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Infection and Immunity, July 2005, p. 4323-4326, Vol. 73, No. 7
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.7.4323-4326.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Effect of Chlamydia pneumoniae on Cellular ATP Content in Mouse Macrophages: Role of Toll-Like Receptor 2

Kambiz Yaraei,1 Lee Ann Campbell,1 Xiaodong Zhu,2 W. Conrad Liles,2 Cho-chou Kuo,1 and Michael E. Rosenfeld1*

Departments of Pathobiology,1 Medicine, University of Washington, Seattle, Washington2

Received 9 December 2004/ Returned for modification 3 February 2005/ Accepted 28 February 2005

Chlamydiae are obligate intracellular gram-negative bacteria and are dependent on the host cell for ATP. Thus, chlamydial infection may alter the intracellular levels of ATP and affect all energy-dependent processes within the cell. We have shown that both live C. pneumoniae and inactivated C. pneumoniae induce markers of cell death prior to completion of the bacterial growth cycle. As depletion of ATP could account for the observed increase in cell death, the effects of C. pneumoniae on ATP concentrations within mouse macrophages were investigated. Live, heat-killed, and UV-inactivated C. pneumoniae cultures (at multiplicities of infection [MOIs] of 0.01, 0.1, and 1.0) were incubated with mouse bone marrow macrophages isolated from C57BL/6J mice and mice deficient in Toll-like receptors. Treatment of the macrophages with both live and inactivated C. pneumoniae increased the ATP content of the cells. In cells infected with live C. pneumoniae, the increase was inversely proportional to the MOI. In cells treated with inactivated C. pneumoniae, the increase in ATP content was smaller than that induced by infection with live organisms and was proportional to the MOI. The increase in ATP content early in the developmental cycle was independent of the growth of C. pneumoniae, while sustained induction required live organisms. The capacity of C. pneumoniae to increase the ATP content was ablated in macrophages deficient in expression of either Toll-like receptor 2 or the Toll-like receptor accessory protein MyD88. In contrast, no effect was observed in macrophages lacking expression of Toll-like receptor 4.

* Corresponding author. Mailing address: Department of Pathobiology, Box 353410, University of Washington, Seattle, WA 98195. Phone: (206) 543-1738. Fax: (206) 616-1245. E-mail: ssmjm{at}u.washington.edu.

Editor: J. N. Weiser

Infection and Immunity, July 2005, p. 4323-4326, Vol. 73, No. 7
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.7.4323-4326.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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