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Infection and Immunity, June 2001, p. 3837-3844, Vol. 69, No. 6
Division of Rheumatology, Department of
Internal Medicine, University of Utah School of Medicine, Salt Lake
City, Utah 84132
Received 6 December 2000/Returned for modification 19 February
2001/Accepted 5 March 2001
The Mycoplasma arthritidis mitogen (MAM)
superantigen (SAg) is a potent activator of human and murine cells and
is produced by an organism that is a cause of acute and chronic
arthritis of rodents. It is phylogenetically unrelated to other
bacterial SAgs and exhibits a number of unique features. We recently
demonstrated that MAM differentially regulates the cytokine responses
of different mouse strains following in vivo administration. Here we
show that the presence in inbred C3H/HeJ mice of the mutant
Lpsd gene, which is associated with a
defect in Toll-like receptor 4 (TLR4), influences MAM regulation of
cytokine profiles in vivo. Whereas the levels of type 1 cytokines (interleukin-2 [IL-2], gamma interferon, IL-12, and tumor
necrosis factor alpha) were depressed in cells from MAM-injected
wild-type C3H/HeSnJ mice, they were elevated in cells from C3H/HeJ
mice. Furthermore, the levels of type 2 cytokines (IL-4, IL-6, and
IL-10) were elevated in Lpsn C3H/HeSnJ
mice but depressed in Lpsd C3H/HeJ
mice. The transcript for IL-12 p40 was highly expressed in C3H/HeJ but
not C3H/HeSnJ mice. F1 mice exhibited the same cytokine
profile as C3H/HeJ mice, indicating that the mutant gene exhibited
dominant-negative inheritance. In addition, C3H/HeJ mice were highly
susceptible to toxic death in comparison with C3H/HeSnJ mice after
injection with live M. arthritidis organisms. Our
results suggest that MAM interacts with the lipopolysaccharide signaling pathway, possibly involving TLR4 or a combinatorial Toll
complex.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.6.3837-3844.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Presence of Lpsd Mutation
Influences Cytokine Regulation In Vivo by the Mycoplasma
arthritidis Mitogen Superantigen and Lethal Toxicity in
Mice Infected with M. arthritidis
*
Corresponding author. Mailing address: Division of
Rheumatology, Department of Internal Medicine, University of Utah
School of Medicine, 50 N. Medical Dr., Salt Lake City, UT 84132. Phone: (801) 581-8845. Fax: (801) 581-6069. E-mail:
Hong.Mu{at}m.cc.utah.edu.
Infection and Immunity, June 2001, p. 3837-3844, Vol. 69, No. 6
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.6.3837-3844.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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