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Infection and Immunity, January 2005, p. 70-78, Vol. 73, No. 1
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.1.70-78.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Osmolarity, a Key Environmental Signal Controlling Expression of Leptospiral Proteins LigA and LigB and the Extracellular Release of LigA

James Matsunaga,1,2* Yolanda Sanchez,1 Xiaoyi Xu,1 and David A. Haake1,2

Division of Infectious Diseases, Veterans Affairs Greater Los Angeles Healthcare System,1 Division of Infectious Diseases, Department of Medicine, UCLA David Geffen School of Medicine Los Angeles, California2

Received 14 July 2004/ Returned for modification 11 August 2004/ Accepted 25 August 2004

The high-molecular-weight leptospiral immunoglobulin-like repeat (Lig) proteins are expressed only by virulent low-passage forms of pathogenic Leptospira species. We examined the effects of growth phase and environmental signals on the expression, surface exposure, and extracellular release of LigA and LigB. LigA was lost from stationary-phase cells, while LigB expression was maintained. The loss of cell-associated LigA correlated with selective release of a lower-molecular-weight form of LigA into the culture supernatant, while LigB and the outer membrane lipoprotein LipL41 remained associated with cells. Addition of tissue culture medium to leptospiral culture medium induced LigA and LigB expression and caused a substantial increase in released LigA. The sodium chloride component of tissue culture medium was primarily responsible for the enhanced release of LigA. Addition of sodium chloride, potassium chloride, or sodium sulfate to leptospiral medium to physiological osmolarity caused the induction of both cell-associated LigA and LigB, indicating that osmolarity regulates the expression of Lig proteins. Osmotic induction of Lig expression also resulted in enhanced release of LigA and increased surface exposure of LigB, as determined by surface immunofluorescence. Osmolarity appears to be a key environmental signal that controls the expression of LigA and LigB.


* Corresponding author. Mailing address: VA Greater Los Angeles Healthcare System, B113/R225, Los Angeles, CA 90073. Phone: (310) 478-3711 ext. 42144. Fax: (310) 268-4142. E-mail: jamesm{at}ucla.edu.

Editor: D. L. Burns


Infection and Immunity, January 2005, p. 70-78, Vol. 73, No. 1
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.1.70-78.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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