Linked Life Data

10882225

Source:http://linkedlifedata.com/resource/pubmed/id/10882225

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-7-14
pubmed:abstractText
Inhalation of Saccharopolyspora rectivirgula (S. rectivirgula) causes farmer's lung disease, a classic example of hypersensitivity pneumonitis (HP). HP is characterized by bronchoalveolar lavage fluid (BALF) neutrophilia (within the first 48 hours after inhalation), followed by BALF lymphocytosis. We utilized a well-described murine model of HP to determine the timing of the appearance of the C-C chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha (MIP-1alpha); the inflammatory cytokines tumor necrosis factor (TNF), interleukin-1alpha (IL-1alpha), and interleukin-6 (IL-6); and the Th1 -differentiating cytokine interleukin-12 (IL-12) in BALF. After a single intratracheal administration of S. rectivirgula, there was remarkable BALF neutrophilia (peak 24 to 48 hours), followed by a BALF lymphocytosis (peak 48 to 72 hours) in both C57Bl/6 and BALB/c mice that was preceded by the appearance of MIP-1alpha in BALF (peak 4 to 6 hours) and MCP-1 (peak at 48 hours). In both strains of mice there was a striking increase of BALF IL-12 (peak 48 to 72 hours). There was also an increase in BALF IL-6, IL-1alpha, and TNF that was greater in the BALB/c mice than in the C57Bl/6 mice. S. rectivirgula induced the secretion of MIP-1alpha, MCP-1, IL-6, IL-1alpha, and IL-12 from the murine macrophage cell line J774A.1; MIP-1alpha, IL-6, IL-1alpha, IL-12, and TNF from C57Bl/6 alveolar macrophages; and IL-1alpha, IL-6, and TNF-but not IL-12-from BALB/c alveolar macrophages. We conclude that chemokines and cytokines induced by intratracheal administration of S. rectivirgula precede BALF neutrophilia and lymphocytosis and may cause differentiation of Th1 cells; we also conclude that pulmonary macrophages represent a potential source of these substances.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-2143
pubmed:author
pubmed:issnType
Print
pubmed:volume
136
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
29-38
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10882225-Alveolitis, Extrinsic Allergic, pubmed-meshheading:10882225-Animals, pubmed-meshheading:10882225-Bronchoalveolar Lavage Fluid, pubmed-meshheading:10882225-Chemokine CCL2, pubmed-meshheading:10882225-Chemokine CCL3, pubmed-meshheading:10882225-Chemokine CCL4, pubmed-meshheading:10882225-Interleukin-12, pubmed-meshheading:10882225-Interleukin-6, pubmed-meshheading:10882225-Leukocyte Count, pubmed-meshheading:10882225-Lymphocytes, pubmed-meshheading:10882225-Macrophage Inflammatory Proteins, pubmed-meshheading:10882225-Macrophages, pubmed-meshheading:10882225-Male, pubmed-meshheading:10882225-Mice, pubmed-meshheading:10882225-Mice, Inbred BALB C, pubmed-meshheading:10882225-Mice, Inbred C57BL, pubmed-meshheading:10882225-Neutrophils, pubmed-meshheading:10882225-Tumor Necrosis Factor-alpha
pubmed:year
2000
pubmed:articleTitle
Mediators of hypersensitivity pneumonitis.
pubmed:affiliation
Department of Medicine, Albuquerque Veterans Affairs Medical Center, University of New Mexico School of Medicine, 87108, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.