Mechanisms of Neutrophil Accumulation in the Lungs Against Bacteria

被引:134
作者
Balamayooran, Gayathriy [1 ,2 ]
Batra, Sanjay [1 ,2 ]
Fessler, Michael B. [3 ]
Happel, Kyle I. [4 ]
Jeyaseelan, Samithamby [1 ,2 ,4 ]
机构
[1] Louisiana State Univ, Dept Pathobiol Sci, Lab Lung Biol, Baton Rouge, LA 70803 USA
[2] Louisiana State Univ, Ctr Expt Infect Dis Res, Baton Rouge, LA 70803 USA
[3] NIEHS, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA
[4] LSU Hlth Sci Ctr, Dept Med, Pulm & Crit Care Med Sect, New Orleans, LA USA
基金
美国国家卫生研究院;
关键词
bacterial pneumonia; lung inflammation; acute lung injury; TUMOR-NECROSIS-FACTOR; INNATE IMMUNE-RESPONSES; NF-KAPPA-B; MYELOID DIFFERENTIATION FACTOR-88; COMMUNITY-ACQUIRED PNEUMONIA; STIMULATING FACTOR RESPONSE; CONTAINING ADAPTER PROTEIN; PULMONARY HOST RESPONSE; PRIOR STATIN USE; FACTOR G-CSF;
D O I
10.1165/rcmb.2009-0047TR
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Bacterial lung diseases are a major cause of morbidity and mortality both in immunocompromised and in immunocompetent individuals. Neutrophil accumulation, a pathological hallmark of bacterial diseases, is critical to host defense, but may also cause acute lung injury/acute respiratory distress syndrome. Toll-like receptors, nucleotide-binding oligomerization domain (NOD)-like receptors, transcription factors, cytokines, and chemokines play essential roles in neutrophil sequestration in the lungs. This review highlights our current understanding of the role of these molecules in the lungs during bacterial infection and their therapeutic potential. We also discuss emerging data on cholesterol and ethanol as environmentally modifiable factors that may impact neutrophil-mediated pulmonary innate host defense. Understanding the precise molecular mechanisms leading to neutrophil influx in the lungs during bacterial infection is critical for the development of more effective therapeutic and prophylactic strategies to control the excessive host response to infection.
引用
收藏
页码:5 / 16
页数:12
相关论文
共 142 条
[11]   Loss of ABCG1 results in chronic pulmonary inflammation [J].
Baldan, Angel ;
Gomes, Aldrin V. ;
Ping, Peipei ;
Edwards, Peter A. .
JOURNAL OF IMMUNOLOGY, 2008, 180 (05) :3560-3568
[12]   HEMATOLOGICAL COMPLICATIONS OF ALCOHOLISM [J].
BALLARD, HS .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1989, 13 (05) :706-720
[13]   Viral recognition by Toll-like receptors [J].
Barton, Gregory M. .
SEMINARS IN IMMUNOLOGY, 2007, 19 (01) :33-40
[14]   Apolipoproteins modulate the inflammatory response to lipopolysaccharide [J].
Berbée, JFP ;
Havekes, LM ;
Rensen, PCN .
JOURNAL OF ENDOTOXIN RESEARCH, 2005, 11 (02) :97-103
[15]   Toll-like receptor 9 regulates the lung macrophage phenotype and host immunity in murine pneumonia caused by Legionella pneumophila [J].
Bhan, Urvashi ;
Trujillo, Glenda ;
Lyn-Kew, Kenneth ;
Newstead, Michael W. ;
Zeng, Xianying ;
Hogaboam, Cory M. ;
Krieg, Arthur M. ;
Standiford, Theodore J. .
INFECTION AND IMMUNITY, 2008, 76 (07) :2895-2904
[16]   TLR9 is required for protective innate immunity in gram-negative bacterial pneumonia: Role of dendritic cells [J].
Bhan, Urvashi ;
Lukacs, Nicholas W. ;
Osterholzer, John J. ;
Newstead, Michael W. ;
Zeng, Xianying ;
Moore, Thomas A. ;
McMillan, Tracy R. ;
Krieg, Arthur M. ;
Akira, Shizuo ;
Standiford, Theodore J. .
JOURNAL OF IMMUNOLOGY, 2007, 179 (06) :3937-3946
[17]   Novel role for the liver X nuclear receptor in the suppression of lung inflammatory responses [J].
Birrell, Mark A. ;
Catley, Matthew C. ;
Hardaker, Elizabeth ;
Wong, Sissie ;
Willson, Timothy M. ;
McCluskie, Kerryn ;
Leonard, Thomas ;
Farrow, Stuart N. ;
Collins, Jon L. ;
Haj-Yahia, Saleem ;
Belvisi, Maria G. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2007, 282 (44) :31882-31890
[18]   Reduced atherosclerosis in MyD88-null mice links elevated serum cholesterol levels to activation of innate immunity signaling pathways [J].
Björkbacka, H ;
Kunjathoor, VV ;
Moore, KJ ;
Koehn, S ;
Ordija, CM ;
Lee, MA ;
Means, T ;
Halmen, K ;
Luster, AD ;
Golenbock, DT ;
Freeman, MW .
NATURE MEDICINE, 2004, 10 (04) :416-421
[19]   Acute ethanol intoxication suppresses lung chemokine production following infection with Streptococcus pneumoniae [J].
Boé, DM ;
Nelson, S ;
Zhang, P ;
Bagby, GJ .
JOURNAL OF INFECTIOUS DISEASES, 2001, 184 (09) :1134-1142
[20]   IL-17 producing γδ T cells are required for a controlled inflammatory response after bleomycin-induced lung injury [J].
Braun, Ruedi K. ;
Ferrick, Christina ;
Neubauer, Paul ;
Sjoding, Michael ;
Sterner-Kock, Anja ;
Kock, Martin ;
Putney, Lei ;
Ferrick, David A. ;
Hyde, Dallas M. ;
Love, Robert B. .
INFLAMMATION, 2008, 31 (03) :167-179