Differential expression of IL-1 and TNF receptors in murine macrophages infected with virulent vs. avirulent Legionella pneumophila

Citation
S. Mchugh et al., Differential expression of IL-1 and TNF receptors in murine macrophages infected with virulent vs. avirulent Legionella pneumophila, CAN J MICRO, 46(10), 2000, pp. 885-891
Citations number
25
Categorie Soggetti
Biotecnology & Applied Microbiology",Microbiology
Journal title
CANADIAN JOURNAL OF MICROBIOLOGY
ISSN journal
00084166 → ACNP
Volume
46
Issue
10
Year of publication
2000
Pages
885 - 891
Database
ISI
SICI code
0008-4166(200010)46:10<885:DEOIAT>2.0.ZU;2-L
Abstract
Infection of macrophages from genetically susceptible A/J mice with Legione lla pneumophila induces high levels of various cytokines in serum as well a s in cultures of spleen or peritoneal cells from the mice. However, modulat ion of receptor expression for these cytokines during infection has not bee n studied in detail, even though these receptors on macrophages have a crit ical role in inflammatory responses during the infection. In the present st udy, the differential expression of mRNA for TNF and IL-1 receptors as well as receptor antigens during infection of macrophages with virulent vs. avi rulent L. pneumophila was investigated. Mouse thioglycollate-elicited perit oneal macrophages showed by RT-PCR constitutive steady-state levels of mRNA for TNF-type I and -type II receptors as well as IL-1 type I receptor. How ever, IL-1 type II receptor mRNA was not expressed in thioglycollate-elicit ed macrophages. Infection of macrophages with virulent bacteria caused an u pregulation of IL-1 type I and TNF type I receptor mRNA, but had no effect on TNF type II receptor message. Avirulent L. pneumophila infection caused much less induction of these receptor mRNAs. The amount of receptor antigen of IL-1 type I on the surface of macrophages was also increased by infecti on with virulent L. pneumophila determined by flow cytometric analysis. The se results indicate that L. pneumophila infection not only causes induction of various cytokines, but also modulation of certain cytokine receptors, w hich may regulate the susceptibility to infection.