Differential expression of IL-1 and TNF receptors in murine macrophages infected with virulent vs. avirulent Legionella pneumophila.
Infection of macrophages from genetically susceptible A/J mice with Legionella pneumophila induces high levels of various cytokines in serum as well as in cultures of spleen or peritoneal cells from the mice. However, modulation of receptor expression for these cytokines during infection has not been studied in detail, even though these receptors on macrophages have a critical role in inflammatory responses during the infection. In the present study, the differential expression of mRNA for TNF and IL-1 receptors as well as receptor antigens during infection of macrophages with virulent vs. avirulent L. pneumophila was investigated. Mouse thioglycollate-elicited peritoneal 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. However, IL-1 type II receptor mRNA was not expressed in thioglycollate-elicited macrophages. Infection of macrophages with virulent bacteria caused an upregulation 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 infection with virulent L. pneumophila determined by flow cytometric analysis. These results indicate that L. pneumophila infection not only causes induction of various cytokines, but also modulation of certain cytokine receptors, which may regulate the susceptibility to infection.
McHugh
S
S
Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa 33612, USA.
Yamamoto
Y
Y
Klein
T W
TW
Friedman
H
H
D000818:Animals; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016952:Legionella pneumophila / Q000276:immunology / Q000472:pathogenicity*; D007877:Legionnaires' Disease / Q000276:immunology / Q000382:microbiology*; D017737:Macrophages, Peritoneal / Q000378:metabolism / Q000382:microbiology*; D051379:Mice; D012333:RNA, Messenger / Q000378:metabolism; D017472:Receptors, Interleukin-1 / Q000378:metabolism*; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D015854:Up-Regulation; D014774:Virulence
D012333:RNA, Messenger; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor