Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-12-4
pubmed:abstractText
We have shown that hypoxia (2% O2 approximately pO2 14 mmHg) as opposed to O2 atmospheric pressure (20.9% O2 approximately pO2 140 mmHg) can deeply affect the production of cytokines in human peripheral mononuclear cells (PBMC) in the presence or absence of a specific T-cell activator such as phytohemagglutinin (PHA). In hypoxia, interleukin (IL)-2, IL-4, and interferon (IFN)-gamma production increased by 110, 70, and 50% over that of controls, respectively, in PHA-stimulated PBMC (P < 0.05). Moreover, in hypoxia, IL-6 production was significantly enhanced in both resting and PHA-stimulated PBMC by 36 and 37%, respectively (P < 0.05). However, in hypoxia, IL-10 production decreased in both resting and stimulated PBMC, being 80 and 67% of controls, respectively (P < 0.05). PBMC proliferation was not significantly affected by hypoxia, although PBMC susceptibility to PHA was about 80% of that of the control (P < 0.05) after 40 hr of treatment, whereas the cycle progression of hypoxic PBMC was delayed. From an evaluation of these results, hypoxia apparently modifies the production of cytokines by PBMC. These results have both theoretical and practical interest because local hypoxia is very common in several conditions, such as inflammation and local ischemia, and is a host-nonspecific defense against infection. Furthermore, these results suggest a differential pattern of cytokine production in vivo in hypoxic tissues.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9541
pubmed:author
pubmed:issnType
Print
pubmed:volume
173
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
335-42
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Hypoxia affects cytokine production and proliferative responses by human peripheral mononuclear cells.
pubmed:affiliation
Institute of General Physiology, University of Siena, Italy. naldini@unisi.it
pubmed:publicationType
Journal Article