PMID- 19842832
OWN - NLM
STAT- MEDLINE
DCOM- 20100202
LR  - 20191027
IS  - 1521-0499 (Electronic)
IS  - 0190-2148 (Linking)
VI  - 35
IP  - 6
DP  - 2009 Aug
TI  - Signal transduction pathways linking the activation of alveolar macrophages with 
      the recruitment of neutrophils to lungs in chronic obstructive pulmonary disease.
PG  - 439-85
AB  - Chronic obstructive pulmonary disease (COPD) is a major and increasing global 
      health problem. It is predicted by the World Health Organization to become the 
      third most common cause of death and the fifth most common cause of disability in 
      the world by 2020. COPD is a complex inflammatory disease involving several types 
      of inflammatory cells and multiple inflammatory mediators. Although abnormal 
      numbers of inflammatory cells such as macrophages, dendritic cells, neutrophils, 
      and T lymphocytes have been documented in COPD, the relationship between these 
      cell types and the sequence of their appearance and persistence is largely 
      unknown. Alveolar macrophages have been identified as one of the major cell types 
      that plays a key role in orchestrating the inflammatory events associated with 
      the pathophysiology of COPD. One of the major functions of macrophages is the 
      secretion of chemotactic factors and this function is markedly increased on 
      exposure to cigarette smoke (CS). This enhanced release of chemoattractants 
      results in increased lung neutrophil infiltration, which is thought to be a key 
      event in the development of COPD. The molecular basis for this amplified 
      inflammatory response is not very clear, but it could be due to an alteration in 
      signal transduction pathways within the macrophage. Based on existing literature, 
      an attempt has been made to create a comprehensive review of the signal 
      transduction pathways that link the activation of macrophages with the increased 
      recruitment of neutrophils into the airways. Some of the major stimuli that 
      activate macrophages and cause them to secrete chemotactic factors have been 
      identified as CS, wood smoke, ozone, bacterial endotoxin, and proinflammatory 
      cytokines such as interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha. 
      These stimuli seem to activate mainly redox-sensitive transcription factors such 
      as nuclear factor (NF)-kappa B and activator protein (AP)-1, both of which play a 
      major role in the synthesis and secretion of chemotactic factors such as IL-8 and 
      leukotriene B(4) (LTB(4)). The pathways involved in the synthesis and secretion 
      of other factors such as macrophage chemotactic protein-1 (MCP-1) and 
      growth-related oncogene-alpha (Gro-alpha) have also been reviewed.
FAU - Murugan, Vidyasaral
AU  - Murugan V
AD  - Jubilant Biosys Ltd., Yeshwanthpur, Bangalore, India.
FAU - Peck, Michael J
AU  - Peck MJ
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Exp Lung Res
JT  - Experimental lung research
JID - 8004944
RN  - 0 (CXCL8 protein, human)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Chemotactic Factors/physiology
MH  - Humans
MH  - Interleukin-1beta/physiology
MH  - Interleukin-8/physiology
MH  - Lipopolysaccharides/toxicity
MH  - Lung/pathology/physiopathology
MH  - Macrophage Activation
MH  - Macrophages, Alveolar/pathology/*physiology
MH  - Models, Biological
MH  - Neutrophils/pathology/*physiology
MH  - Pulmonary Disease, Chronic Obstructive/*etiology/pathology/physiopathology
MH  - Risk Factors
MH  - Signal Transduction
MH  - Smoking/adverse effects
MH  - Tumor Necrosis Factor-alpha/physiology
RF  - 177
EDAT- 2009/10/22 06:00
MHDA- 2010/02/03 06:00
CRDT- 2009/10/22 06:00
PHST- 2009/10/22 06:00 [entrez]
PHST- 2009/10/22 06:00 [pubmed]
PHST- 2010/02/03 06:00 [medline]
AID - 10.1080/01902140902759290 [pii]
AID - 10.1080/01902140902759290 [doi]
PST - ppublish
SO  - Exp Lung Res. 2009 Aug;35(6):439-85. doi: 10.1080/01902140902759290.