Linked Life Data

17785791

Source:http://linkedlifedata.com/resource/pubmed/id/17785791

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-9-5
pubmed:abstractText
The MAPK family member JNK/stress-activated MAPK (SAPK) is involved in extracellular stress and proinflammatory cytokine responses, including production of cytokines such as IL-12. The JNK1 and 2 isoforms are widely expressed, but JNK3 is largely restricted to tissues of the brain, testis, and heart. In this study, we focus on mouse neutrophils, a cell type in which JNK/SAPK expression and activity has been given little study. We used Western blot analysis to examine expression patterns of JNK/SAPK in wild-type and JNK2-/- polymorphonuclear leukocytes (PMN). Surprisingly, neutrophils displayed a major deficiency in JNK1 expression, in contrast to macrophages that expressed high levels of both JNK1 and JNK2 MAPK. JNK1 expression was steadily reduced during the neutrophil maturation in bone marrow. We used PMN infection with the protozoan parasite Toxoplasma gondii to determine whether neutrophil JNK2 was functional. The parasite induced rapid JNK2 phosphorylation and intracellular FACS staining demonstrated preferential activation in infected neutrophils. Use of JNK2-/- neutrophils revealed that this MAPK family member was required for PMN IL-12p40 and CCL2/MCP-1 production. The chemotactic response displayed a minor JNK2 dependence but phagocytosis and oxidative burst activity did not require this MAPK. These findings are important because they demonstrate 1) a previously unrecognized unusual JNK expression pattern in mouse neutrophils, 2) JNK2 in PMN is activated by Toxoplasma invasion, and 3) a requirement for JNK2 in PMN IL-12p40 and CCL2/MCP-1 production in response to a microbial pathogen.
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
15
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3570-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17785791-Animals, pubmed-meshheading:17785791-Ascitic Fluid, pubmed-meshheading:17785791-Bystander Effect, pubmed-meshheading:17785791-Cell Differentiation, pubmed-meshheading:17785791-Chemokine CCL2, pubmed-meshheading:17785791-Chemotaxis, Leukocyte, pubmed-meshheading:17785791-Down-Regulation, pubmed-meshheading:17785791-Enzyme Activation, pubmed-meshheading:17785791-Female, pubmed-meshheading:17785791-Interleukin-12 Subunit p40, pubmed-meshheading:17785791-Mice, pubmed-meshheading:17785791-Mice, Inbred C57BL, pubmed-meshheading:17785791-Mice, Knockout, pubmed-meshheading:17785791-Mice, Transgenic, pubmed-meshheading:17785791-Mitogen-Activated Protein Kinase 8, pubmed-meshheading:17785791-Mitogen-Activated Protein Kinase 9, pubmed-meshheading:17785791-Neutrophils, pubmed-meshheading:17785791-Phagocytosis, pubmed-meshheading:17785791-Respiratory Burst, pubmed-meshheading:17785791-Toxoplasma
pubmed:year
2007
pubmed:articleTitle
Mouse neutrophils require JNK2 MAPK for Toxoplasma gondii-induced IL-12p40 and CCL2/MCP-1 release.
pubmed:affiliation
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural