Inflammatory response to infectious pulmonary injury

被引:57
作者
Delclaux, C
Azoulay, E
机构
[1] Hop Henri Mondor, Serv Physiol Explorat Fonctionnelles, AP HP, F-94010 Creteil, France
[2] Univ Paris 12, INSERM, U492, Fac Med, Creteil, France
[3] Hop St Louis, Serv Reanimat Med, AP HP, Paris, France
关键词
alveolar macrophage; bacteria; cytokine; innate immunity; neutrophil; RESPIRATORY-DISTRESS SYNDROME; HOST-DEFENSE; BACTERIAL PNEUMONIA; INNATE IMMUNITY; PARTS; NEUTROPHILS; LUNG; PERMEABILITY; MACROPHAGES; IMMUNOLOGY;
D O I
10.1183/09031936.03.00420203
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
This review describing the inflammatory response to infectious pulmonary injury is focused on the innate immunity of the distal lung to bacterial pneumonia. The fact that the inflammatory response varies to some extent with the bacterial strain responsible for the infection is emphasised. The key cellular components present in the distal lung are described. The major role of alveolar macrophage is described, inasmuch as it responds to the usual daily challenges of bacteria entering the terminal airways and is capable of initiating an inflammatory reaction if the microbial challenge is either too large or too virulent. Under these conditions, the alveolar macrophages initiate an inflammatory response that recruits large numbers of neutrophils into the alveolar spaces. The strategy of the innate immune response may not be to recognise every possible antigen, but rather to focus on a few, highly conserved structures present in large groups of microorganisms. These structures are referred to as pathogen-associated molecular patterns and the receptors of the innate immune system that evolved to recognise them are called pattern-recognition receptors. The soluble factors in innate defence, such as cytokines, are described, and a last paragraph discusses whether a specific inflammatory response could characterise nosocomial pneumonia.
引用
收藏
页码:10S / 14S
页数:5
相关论文
共 29 条
[11]  
Greenberger MJ, 1996, J IMMUNOL, V157, P3006
[12]   Upregulation of two death pathways of perforin/granzyme and FasL/Fas in septic acute respiratory distress syndrome [J].
Hashimoto, S ;
Kobayashi, A ;
Kooguchi, K ;
Kitamura, Y ;
Onodera, H ;
Nakajima, H .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2000, 161 (01) :237-243
[13]   Granulocyte apoptosis and its role in the resolution and control of lung inflammation [J].
Haslett, C .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1999, 160 (05) :S5-S11
[14]   PROTEIN PERMEABILITY IN THE ADULT RESPIRATORY-DISTRESS SYNDROME - LOSS OF SIZE SELECTIVITY OF THE ALVEOLAR EPITHELIUM [J].
HOLTER, JF ;
WEILAND, JE ;
PACHT, ER ;
GADEK, JE ;
DAVIS, WB .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 78 (06) :1513-1522
[15]   RECOMBINANT TUMOR NECROSIS FACTOR INCREASES PULMONARY VASCULAR-PERMEABILITY INDEPENDENT OF NEUTROPHILS [J].
HORVATH, CJ ;
FERRO, TJ ;
JESMOK, G ;
MALIK, AB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (23) :9219-9223
[16]   CYTOKINES OF THE LUNG [J].
KELLEY, J .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1990, 141 (03) :765-788
[17]   Exhaled markers of pulmonary disease [J].
Kharitonov, SA ;
Barnes, PJ .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2001, 163 (07) :1693-1722
[18]   Pathogenesis of septic shock in Pseudomonas aeruginosa pneumonia [J].
Kurahashi, K ;
Kajikawa, O ;
Sawa, T ;
Ohara, M ;
Gropper, MA ;
Frank, DW ;
Martin, TR ;
Wiener-Kronish, JP .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (06) :743-750
[19]   Advances in immunology: Innate immunity. [J].
Medzhitov, R ;
Janeway, CJ .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (05) :338-344
[20]  
Monton C, 1998, Monaldi Arch Chest Dis, V53, P56