Association between early airway damage-associated molecular patterns and subsequent bacterial infection in patients with inhalational and burn injury

American Journal of Physiology - Lung Cellular and Molecular Physiology

Volumn 308, Issue 9, 2015, Pages L855-L860

  Mail, Robert ^a,b   Jones, Samuel ^a,b   Pan, Yinghao ^c   Zhou, Haibo ^c   Jaspers, Ilona ^a   Peden, David B ^a   Cairns, Bruce A ^a,b   Noah, Terry L ^a  

^a UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE   (United States)

^b North Carolina Jaycee Burn Center   (United States)

^c University of North Carolina at Chapel Hill   (United States)

Author keywords

Acute lung injury; Burn injury; Inhalational injury; Innate immunology; Respiratory infection

Indexed keywords

BIOLOGICAL MARKER; DAMAGE ASSOCIATED MOLECULAR PATTERN; DOUBLE STRANDED DNA; GAMMA INTERFERON; HEAT SHOCK PROTEIN 70; HIGH MOBILITY GROUP B1 PROTEIN; HYALURONIC ACID; INTERLEUKIN 10; INTERLEUKIN 12P70; INTERLEUKIN 1BETA; INTERLEUKIN 6; INTERLEUKIN 8; TRANSFORMING GROWTH FACTOR BETA; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG; DNA; HMGB1 PROTEIN, HUMAN; IL10 PROTEIN, HUMAN;

ACUTE LUNG INJURY; ADULT; ARTICLE; ARTIFICIAL VENTILATION; BACTERIAL INFECTION; BACTERIUM CULTURE; BODY SURFACE; BRONCHOSCOPY; BURN; BURN PATIENT; BURN UNIT; CLINICAL FEATURE; CONTROLLED STUDY; CYTOKINE PRODUCTION; DISEASE ASSOCIATION; FEMALE; HUMAN; HUMAN TISSUE; INFLAMMATION; INJURY SEVERITY; LUNG BURN; MAJOR CLINICAL STUDY; MALE; MEDIATOR RELEASE; MIDDLE AGED; OBSERVATIONAL STUDY; PRIORITY JOURNAL; PROSPECTIVE STUDY; TISSUE INJURY; TRACHEOBRONCHIAL TOILET; UNITED STATES; UNIVERSITY HOSPITAL; LUNG; LUNG INJURY; METABOLISM; PATHOLOGY;

ADULT; BACTERIAL INFECTIONS; BIOMARKERS; BRONCHOSCOPY; BURNS, INHALATION; DNA; FEMALE; HMGB1 PROTEIN; HSP70 HEAT-SHOCK PROTEINS; HUMANS; HYALURONIC ACID; INTERLEUKIN-10; LUNG; LUNG INJURY; MALE; MIDDLE AGED; PROSPECTIVE STUDIES; RESPIRATION, ARTIFICIAL;

EID: 84929678126     PISSN: 10400605     EISSN: 15221504     Source Type: Journal    
DOI: 10.1152/ajplung.00321.2014     Document Type: Article

References (31)

1. Beutler B. Inferences, questions and possibilities in Toll-like receptor signalling. Nature 430: 257–263, 2004.
2. Beutler B. Innate immune sensing of microbial infection: the mechanism and the therapeutic challenge. Wien Med Wochenschr 152: 547–551, 2002.
3. Bianchi ME. DAMPs, PAMPs and alarmins: all we need to know about danger. J Leukoc Biol 81: 1–5, 2007.
4. Biswas SK, Chittezhath M, Shalova IN, Lim JY. Macrophage polarization and plasticity in health and disease. Immunol Res 53: 11–24, 2012.
5. Cairns BA, Barnes CM, Mlot S, Meyer AA, Maile R. Toll-like receptor 2 and 4 ligation results in complex altered cytokine profiles early and late after burn injury. J Trauma 64: 1069–1077; discussion 1077–1068, 2008.
6. Carr JA, Phillips BD, Bowling WM. The utility of bronchoscopy after inhalation injury complicated by pneumonia in burn patients: results from the National Burn Repository. J Burn Care Res 30: 967–974, 2009.
7. Cohen MJ, Carroll C, He LK, Muthu K, Gamelli RL, Jones SB, Shankar R. Severity of burn injury and sepsis determines the cytokine responses of bone marrow progenitor-derived macrophages. J Trauma 62: 858–867, 2007.
8. Csontos C, Foldi V, Palinkas L, Bogar L, Roth E, Weber G, Lantos J. Time course of pro- and anti-inflammatory cytokine levels in patients with burns–prognostic value of interleukin-10. Burns 36: 483–494, 2010.
9. D’Avignon LC, Hogan BK, Murray CK, Loo FL, Hospenthal DR, Cancio LC, Kim SH, Renz EM, Barillo D, Holcomb JB, Wade CE, Wolf SE. Contribution of bacterial and viral infections to attributable mortality in patients with severe burns: an autopsy series. Burns 36: 773–779, 2010.
10. Harter L, Mica L, Stocker R, Trentz O, Keel M. Increased expression of toll-like receptor-2 and -4 on leukocytes from patients with sepsis. Shock 22: 403–409, 2004.
11. Hauser CJ, Sursal T, Rodriguez EK, Appleton PT, Zhang Q, Itagaki K. Mitochondrial damage associated molecular patterns from femoral reamings activate neutrophils through formyl peptide receptors and P44/42 MAP kinase. J Orthop Trauma 24: 534–538, 2010.
12. Hotchkiss RS, Coopersmith CM, McDunn JE, Ferguson TA. The sepsis seesaw: tilting toward immunosuppression. Nat Med 15: 496–497, 2009.
13. Huebener P, Pradere JP, Hernandez C, Gwak GY, Caviglia JM, Mu X, Loike JD, Jenkins RE, Antoine DJ, Schwabe RF. The HMGB1/ RAGE axis triggers neutrophil-mediated injury amplification following necrosis. J Clin Invest 125: 539–550, 2015.
14. Jones SW, Zhou H, Ortiz-Pujols SM, Maile R, Herbst M, Joyner BL Jr, Zhang H, Kesic M, Jaspers I, Short KA, Meyer AA, Peden DB, Cairns BA, Noah TL. Bronchoscopy-derived correlates of lung injury following inhalational injuries: a prospective observational study. PLoS One 8: e64250, 2013.
15. Kasten KR, Muenzer JT, Caldwell CC. Neutrophils are significant producers of IL-10 during sepsis. Biochem Biophys Res Commun 393: 28–31, 2010.
16. Kuipers MT, van der Poll T, Schultz MJ, Wieland CW. Bench-tobedside review: damage-associated molecular patterns in the onset of ventilator-induced lung injury. Crit Care 15: 235, 2011.
17. Lange M, Hamahata A, Traber DL, Esechie A, Jonkam C, Bansal K, Nakano Y, Traber LD, Enkhbaatar P. A murine model of sepsis following smoke inhalation injury. Biochem Biophys Res Commun 391: 1555–1560, 2010.
18. Martins PS, Brunialti MK, Martos LS, Machado FR, Assuncao MS, Blecher S, Salomao R. Expression of cell surface receptors and oxidative metabolism modulation in the clinical continuum of sepsis. Crit Care 12: R25, 2008.
19. Murakami K, Traber DL. Pathophysiological basis of smoke inhalation injury. News Physiol Sci 18: 125–129, 2003.
20. Murray PJ, Allen JE, Biswas SK, Fisher EA, Gilroy DW, Goerdt S, Gordon S, Hamilton JA, Ivashkiv LB, Lawrence T, Locati M, Mantovani A, Martinez FO, Mege JL, Mosser DM, Natoli G, Saeij JP, Schultze JL, Shirey KA, Sica A, Suttles J, Udalova I, van Ginderachter JA, Vogel SN, Wynn TA. Macrophage activation and polarization: nomenclature and experimental guidelines. Immunity 41: 14–20, 2014.
21. Neely CJ, Maile R, Wang MJ, Vadlamudi S, Meyer AA, Cairns BA. Th17 (IFNgamma- IL17_) CD4_ T cells generated after burn injury may be a novel cellular mechanism for postburn immunosuppression. J Trauma 70: 681–690, 2011.
22. Noel G, Wang Q, Schwemberger S, Hanson C, Giacalone N, Haar L, Ogle CK. Neutrophils, not monocyte/macrophages, are the major splenic source of postburn IL-10. Shock 36: 149–155, 2011.
23. Qin H, Holdbrooks AT, Liu Y, Reynolds SL, Yanagisawa LL, Benveniste EN. SOCS3 deficiency promotes M1 macrophage polarization and inflammation. J Immunol 189: 3439–3448, 2012.
24. Schwacha MG, Chaudry IH, Alexander M. Regulation of macrophage IL-10 production postinjury via beta2 integrin signaling and the P38 MAP kinase pathway. Shock 20: 529–535, 2003.
25. Steinhauser ML, Hogaboam CM, Kunkel SL, Lukacs NW, Strieter RM, Standiford TJ. IL-10 is a major mediator of sepsis-induced impairment in lung antibacterial host defense. J Immunol 162: 392–399, 1999.
26. Sun L, Guo RF, Newstead MW, Standiford TJ, Macariola DR, Shanley TP. Effect of IL-10 on neutrophil recruitment and survival after Pseudomonas aeruginosa challenge. Am J Respir Cell Mol Biol 41: 76–84, 2009.
27. Tolle LB, Standiford TJ. Danger-associated molecular patterns (DAMPs) in acute lung injury. J Pathol 229: 145–156, 2013.
28. Yamaguchi T, Hirakata Y, Izumikawa K, Miyazaki Y, Maesaki S, Tomono K, Yamada Y, Kohno S, Kamihira S. Prolonged survival of mice with Pseudomonas aeruginosa-induced sepsis by rIL-12 modulation of IL-10 and interferon-gamma. J Med Microbiol 49: 701–707, 2000.
29. Zhang Q, Itagaki K, Hauser CJ. Mitochondrial DNA is released by shock and activates neutrophils via p38 map kinase. Shock 34: 55–59, 2010.
30. Zhang Q, Raoof M, Chen Y, Sumi Y, Sursal T, Junger W, Brohi K, Itagaki K, Hauser CJ. Circulating mitochondrial DAMPs cause inflammatory responses to injury. Nature 464: 104–107, 2010.
31. Zhang X, Mosser DM. Macrophage activation by endogenous danger signals. J Pathol 214: 161–178, 2008.