. Alternative activation of macrophages: mechanism and functions. Immunity. 2010;32(5):593-604.
  21. Mantovani A, Biswas SK, Galdiero MR, Sica A, Locati M. Macrophage plasticity and polarization. Nat Rev Immunol. 2013;13(10):759-767.
  22. Chovatiya R, Medzhitov R. Stress, inflammation, and defense of homeostasis. Mol Cell. 2014;54(2):281-288.
  23. Kotas ME, Medzhitov R. Homeostasis, inflammation, and disease susceptibility. Cell. 2015;160(5):816-827.
  24. Tabas I, Glass CK. Anti-inflammatory therapy in chronic disease: challenges and opportunities. Science. 2013;339(6116):166-172.
  25. Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med. 2017;377(12):1119-1131.
  26. Calder PC. Omega-3 fatty acids and inflammatory processes. Nutrients. 2010;2(3):355-374.
  27. Sugimoto MA, Vago JP, Teixeira MM, Sousa LP. Annexin A1 and the resolution of inflammation. J Immunol Res. 2016;2016:8239258.
  28. Fullerton JN, Gilroy DW. Resolution of inflammation: a new therapeutic frontier. Nat Rev Drug Discov. 2016;15(8):551-567.
  29. Lawrence T. The nuclear factor NF-κB pathway in inflammation. Cold Spring Harb Perspect Biol. 2009;1(6):a001651.
  30. Karin M, Clevers H. Reparative inflammation takes charge of tissue regeneration. Nature. 2016;529(7586):307-315.
  31. Greten FR, Grivennikov SI. Inflammation and cancer: triggers, mechanisms, and consequences. Immunity. 2019;51(1):27-41.
  32. Grivennikov SI, Greten FR, Karin M. Immunity, inflammation, and cancer. Cell. 2010;140(6):883-899.
  33. Serhan CN, Levy BD. Resolvins in inflammation: emergence of the pro-resolving superfamily of mediators. J Clin Invest. 2018;128(7):2657-2669.
Print Friendly, PDF & Email