Linked Life Data

8360489

Source:http://linkedlifedata.com/resource/pubmed/id/8360489

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1993-9-28
pubmed:abstractText
Inhaled inert particles and organisms cause a spectrum of pulmonary responses, ranging from minimal changes to marked acute inflammation. During ingestion and clearance of such particles, alveolar macrophages (AM) can initiate pulmonary inflammation by production of TNF and neutrophil chemoattractant cytokines. We tested the role of opsonization in determining the AM response to ingestion of inert particles in vitro and in vivo. As measures of AM activation after phagocytosis in vitro, we measured release of TNF and mRNA expression for the platelet-factor 4 family neutrophil chemoattractants, KC and macrophage-inflammatory protein-2 (MIP-2). Using albumin-coated fluorescent latex particle as phagocytic targets, we found a marked release of TNF by AM ingesting particles opsonized with antialbumin IgG, although uptake of similar numbers of unopsonized particles caused little or no release (e.g., 4648 +/- 1147 pg/ml, opsonized beads vs 576 +/- 205 unopsonized, 10:1 particle:cell ratio, n = 4, mean +/- SD). Flow cytometry confirmed equal uptake of the two particle types. Northern analysis of AM mRNA showed marked induction of KC and MIP-2 mRNA after ingestion of opsonized particles only. Instillation of opsonized particles into hamster lungs caused a marked neutrophil influx, although unopsonized particles did not. TNF was elevated in lavage fluid after instillation of opsonized particles, but not after unopsonized beads (92.7 +/- 136 pg/ml opsonized, n = 7 vs 1.3 +/- 3.6 unopsonized, n = 6). KC and MIP-2 mRNA were induced in lavaged cells after instillation of opsonized but not after unopsonized particles or vehicle control. The nature of particle interaction with the AM surface during phagocytosis determines the subsequent AM response. Although many unopsonized inert particles are ingested with minimal AM activation, specific opsonization of pathogens or non-specific adsorption of Ig onto other particles may activate AM and lead to pulmonary inflammation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
151
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2753-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Particle opsonization and lung macrophage cytokine response. In vitro and in vivo analysis.
pubmed:affiliation
Department of Environmental Health, Harvard School of Public Health, Boston, MA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't