Pneumonia models and innate immunity to respiratory bacterial pathogens

被引:44
作者
Knapp, S
Schultz, MJ
van der Poll, T
机构
[1] Med Univ Vienna, Dept Internal Med, A-1090 Vienna, Austria
[2] Univ Amsterdam, Dept Intens Care, NL-1105 AZ Amsterdam, Netherlands
[3] Univ Amsterdam, Dept Infect Dis Trop Med & AIDS, NL-1105 AZ Amsterdam, Netherlands
来源
SHOCK | 2005年 / 24卷
关键词
sepsis; immunomodulating agents; community-acquired pneumonia; nosocomial/hospital-acquired pneumonia;
D O I
10.1097/01.shk.0000191385.41689.f3
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Preclinical sepsis models have been used for decades to study the pathophysiologic processes during sepsis and shock. Although these studies revealed promising immunomodulating agents for the treatment of sepsis, clinical trials evaluating the efficacy of these new agents in patients with sepsis were disappointing. The main reason for this unsatisfactory experience might be that unlike the clinical situation, most of these preclinical models are devoid of a localized infectious source from which the infection disseminates. Studies on the effects of several immunomodulating strategies have demonstrated strikingly opposite results when sepsis models with a more natural route of infection, such as pneumonia, were used. In this review, we will give insights into pneumonia models and discuss results and differences in the innate immune responses during distinct pulmonary infection models.
引用
收藏
页码:12 / 18
页数:7
相关论文
共 73 条
[11]   COMPARTMENTALIZED CYTOKINE PRODUCTION WITHIN THE HUMAN LUNG IN UNILATERAL PNEUMONIA [J].
DEHOUX, MS ;
BOUTTEN, A ;
OSTINELLI, J ;
SETA, N ;
DOMBRET, MC ;
CRESTANI, B ;
DESCHENES, M ;
TROUILLET, JL ;
AUBIER, M .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 150 (03) :710-716
[12]  
Dinarello CA, 2002, CLIN EXP RHEUMATOL, V20, pS1
[13]   Monocyte deactivation in septic patients: Restoration by IFN-gamma treatment [J].
Docke, WD ;
Randow, F ;
Syrbe, U ;
Krausch, D ;
Asadullah, K ;
Reinke, P ;
VolK, HD ;
Kox, W .
NATURE MEDICINE, 1997, 3 (06) :678-681
[14]   Alveolar macrophage apoptosis contributes to pneumococcal clearance in a resolving model of pulmonary infection [J].
Dockrell, DH ;
Marriott, HM ;
Prince, LR ;
Ridger, VC ;
Ince, PG ;
Hellewell, PG ;
Whyte, MKB .
JOURNAL OF IMMUNOLOGY, 2003, 171 (10) :5380-5388
[15]  
DOERSCHUK CM, 1990, J IMMUNOL, V144, P2327
[16]   Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-β, PGE2, and PAF [J].
Fadok, VA ;
Bratton, DL ;
Konowal, A ;
Freed, PW ;
Westcott, JY ;
Henson, PM .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (04) :890-898
[17]  
FrankeUllmann G, 1996, J IMMUNOL, V157, P3097
[18]   Effect of CD14 blockade in rabbits with Escherichia coli pneumonia and sepsis [J].
Frevert, CW ;
Matute-Bello, G ;
Skerrett, SJ ;
Goodman, RB ;
Kajikawa, O ;
Sittipunt, C ;
Martin, TR .
JOURNAL OF IMMUNOLOGY, 2000, 164 (10) :5439-5445
[19]   ROLE OF TUMOR-NECROSIS-FACTOR-ALPHA IN INNATE RESISTANCE TO MOUSE PULMONARY INFECTION WITH PSEUDOMONAS-AERUGINOSA [J].
GOSSELIN, D ;
DESANCTIS, J ;
BOULE, M ;
SKAMENE, E ;
MATOUK, C ;
RADZIOCH, D .
INFECTION AND IMMUNITY, 1995, 63 (09) :3272-3278
[20]  
Greenberger MJ, 1996, J IMMUNOL, V157, P3006