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Semin Respir Crit Care Med 2004; 25(1): 85-93
DOI: 10.1055/s-2004-822308
DOI: 10.1055/s-2004-822308
Sepsis and the Lung Host Response
Further Information
Publication History
Publication Date:
12 March 2004 (online)
Sepsis is the leading cause of death in critically ill patients and is the most common risk factor for the development of acute lung injury in medical patients. Initially investigators hypothesized that an excessive proinflammatory response contributed to the pathogenesis of sepsis. However, this hypothesis overlooked the beneficial effects of proinflammatory mediators and the detrimental effects of an excessive anti-inflammatory response. This has led to a new hypothesis where sepsis is characterized by imbalances of the pro- and anti-inflammatory responses, with tissue injury the result of an excessive proinflammatory response and impaired pulmonary host defense the result of an excessive anti-inflammatory response. This article reviews clinical studies and animal models which show that sepsis results in an impaired lung host response to bacteria. Information in this article should provide the reader with an increased understanding of the pathogenesis of sepsis and the realization that new therapeutic strategies for sepsis need to take into account the need to balance pro- and anti-inflammatory responses to maintain pulmonary host defenses and prevent the development of acute lung injury.
KEYWORDS
Sepsis - innate immunity - pulmonary host defenses
REFERENCES
- 1 Brun-Buisson C, Doyon F, Carlet J et al.. Incidence, risk factors, and outcome of severe sepsis and septic shock in adults. JAMA. 1995; 274 968-974
- 2 Angus D C, Linde-Zwirble W T, Lidicker J et al.. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med. 2001; 29 1303-1310
- 3 Pinner R W, Teutsch S M, Simonsen L et al.. Trends in infectious diseases mortality in the United States. JAMA. 1996; 275 189-193
- 4 Simonsen L, Conn L A, Pinner R W, Teutsch S. Trends in infectious disease hospitalizations in the United States, 1980-1994. Arch Intern Med. 1998; 158 1923-1928
- 5 McBean M, Rajamani S. Increasing rates of hospitalization due to septicemia in the US elderly population, 1986-1997. J Infect Dis. 2001; 183 596-603
- 6 Bone R C, Balk R A, Cerra F B et al.. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. Chest. 1992; 101 1644-1655
- 7 Bone R C. Why sepsis trials fail. JAMA. 1996; 276 565-566
- 8 Goldie A S, Fearon K C, Ross J A et al.. Natural cytokine antagonists and endogenous antiendotoxin core antibodies in sepsis syndrome. The Sepsis Intervention Group. JAMA. 1995; 274 172-177
- 9 Bone R C, Grodzin C J, Balk R A. Sepsis: a new hypothesis for pathogenesis of the disease process. Chest. 1997; 112 235-243
- 10 Nelson S. A question of balance. Am J Respir Crit Care Med. 1999; 159(5 Pt 1) 1365-1367
- 11 Munford R S, Pugin J. Normal responses to injury prevent systemic inflammation and can be immunosuppressive. Am J Respir Crit Care Med. 2001; 163 316-321
- 12 Hotchkiss R S, Karl I E. The pathophysiology and treatment of sepsis. N Engl J Med. 2003; 348 138-150
- 13 Sibille Y, Reynolds H Y. Macrophages and polymorphonuclear neutrophils in lung defense and injury. Am Rev Respir Dis. 1990; 141 471-501
- 14 Standiford T J, Kunkel S L, Greenberger M J, Laichalk L L, Strieter R M. Expression and regulation of chemokines in bacterial pneumonia. J Leukoc Biol. 1996; 59 24-28
- 15 Zhang P, Summer W R, Bagby G J, Nelson S. Innate immunity and pulmonary host defense. Immunol Rev. 2000; 173 39-51
- 16 Gordon S B, Read R C. Macrophage defences against respiratory tract infections. Br Med Bull. 2002; 61 45-61
- 17 Hensler T, Hecker H, Heeg K et al.. Distinct mechanisms of immunosuppression as a consequence of major surgery. Infect Immun. 1997; 65 2283-2291
- 18 Hensler T, Heidecke C D, Hecker H et al.. Increased susceptibility to postoperative sepsis in patients with impaired monocyte IL-12 production. J Immunol. 1998; 161 2655-2659
- 19 van der Poll T, de Wall Malefyt R, Coyle S M, Lowry S F. Antiinflammatory cytokine responses during clinical sepsis and experimental endotoxemia: sequential measurements of plasma soluble interleukin (IL)-1 receptor type II, IL-10, and IL-13. J Infect Dis. 1997; 175 118-122
- 20 Ferguson N R, Galley H F, Webster N R. T helper cell subset ratios in patients with severe sepsis. Intensive Care Med. 1999; 25 106-109
- 21 Zimmer S, Pollard V, Marshall G D et al.. Effects of endotoxin on the Th1/Th2 response in humans. J Burn Care Rehabil. 1996; 17(6 Pt 1) 491-496
- 22 Lauw F N, ten Hove T, Dekkers P E et al.. Reduced Th1, but not Th2, cytokine production by lymphocytes after in vivo exposure of healthy subjects to endotoxin. Infect Immun. 2000; 68 1014-1018
- 23 Olszyna D P, Pajkrt D, van Deventer S J, van der Poll T. Effect of interleukin 10 on the release of the CXC chemokines growth related oncogene GRO-alpha and epithelial cell-derived neutrophil activating peptide (ENA)-78 during human endotoxemia. Immunol Lett. 2001; 78 41-44
- 24 Olszyna D P, Pajkrt D, Lauw F N, van Deventer S J, van Der Poll T. Interleukin 10 inhibits the release of CC chemokines during human endotoxemia. J Infect Dis. 2000; 181 613-620
- 25 Pajkrt D, Camoglio L, Buul T et al.. Attenuation of proinflammatory response by recombinant human IL-10 in human endotoxemia: effect of timing of recombinant human IL-10 administration. J Immunol. 1997; 158 3971-3977
- 26 Janeway Jr C A, Medzhitov R. Innate immune recognition. Annu Rev Immunol. 2002; 20 197-216
- 27 Aderem A, Ulevitch R J. Toll-like receptors in the induction of the innate immune response. Nature. 2000; 406 782-787
- 28 West M A, Heagy W. Endotoxin tolerance: a review. Crit Care Med. 2002; 30(suppl 1) S64-S73
- 29 Dobrovolskaia M A, Vogel S N. Toll receptors, CD14, and macrophage activation and deactivation by LPS. Microbes Infect. 2002; 4 903-914
- 30 Munoz C, Carlet J, Fitting C et al.. Dysregulation of in vitro cytokine production by monocytes during sepsis. J Clin Invest. 1991; 88 1747-1754
- 31 Volk H D, Thieme M, Heym S et al.. Alterations in function and phenotype of monocytes from patients with septic disease: predictive value and new therapeutic strategies. Behring Inst Mitt. 1991; 88 208-215
- 32 Wilson C S, Seatter S C, Rodriguez J L et al.. In vivo endotoxin tolerance: impaired LPS-stimulated TNF release of monocytes from patients with sepsis, but not SIRS. J Surg Res. 1997; 69 101-106
- 33 Docke W D, Randow F, Syrbe U et al.. Monocyte deactivation in septic patients: restoration by IFN-γ treatment. Nat Med. 1997; 3 678-681
- 34 Wolk K, Docke W D, von Baehr V, Volk H D, Sabat R. Impaired antigen presentation by human monocytes during endotoxin tolerance. Blood. 2000; 96 218-223
- 35 Adib-Conquy M, Adrie C, Moine P et al.. NF-kappaB expression in mononuclear cells of patients with sepsis resembles that observed in lipopolysaccharide tolerance. Am J Respir Crit Care Med. 2000; 162 1877-1883
- 36 Sugawara S, Nemoto E, Tada H et al.. Proteolysis of human monocyte CD14 by cysteine proteinases (gingipains) from Porphyromonas gingivalis leading to lipopolysaccharide hyporesponsiveness. J Immunol. 2000; 165 411-418
- 37 Randow F, Syrbe U, Meisel C et al.. Mechanism of endotoxin desensitization: involvement of interleukin 10 and transforming growth factor beta. J Exp Med. 1995; 181 1887-1892
- 38 Park D R, Skerrett S J. IL-10 enhances the growth of Legionella pneumophila in human mononuclear phagocytes and reverses the protective effect of IFN-gamma: differential responses of blood monocytes and alveolar macrophages. J Immunol. 1996; 157 2528-2538
- 39 Raychaudhuri B, Fisher C J, Farver C F et al.. Interleukin 10 (IL-10)-mediated inhibition of inflammatory cytokine production by human alveolar macrophages. Cytokine. 2000; 12 1348-1355
- 40 Cummings C J, Martin T R, Frevert C W et al.. Expression and function of the chemokine receptors CXCR1 and CXCR2 in sepsis. J Immunol. 1999; 162 2341-2346
- 41 Tavares-Murta B M, Zaparoli M, Ferreira R B et al.. Failure of neutrophil chemotactic function in septic patients. Crit Care Med. 2002; 30 1056-1061
- 42 Skoutelis A T, Kaleridis V, Athanassiou G M et al.. Neutrophil deformability in patients with sepsis, septic shock, and adult respiratory distress syndrome. Crit Care Med. 2000; 28 2355-2359
- 43 Schultz M J, Olszyna D P, de Jonge E et al.. Reduced ex vivo chemokine production by polymorphonuclear cells after in vivo exposure of normal humans to endotoxin. J Infect Dis. 2000; 182 1264-1267
- 44 Ahmed N A, McGill S, Yee J et al.. Mechanisms for the diminished neutrophil exudation to secondary inflammatory sites in infected patients with a systemic inflammatory response (sepsis). Crit Care Med. 1999; 27 2459-2468
- 45 Laichalk L L, Danforth J M, Standiford T J. Interleukin-10 inhibits neutrophil phagocytic and bactericidal activity. FEMS Immunol Med Microbiol. 1996; 15 181-187
- 46 Wright J R, Borron P, Brinker K G, Folz R J. Surfactant protein A: regulation of innate and adaptive immune responses in lung inflammation. Am J Respir Cell Mol Biol. 2001; 24 513-517
- 47 Korfhagen T R. Surfactant protein A (SP-A)-mediated bacterial clearance: SP-A and cystic fibrosis. Am J Respir Cell Mol Biol. 2001; 25 668-672
- 48 Crouch E, Wright J R. Surfactant proteins A and D and pulmonary host defense. Annu Rev Physiol. 2001; 63 521-554
- 49 Tobias P S, Ulevitch R J. Lipopolysaccharide binding protein and CD14 in LPS dependent macrophage activation. Immunobiology. 1993; 187 227-232
- 50 Raymondos K, Leuwer M, Haslam P L et al.. Compositional, structural, and functional alterations in pulmonary surfactant in surgical patients after the early onset of systemic inflammatory response syndrome or sepsis. Crit Care Med. 1999; 27 82-89
- 51 Greene K E, Wright J R, Steinberg K P et al.. Serial changes in surfactant-associated proteins in lung and serum before and after onset of ARDS. Am J Respir Crit Care Med. 1999; 160 1843-1850
- 52 Cheng I W, Ware L B, Greene K E et al.. Prognostic value of surfactant proteins A and D in patients with acute lung injury. Crit Care Med. 2003; 31 20-27
- 53 Wurfel M M, Radella II F, Ruzinski J T et al.. Bronchoalveolar lavage fluid from patients with acute respiratory distress syndrome facilitates bacterial lipopolysaccharide recognition: role for lipopolysaccharide-binding protein. Am J Respir Crit Care Med. 2003; 167 A760
- 54 Reddy R C, Chen G H, Tekchandani P K, Standiford T J. Sepsis-induced immunosuppression: from bad to worse. Immunol Res. 2001; 24 273-287
- 55 van der Poll T, Marchant A, Buurman W A et al.. Endogenous IL-10 protects mice from death during septic peritonitis. J Immunol. 1995; 155 5397-5401
- 56 van der Poll T, Jansen P M, Montegut W J et al.. Effects of IL-10 on systemic inflammatory responses during sublethal primate endotoxemia. J Immunol. 1997; 158 1971-1975
- 57 van der Poll T, Marchant A, Keogh C V, Goldman M, Lowry S F. Interleukin-10 impairs host defense in murine pneumococcal pneumonia. J Infect Dis. 1996; 174 994-1000
- 58 Greenberger M J, Strieter R M, Kunkel S L et al.. Neutralization of IL-10 increases survival in a murine model of Klebsiella pneumonia. J Immunol. 1995; 155 722-729
- 59 Steinhauser M L, Hogaboam C M, Kunkel S L et al.. IL-10 is a major mediator of sepsis-induced impairment in lung antibacterial host defense. J Immunol. 1999; 162 392-399
- 60 Reddy R C, Chen G H, Newstead M W et al.. Alveolar macrophage deactivation in murine septic peritonitis: role of interleukin 10. Infect Immun. 2001; 69 1394-1401
- 61 Kurahashi K, Kajikawa O, Sawa T et al.. Pathogenesis of septic shock in Pseudomonas aeruginosa pneumonia. J Clin Invest. 1999; 104 743-750
- 62 Sewnath M E, Olszyna D P, Birjmohun R et al.. IL-10-deficient mice demonstrate multiple organ failure and increased mortality during Escherichia coli peritonitis despite an accelerated bacterial clearance. J Immunol. 2001; 166 6323-6331
- 63 Hashimoto S, Pittet J F, Hong K et al.. Depletion of alveolar macrophages decreases neutrophil chemotaxis to Pseudomonas airspace infections. Am J Physiol. 1996; 270 L819-L828
- 64 Broug-Holub E, Toews G B, van Iwaarden J F et al.. Alveolar macrophages are required for protective pulmonary defenses in murine Klebsiella pneumonia: elimination of alveolar macrophages increases neutrophil recruitment but decreases bacterial clearance and survival. Infect Immun. 1997; 65 1139-1146
- 65 Heagy W, Hansen W, Nieman K et al.. Impaired ex vivo lipopolysaccharide-stimulated whole blood tumor necrosis factor production may identify “septic” intensive care unit patients. Shock. 2000; 14 271-276; discussion 276-277
- 66 Nomura F, Akashi S, Sakao Y et al.. Endotoxin tolerance in mouse peritoneal macrophages correlates with down-regulation of surface toll-like receptor 4 expression. J Immunol. 2000; 164 3476-3479
- 67 Sato S, Nomura F, Kawai T et al.. Synergy and cross-tolerance between toll-like receptor (TLR) 2- and TLR-4-mediated signaling pathways. J Immunol. 2000; 165 7096-7101
- 68 Fahmi H, Chaby R. Desensitization of macrophages to endotoxin effects is not correlated with a down-regulation of lipopolysaccharide-binding sites. Cell Immunol. 1993; 150 219-229
- 69 Jacinto R, Hartung T, McCall C, Li L. Lipopolysaccharide- and lipoteichoic acid-induced tolerance and cross-tolerance: distinct alterations in il-1 receptor-associated kinase. J Immunol. 2002; 168 6136-6141
- 70 Shennib H, Chu-Jeng R, Mulder D, Richards G, Prentis J. Pulmonary bacterial clearance and alveolar macrophage function in septic shock lung. Am Rev Respir Dis. 1984; 130 444-449
- 71 Jacobs R F, Kiel D P, Balk R A. Alveolar macrophage function in a canine model of endotoxin-induced lung injury. Am Rev Respir Dis. 1986; 134 745-751
- 72 Jacobs R F, Dorsey D R, Tryka A F, Tabor D R. Pulmonary macrophage antimicrobial activity in canine endotoxin shock and lung injury. Exp Lung Res. 1988; 14 359-374
- 73 Tabor D, Kiel D, Jacobs R. Receptor-mediated ingestion responses by lung macrophages from a canine model of ARDS. J Leukoc Biol. 1987; 41 539-543
- 74 Mason C M, Dobard E, Summer W R, Nelson S. Intraportal lipopolysaccharide suppresses pulmonary antibacterial defense mechanisms. J Infect Dis. 1997; 176 1293-1302
- 75 Christman J W, Petras S F, Hacker M, Absher P M, Davis G S. Alveolar macrophage function is selectively altered after endotoxemia in rats. Infect Immun. 1988; 56 1254-1259
- 76 Frevert C W, Warner A E, Weller E, Brain J D. The effect of endotoxin on in vivo rat alveolar macrophage phagocytosis. Exp Lung Res. 1998; 24 745-758
- 77 Harris S E, Nelson S, Astry C L, Bainton B G, Summer W R. Endotoxin-induced suppression of pulmonary antibacterial defenses against Staphylococcus aureus. Am Rev Respir Dis. 1988; 138 1439-1443
- 78 Goya T, Abe M, Shimura H, Torisu M. Characteristics of alveolar macrophages in experimental septic lung. J Leukoc Biol. 1992; 52 236-243
- 79 Coffey M J, Phare S M, Peters-Golden M. Prolonged exposure to lipopolysaccharide inhibits macrophage 5-lipoxygenase metabolism via induction of nitric oxide synthesis. J Immunol. 2000; 165 3592-3598
- 80 Toews G B, Gross G N, Pierce A K. The relationship of inoculum size to lung bacterial clearance and phagocytic cell response in mice. Am Rev Respir Dis. 1979; 120 559-566
- 81 Rehm S R, Gross G N, Pierce A K. Early bacterial clearance from murine lungs. Species-dependent phagocyte response. J Clin Invest. 1980; 66 194-199
- 82 Onofrio J M, Toews G B, Lipscomb M F, Pierce A K. Granulocyte-alveolar-macrophage interaction in the pulmonary clearance of Staphylococcus aureus . Am Rev Respir Dis. 1983; 127 335-341
- 83 White J C, Nelson S, Winkelstien J, Booth F, Jakab G. Impairment of antibacterial defense mechanisms of the lung by extrapulmonary infection. J Infect Dis. 1986; 153 202-208
- 84 Nelson S, Chidiac C, Bagby G, Summer W R. Endotoxin-induced suppression of lung host defenses. J Med. 1990; 21 85-103
- 85 Nelson S, Mason C, Bagby G, Nakamura C, Summer W. Lipopolysaccharide-induced inhibition of intrapulmonary tumor necrosis factor and lung antibacterial defenses. Am Rev Respir Dis. 1990; 141 A512
- 86 Frevert C W, Warner A E, Kobzik L. Defective pulmonary recruitment of neutrophils in a rat model of endotoxemia. Am J Respir Cell Mol Biol. 1994; 11 716-723
- 87 Hirano S. Migratory responses of PMN after intraperitoneal and intratracheal administration of lipopolysaccharide. Am J Physiol. 1996; 270(5 Pt 1) L836-L845
- 88 Wagner J G, Harkema J R, Roth R A. Pulmonary leukostasis and the inhibition of airway neutrophil recruitment are early events in the endotoxemic rat. Shock. 2002; 17 151-158
- 89 Hartiala K T, Langlois L, Goldstein I M, Rosenbaum J T. Endotoxin-induced selective dysfunction of rabbit polymorphonuclear leukocytes in response to endogenous chemotactic factors. Infect Immun. 1985; 50 527-533
- 90 Wagner J G, Driscoll K E, Roth R A. Inhibition of pulmonary neutrophil trafficking during endotoxemia is dependent on the stimulus for migration. Am J Respir Cell Mol Biol. 1999; 20 769-776
- 91 Bignold L P, Rogers S D, Siaw T M, Bahnisch J. Inhibition of chemotaxis of neutrophil leukocytes to interleukin-8 by endotoxins of various bacteria. Infect Immun. 1991; 59 4255-4258
- 92 Gimbrone Jr M A, Obin M S, Brock A F et al.. Endothelial interleukin-8: a novel inhibitor of leukocyte-endothelial interactions. Science. 1989; 246 1601-1603
- 93 Hechtman D H, Cybulsky M I, Fuchs H J, Baker J B, Gimbrone M J. Intravascular IL-8: inhibitor of polymorphonuclear leukocyte accumulation at sites of acute inflammation. J Immunol. 1991; 147 883-892
- 94 Sano H, Sata T, Nanri H, Ikeda M, Shigematsu A. Thioredoxin is associated with endotoxin tolerance in mice. Crit Care Med. 2002; 30 190-194
- 95 Nakamura H, Herzenberg L A, Bai J et al.. Circulating thioredoxin suppresses lipopolysaccharide-induced neutrophil chemotaxis. Proc Natl Acad Sci USA. 2001; 98 15143-15148
- 96 Blackwell T S, Lancaster L H, Blackwell T R, Venkatakrishnan A, Christman J W. Chemotactic gradients predict neutrophilic alveolitis in endotoxin-treated rats. Am J Respir Crit Care Med. 1999; 159 1644-1652
- 97 Duffy A J, Nolan B, Sheth K et al.. Inhibition of alveolar neutrophil immigration in endotoxemia is macrophage inflammatory protein 2 independent. J Surg Res. 2000; 90 51-57
- 98 Ferri L E, Swartz D, Christou N V. Soluble L-selectin at levels present in septic patients diminishes leukocyte-endothelial cell interactions in mice in vivo: a mechanism for decreased leukocyte delivery to remote sites in sepsis. Crit Care Med. 2001; 29 117-122
- 99 Benjamim C F, Ferreira S H, Cunha F Q. Role of nitric oxide in the failure of neutrophil migration in sepsis. J Infect Dis. 2000; 182 214-223
- 100 Benjamim C F, Silva J S, Fortes Z B et al.. Inhibition of leukocyte rolling by nitric oxide during sepsis leads to reduced migration of active microbicidal neutrophils. Infect Immun. 2002; 70 3602-3610
- 101 Crosara-Alberto D P, Darini A L, Inoue R Y et al.. Involvement of NO in the failure of neutrophil migration in sepsis induced by Staphylococcus aureus . Br J Pharmacol. 2002; 136 645-658
- 102 Matute-Bello G, Frevert C W, Kajikawa O et al.. Septic shock and acute lung injury in rabbits with peritonitis. failure of the neutrophil response to localized infection. Am J Respir Crit Care Med. 2001; 163 234-243
- 103 Hotchkiss R S, Swanson P E, Freeman B D et al.. Apoptotic cell death in patients with sepsis, shock, and multiple organ dysfunction. Crit Care Med. 1999; 27 1230-1251
- 104 Hotchkiss R S, Tinsley K W, Swanson P E et al.. Depletion of dendritic cells, but not macrophages, in patients with sepsis. J Immunol. 2002; 168 2493-2500
- 105 Hotchkiss R S, Tinsley K W, Swanson P E et al.. Prevention of lymphocyte cell death in sepsis improves survival in mice. Proc Natl Acad Sci USA. 1999; 96 14541-14546
- 106 Hotchkiss R S, Chang K C, Swanson P E et al.. Caspase inhibitors improve survival in sepsis: a critical role of the lymphocyte. Nat Immunol. 2000; 1 496-501
- 107 Tinsley K W, Grayson M H, Swanson P E et al.. Sepsis induces apoptosis and profound depletion of splenic interdigitating and follicular dendritic cells. J Immunol. 2003; 171 909-914
- 108 Fadok V A, Bratton D L, Konowal A et al.. Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF. J Clin Invest. 1998; 101 890-898
- 109 Fadok V A, Bratton D L, Henson P M. Phagocyte receptors for apoptotic cells: recognition, uptake, and consequences. J Clin Invest. 2001; 108 957-962
- 110 Fadok V A, Chimini G. The phagocytosis of apoptotic cells. Semin Immunol. 2001; 13 365-372
- 111 Hotchkiss R S, Chang K C, Grayson M H et al.. Adoptive transfer of apoptotic splenocytes worsens survival, whereas adoptive transfer of necrotic splenocytes improves survival in sepsis. Proc Natl Acad Sci USA. 2003; 100 6724-6729
- 112 Martin T R. Recognition of bacterial endotoxin in the lungs. Am J Respir Cell Mol Biol. 2000; 23 128-132
- 113 Fan M H, Klein R D, Steinstraesser L et al.. An essential role for lipopolysaccharide-binding protein in pulmonary innate immune responses. Shock. 2002; 18 248-254
- 114 Le Roy D, Di Padova F, Adachi Y et al.. Critical role of lipopolysaccharide-binding protein and CD14 in immune responses against gram-negative bacteria. J Immunol. 2001; 167 2759-2765
- 115 McCormack F X, Whitsett J A. The pulmonary collectins, SP-A and SP-D, orchestrate innate immunity in the lung. J Clin Invest. 2002; 109 707-712
- 116 Sano H, Chiba H, Iwaki D et al.. Surfactant proteins A and D bind CD14 by different mechanisms. J Biol Chem. 2000; 275 22442-22451
- 117 Guillot L, Balloy V, McCormack F X et al.. Cutting edge: the immunostimulatory activity of the lung surfactant protein-A involves Toll-like receptor 4. J Immunol. 2002; 168 5989-5992
- 118 Wright J R. Immunomodulatory functions of surfactant. Physiol Rev. 1997; 77 931-962
- 119 Awasthi S, Coalson J J, Yoder B A, Crouch E, King R J. Deficiencies in lung surfactant proteins A and D are associated with lung infection in very premature neonatal baboons. Am J Respir Crit Care Med. 2001; 163 389-397
- 120 LeVine A M, Kurak K E, Bruno M D et al.. Surfactant protein-A-deficient mice are susceptible to Pseudomonas aeruginosa infection. Am J Respir Cell Mol Biol. 1998; 19 700-708
- 121 LeVine A M, Kurak K E, Wright J R et al.. Surfactant protein-A binds group B streptococcus enhancing phagocytosis and clearance from lungs of surfactant protein-A-deficient mice. Am J Respir Cell Mol Biol. 1999; 20 279-286
- 122 Chabot S, Salez L, McCormack F X, Touqui L, Chignard M. Surfactant protein A inhibits lipopolysaccharide-induced in vivo production of interleukin-10 by mononuclear phagocytes during lung inflammation. Am J Respir Cell Mol Biol. 2003; 28 347-353
- 123 Abraham E. Neutrophils and acute lung injury. Crit Care Med. 2003; 31(suppl 4) S195-199
- 124 LeVine A M, Whitsett J A, Gwozdz J A et al.. Distinct effects of surfactant protein A or D deficiency during bacterial infection on the lung. J Immunol. 2000; 165 3934-3940
- 125 Bufler P, Schmidt B, Schikor D et al.. Surfactant protein A and D differently regulate the immune response to nonmucoid Pseudomonas aeruginosa and its lipopolysaccharide. Am J Respir Cell Mol Biol. 2003; 28 249-256
- 126 Augusto L A, Synguelakis M, Johansson J et al.. Interaction of pulmonary surfactant protein C with CD14 and lipopolysaccharide. Infect Immun. 2003; 71 61-67
- 127 Augusto L A, Synguelakis M, Espinassous Q et al.. Cellular anti-endotoxin activities of lung surfactant protein C in lipid vesicles. Am J Respir Crit Care Med. 2003; 168 335-341
- 128 Wang S C, Klein R D, Wahl W L et al.. Tissue coexpression of LBP and CD14 mRNA in a mouse model of sepsis. J Surg Res. 1998; 76 67-73
- 129 Malloy J, Mccaig L, Veldhuizen R et al.. Alterations of the endogenous surfactant system in septic adult rats. Am J Respir Crit Care Med. 1997; 156 617-623
- 130 Herbein J F, Wright J R. Enhanced clearance of surfactant protein D during LPS-induced acute inflammation in rat lung. Am J Physiol Lung Cell Mol Physiol. 2001; 281 L268-L277
- 131 Martin T R. Lung Cytokines and ARDS. Chest. 1999; 116 2S-8S
- 132 Martin T R, Goodman R B. The role of chemokines in the pathophysiology of the acute respiratory distress syndrome
(ARDS). In: Hebert CA Chemokines in Disease: Biology and Clinical Research. Totowa, NJ; Humana 1999: 81-110
MissingFormLabel
- 133 Martin T R, Matute-Bello G, Skerrett S J, Frevert C W. Extrapulmonary sepsis and cytokines in lung injury and defenses. In: Nelson S, Martin TR Cytokines in Pulmonary Disease: Infection and Inflammation. New York; Marcel Dekker 2000: 403-458
MissingFormLabel
- 134 Ware L B, Matthay M A. The acute respiratory distress syndrome. N Engl J Med. 2000; 342 1334-1349
Charles W FrevertD.V.M. Sc.D.
VA Puget Sound Medical Center
GMR151-L, 1660 South Columbian Way
Seattle, WA
Email: cfrevert@u.washington.edu