IMMUNE RESPONSE TO TRAUMATIC INJURY: BALANCE AND DISRUPTION OF IMMUNE SYSTEM HOMEOSTASIS
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Аннотация:
Trauma is a leading cause of death globally, disrupting immune system balance and potentially causing infections and inflammatory issues. A major challenge is preventing multiple organ dysfunction syndrome (MODS) due to septic complications following severe trauma. Typically, after a severe injury, the immune system shifts from a pro-inflammatory to a counter-inflammatory state, which is seen as a protective response to balance the innate and adaptive immune systems. Our research shows that injury activates inflammasomes and primes Toll-like receptors, enhancing the innate immune system’s antimicrobial defense. However, trauma can also cause a "two-hit" response. Additionally, we found that injury increases regulatory T cell activity, which can influence this "two-hit" response. This paper explores how traumatic injury triggers a unique immune response, possibly initiated by damage-associated molecular pattern molecules (DAMPs), a mix of endogenous danger signals, including alarmins and pathogen-associated molecular pattern molecules (PAMPs).
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Библиографические ссылки:
World Health Organization . The global burden of disease [database on the Internet]. 2013. [Cited 19 Aug 2013]. Available from URL: http://www.who.int/healthinfo/global_burden_disease/en/
Trunkey DD. Trauma. Accidental and intentional injuries account for more years of life lost in the U.S. than cancer and heart disease. Among the prescribed remedies are improved preventive efforts, speedier surgery and further research. Sci. Am. 1983; 249: 28–35. [PubMed] [Google Scholar]
Wafaisade A, Lefering R, Bouillon B et al Epidemiology and risk factors of sepsis after multiple trauma: an analysis of 29,829 patients from the Trauma Registry of the German Society for Trauma Surgery. Crit. Care Med. 2011; 39: 621–628. [PubMed] [Google Scholar]
Moore FA, Moore EE, Read RA. Postinjury multiple organ failure: role of extrathoracic injury and sepsis in adult respiratory distress syndrome. New Horiz. 1993; 1: 538–549. [PubMed] [Google Scholar]
Baue AE, Durham R, Faist E. Systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), multiple organ failure (MOF): are we winning the battle? Shock 1998; 10: 79–89. [PubMed] [Google Scholar]
Baue AE. MOF, MODS, and SIRS: what is in a name or an acronym? Shock 2006; 26: 438–449. [PubMed] [Google Scholar]
Bone RC. Sir Isaac Newton, sepsis, SIRS, and CARS. Crit. Care Med. 1996; 24: 1125–1128. [PubMed] [Google Scholar]
Osuchowski MF, Welch K, Siddiqui J, Remick DG. Circulating cytokine/inhibitor profiles reshape the understanding of the SIRS/CARS continuum in sepsis and predict mortality. J. Immunol. 2006; 177: 1967–1974. [PubMed] [Google Scholar]
Matzinger P. The danger model: a renewed sense of self. Science 2002; 296: 301–305. [PubMed] [Google Scholar]
Harris HE, Raucci A. Alarmin(g) news about danger: workshop on innate danger signals and HMGB1. EMBO Rep. 2006; 7: 774–778. [PMC free article] [PubMed] [Google Scholar]
Oppenheim JJ, Yang D. Alarmins: chemotactic activators of immune responses. Curr. Opin. Immunol. 2005; 17: 359–365. [PubMed] [Google Scholar]
Manson J, Thiemermann C, Brohi K. Trauma alarmins as activators of damage‐induced inflammation. Br. J. Surg. 2012; 99(Suppl. 1): 12–20. [PubMed] [Google Scholar]
Matzinger P. An innate sense of danger. Ann. N. Y. Acad. Sci. 2002; 961: 341–342. [PubMed] [Google Scholar]
Ogura H, Tanaka H, Koh T et al Priming, second‐hit priming, and apoptosis in leukocytes from trauma patients. J. Trauma 1999; 46: 774–781, discussion 81–3. [PubMed] [Google Scholar]
Hoover L, Bochicchio GV, Napolitano LM et al Systemic inflammatory response syndrome and nosocomial infection in trauma. J. Trauma 2006; 61: 310–316, discussion 6–7. [PubMed] [Google Scholar]
Osuka A, Hanschen M, Stoecklein V, Lederer JA. A protective role for inflammasome activation following injury. Shock 2012; 37: 47–55. [PMC free article] [PubMed] [Google Scholar]
Mizushima Y, Ueno M, Idoguchi K, Ishikawa K, Matsuoka T. Fever in trauma patients: friend or foe? J. Trauma 2009; 67: 1062–1065. [PubMed] [Google Scholar]
Paterson HM, Murphy TJ, Purcell EJ et al Injury primes the innate immune system for enhanced Toll‐like receptor reactivity. J. Immunol. 2003; 171: 1473–1483. [PubMed] [Google Scholar]
Zang Y, Dolan SM, Ni Choileain N et al Burn injury initiates a shift in superantigen‐induced T cell responses and host survival. J. Immunol. 2004; 172: 4883–4892. [PubMed] [Google Scholar]
Maung AA, Fujimi S, MacConmara MP et al Injury enhances resistance to Escherichia coli infection by boosting innate immune system function. J. Immunol. 2008; 180: 2450–2458. [PubMed] [Google Scholar]
Southard R, Ghosh S, Hilliard J et al Pulmonary contusion is associated with toll‐like receptor 4 upregulation and decreased susceptibility to pseudomonas pneumonia in a mouse model. Shock 2012; 7: 629–633. [PMC free article] [PubMed] [Google Scholar]
Grossman JA, Adams JP, Kunec J. Prophylactic antibiotics in simple hand lacerations. JAMA 1981; 245: 1055–1056. [PubMed] [Google Scholar]
Fan J, Li Y, Levy RM et al Hemorrhagic shock induces NAD(P)H oxidase activation in neutrophils: role of HMGB1‐TLR4 signaling. J. Immunol. 2007; 178: 6573–6580. [PubMed] [Google Scholar]
Fan J, Kapus A, Li YH, Rizoli S, Marshall JC, Rotstein OD. Priming for enhanced alveolar fibrin deposition after hemorrhagic shock: role of tumor necrosis factor. Am. J. Respir. Cell Mol. Biol. 2000; 22: 412–421. [PubMed] [Google Scholar]
Bone RC. Immunologic dissonance: a continuing evolution in our understanding of the systemic inflammatory response syndrome (SIRS) and the multiple organ dysfunction syndrome (MODS). Ann. Intern. Med. 1996; 125: 680–687. [PubMed] [Google Scholar]
Sauaia A, Moore FA, Moore EE, Lezotte DC. Early risk factors for postinjury multiple organ failure. World J. Surg. 1996; 20: 392–400. [PubMed] [Google Scholar]
Ninnemann JL, Fisher JC, Frank HA. Prolonged survival of human skin allografts following thermal injury. Transplantation 1978; 25: 69–72. [PubMed] [Google Scholar]
Lederer JA, Rodrick ML, Mannick JA. The effects of injury on the adaptive immune response. Shock 1999; 11: 153–159. [PubMed] [Google Scholar]
Faist E, Schinkel C, Zimmer S. Update on the mechanisms of immune suppression of injury and immune modulation. World J. Surg. 1996; 20: 454–459. [PubMed] [Google Scholar]
De AK, Kodys KM, Pellegrini J et al Induction of global anergy rather than inhibitory Th2 lymphokines mediates posttrauma T cell immunodepression. Clin. Immunol. 2000; 96: 52–66. [PubMed] [Google Scholar]
Kelly JL, O'Suilleabhain CB, Soberg CC, Mannick JA, Lederer JA. Severe injury triggers antigen‐specific T‐helper cell dysfunction. Shock 1999; 12: 39–45. [PubMed] [Google Scholar]
Murphy T, Paterson H, Rogers S, Mannick JA, Lederer JA. Use of intracellular cytokine staining and bacterial superantigen to document suppression of the adaptive immune system in injured patients. Ann. Surg. 2003; 238: 401–410, discussion 10–1. [PMC free article] [PubMed] [Google Scholar]
O'Sullivan ST, Lederer JA, Horgan AF, Chin DH, Mannick JA, Rodrick ML. Major injury leads to predominance of the T helper‐2 lymphocyte phenotype and diminished interleukin‐12 production associated with decreased resistance to infection. Ann. Surg. 1995; 222: 482–490, discussion 90–2. [PMC free article] [PubMed] [Google Scholar]
Mack VE, McCarter MD, Naama HA, Calvano SE, Daly JM. Candida infection following severe trauma exacerbates Th2 cytokines and increases mortality. J. Surg. Res. 1997; 69: 399–407. [PubMed] [Google Scholar]
Guo Z, Kavanagh E, Zang Y et al Burn injury promotes antigen‐driven Th2‐type responses in vivo. J. Immunol. 2003; 171: 3983–3990. [PubMed] [Google Scholar]