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Infection and Immunity, January 2000, p. 87-92, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Resistance of Transgenic Mice Expressing Human Group II Phospholipase A2 to Escherichia coli Infection

V. Jukka O. Laine,1,* David S. Grass,2 and Timo J. Nevalainen1

Department of Pathology, University of Turku, 20520 Turku, Finland,1 and Chrysalis DNX Transgenics, Princeton, New Jersey 085402

Received 10 June 1999/Returned for modification 11 August 1999/Accepted 20 October 1999

Group II phospholipase A2 (PLA2) is a newly recognized antibacterial acute-phase protein. Recently we observed that transgenic mice expressing group II PLA2 (PLA2+ mice) were able to resist experimental Staphylococcus aureus infection by killing the bacteria, as indicated by improved survival and by the small numbers of live bacteria in their tissues (V. J. O. Laine, D. S. Grass, and T. J. Nevalainen, J. Immunol. 162:7402-7408, 1999). To establish the role of group II PLA2 in Escherichia coli infection, the host responses of PLA2+ mice and their PLA2-deficient C57BL/6J littermates (PLA2- mice) were studied after intraperitoneal administration of E. coli. The levels of group II PLA2 in sera of PLA2+ mice increased after the administration of E. coli, and the concentration of group II PLA2 correlated significantly with the catalytic activity of PLA2 in serum. PLA2+ mice showed lower rates of mortality and less bacterial growth in peritoneal lavage fluid, blood, and spleen and liver tissues than PLA2- mice. Unlike the observations with staphylococcal infection, serum and peritoneal lavage fluid did not inhibit the growth of E. coli in vitro. The results indicate that expression of the group II PLA2 transgene improves the host defense of mice against E. coli infection.

* Corresponding author. Mailing address: Department of Pathology, University of Turku, Kiinamyllynkatu 10, FIN-20520 Turku, Finland. Phone: (358) 2-261 2670. Fax: (358) 2-333 7459. E-mail: vellai{at}utu.fi.

Infection and Immunity, January 2000, p. 87-92, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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