dc.contributor.author |
Fernandez-Bustamante, A |
|
dc.contributor.author |
Agazio, A |
|
dc.contributor.author |
Wilson, P |
|
dc.contributor.author |
Elkins, N |
|
dc.contributor.author |
Domaleski, L |
|
dc.contributor.author |
He, Q |
|
dc.contributor.author |
Baer, KA |
|
dc.contributor.author |
Moss, AF |
|
dc.contributor.author |
Wischmeyer, Paul Edmund |
|
dc.contributor.author |
Repine, JE |
|
dc.coverage.spatial |
United States |
|
dc.date.accessioned |
2016-11-06T18:01:56Z |
|
dc.date.issued |
2015 |
|
dc.identifier |
http://www.ncbi.nlm.nih.gov/pubmed/26147379 |
|
dc.identifier |
PONE-D-14-47188 |
|
dc.identifier.uri |
https://hdl.handle.net/10161/12988 |
|
dc.description.abstract |
BACKGROUND: Glutamine (GLN) attenuates acute lung injury (ALI) but its effect on alveolar
macrophages is unknown. We hypothesized that GLN pretreatment would induce the anti-inflammatory
CD163/heme oxygenase (HO)-1/p38-MAPK dephosphorylation pathway in alveolar macrophages
and reduce ALI in rats insufflated with interleukin-1 (IL-1) and lipopolysaccharide
(LPS). METHODS: Male Sprague-Dawley rats were randomized to the following groups:
GLN-IL-1/LPS-, GLN+IL-1/LPS-, GLN-IL-1/LPS+, and GLN+IL-1/LPS+. GLN pretreatment was
given via gavage (1 g/kg L-alanyl-L-glutamine) daily for 2 days. ALI was subsequently
induced by insufflating 50 ng IL-1 followed by 5mg/kg E.coli LPS. After 24h, bronchoalveolar
lavage (BAL) protein, lactate dehydrogenase (LDH) and neutrophil concentrations were
analyzed. BAL alveolar macrophage CD163+ expression, HO-1 and p38-MAPK concentrations
were measured, as well as alveolar macrophage tumor necrosis factor (TNF)-α and interleukin
(IL)-10 concentrations. Histology and immunofluorescence studies were also performed.
RESULTS: Following IL-1/LPS insufflation, GLN pretreated rats had significantly decreased
BAL protein and LDH concentrations, but not BAL neutrophil counts, compared to non-GLN
pretreated rats. The number of alveolar macrophages and the number of CD163+ macrophages
were significantly increased in GLN pretreated IL-1/LPS-insufflated rats compared
to non-GLN pretreated, IL-1/LPS-insufflated rats. GLN pretreatment before IL-1/LPS
also significantly increased HO-1 concentrations and dephosphorylated p38-MAPK levels
but not cytokine levels in alveolar macrophages. Immunofluorescence localized CD163
and HO-1 in alveolar macrophages. CONCLUSION: Short-term GLN pretreatment activates
the anti-inflammatory CD163/HO-1/p38-MAPK dephosphorylation pathway of alveolar macrophages
and decreases capillary damage but not neutrophil recruitment in IL-1/LPS-insufflated
rats.
|
|
dc.language |
eng |
|
dc.relation.ispartof |
PLoS One |
|
dc.relation.isversionof |
10.1371/journal.pone.0130764 |
|
dc.subject |
Acute Lung Injury |
|
dc.subject |
Animals |
|
dc.subject |
Antigens, CD |
|
dc.subject |
Antigens, Differentiation, Myelomonocytic |
|
dc.subject |
Bronchoalveolar Lavage Fluid |
|
dc.subject |
Capillaries |
|
dc.subject |
Glutamine |
|
dc.subject |
Heme Oxygenase-1 |
|
dc.subject |
Interleukin-1 |
|
dc.subject |
Lipopolysaccharides |
|
dc.subject |
Macrophages, Alveolar |
|
dc.subject |
Mitogen-Activated Protein Kinases |
|
dc.subject |
Phosphorylation |
|
dc.subject |
Rats |
|
dc.subject |
Rats, Sprague-Dawley |
|
dc.subject |
Receptors, Cell Surface |
|
dc.title |
Brief Glutamine Pretreatment Increases Alveolar Macrophage CD163/Heme Oxygenase-1/p38-MAPK
Dephosphorylation Pathway and Decreases Capillary Damage but Not Neutrophil Recruitment
in IL-1/LPS-Insufflated Rats.
|
|
dc.type |
Journal article |
|
pubs.author-url |
http://www.ncbi.nlm.nih.gov/pubmed/26147379 |
|
pubs.begin-page |
e0130764 |
|
pubs.issue |
7 |
|
pubs.organisational-group |
Anesthesiology |
|
pubs.organisational-group |
Anesthesiology, Critical Care Medicine |
|
pubs.organisational-group |
Clinical Science Departments |
|
pubs.organisational-group |
Duke |
|
pubs.organisational-group |
Duke Clinical Research Institute |
|
pubs.organisational-group |
Institutes and Centers |
|
pubs.organisational-group |
School of Medicine |
|
pubs.publication-status |
Published online |
|
pubs.volume |
10 |
|
dc.identifier.eissn |
1932-6203 |
|