Published ahead of print on September 8, 2009 Am. J. Respir. Cell Mol. Biol. 2009, doi:10.1165/rcmb.2009-0047TR
Submitted on February 3, 2009 Mechanisms of Neutrophil Accumulation in the Lungs Against BacteriaGayathriy Balamayooran1,1 Laboratory of Lung Biology, Department of Pathobiological Sciences and Center for Experimental Infectious Disease Research, Louisiana State University, Baton Rouge, Louisiana, United States, 2 Laboratory of Respiratory Biolgy, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States, 3 Department of Medicine, Section of Pulmonary and Critical Care Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana, United States, 4 Laboratory of Lung Biology, Department of Pathobiological Sciences and Center for Experimental Infectious Disease Research, Louisiana State University, Baton Rouge, Louisiana, United States; Department of Medicine, Section of Pulmonary and Critical Care Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana, United States * To whom correspondence should be addressed. E-mail: jey{at}lsu.edu.
Bacterial lung diseases are a major cause of morbidity and mortality both in immunocompromised and immunocompetent individuals. Neutrophil accumulation, a pathological hallmark of bacterial diseases, is critical to host defense, but may also cause ALI/ARDS. Toll-like receptors, 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 neutrophilmediated 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. Key words: Neutrophil Lung Bacteria Cytokine Chemokine
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