Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 299, Issue 3, Pages L334-L344Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00017.2010
Keywords
cystic fibrosis; immunodeficiency; nerve growth factor; neuroimmunomodulation
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Funding
- National Institute of General Medical Sciences, National Institutes of Health [GM-061347]
- National Heart, Lung, and Blood Institute, National Institutes of Health [HL-61007]
- National Institute of Child Health and Human Development, National Institutes of Health [NCS-07-11]
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Cardenas S, Scuri M, Samsell L, Ducatman B, Bejarano P, Auais A, Doud M, Mathee K, Piedimonte G. Neurotrophic and neuroimmune responses to early-life Pseudomonas aeruginosa infection in rat lungs. Am J Physiol Lung Cell Mol Physiol 299: L334-L344, 2010. First published June 11, 2010; doi:10.1152/ajplung.00017.2010.-Early-life respiratory infection with Pseudomonas aeruginosa is common in children with cystic fibrosis or immune deficits. Although many of its clinical manifestations involve neural reflexes, little information is available on the peripheral nervous system of infected airways. This study sought to determine whether early-life infection triggers a neurogenic-mediated immunoinflammatory response, the mechanisms of this response, and its relationship with other immunoinflammatory pathways. Weanling and adult rats were inoculated with suspensions containing P. aeruginosa (PAO1) coated on alginate microspheres suspended in Tris-CaCl2 buffer. Five days after infection, rats were injected with capsaicin to stimulate nociceptive nerves in the airway mucosa, and microvascular permeability was measured using Evans blue as a tracer. PAO1 increased neurogenic inflammation in the extra-and intrapulmonary compartments of weanlings but not in adults. The mechanism involves selective overexpression of NGF, which is critical for the local increase in microvascular permeability and for the infiltration of polymorphonuclear leukocytes into infected lung parenchyma. These effects are mediated in part by induction of downstream inflammatory cytokines and chemokines, especially IL-1 beta, IL-18, and leptin. Our data suggest that neurogenic-mediated immunoinflammatory mechanisms play important roles in airway inflammation and hyperreactivity associated with P. aeruginosa when infection occurs early in life.
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