@article {DÖRING:1989:0803-5253:37,
title = "Host Response to Pseudomonas aeruginosa",
journal = "Acta Pædiatrica",
parent_itemid = "infobike://bpl/apa",
publishercode ="bp",
year = "1989",
volume = "78",
number = "1",
publication date ="1989-11-01T00:00:00",
pages = "37-40",
itemtype = "ARTICLE",
issn = "0803-5253",
eissn = "1651-2227",
url = "https://www.ingentaconnect.com/content/bpl/apa/1989/00000078/a363s363/art00008",
doi = "doi:10.1111/apa.1989.78.s363.37",
author = "D{\"O}RING, GERD",
abstract = "Patients with cystic fibrosis (CF) do not reveal a primary immune defect and respond with high numbers of functional polymorphonuclear leukocytes (PMN) and specific antibodies to lung infection with Pseudomonas aeruginosa. The mucoid character of P. aeruginosa, an altered
epithelial cell surface, and high concentrations of PMNderived lysosomal enzymes contribute to impaired bacterial lung clearance and result in chronic infection. Released PMNelastase inactivates exotoxin A, the major toxin of P. aeruginosa, thus reducing its virulence.
The imbalance between PMNproteinases and their inhibitors leads to lung tissue damage, impaired opsonophagocytosis, and Tcell and Bcell imbalance. New therapeutical concepts in CF therefore combine antiinflammatory drugs with effective antibiotics.",
}