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Infection and Immunity, July 2003, p. 4102-4111, Vol. 71, No. 7
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.7.4102-4111.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

CD44-Regulated Intracellular Proliferation of Listeria monocytogenes

Microbiology & Tumorbiology Center, Karolinska Institute, Stockholm,¹ Department of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Upsala, Sweden,³ Department of Veterinary Microbiology, The Royal Veterinary and Agricultural University, Frederiksberg, Denmark²

Received 9 December 2002/ Returned for modification 11 February 2003/ Accepted 14 April 2003

CD44 has been implicated in immune and inflammatory processes. We have analyzed the role of CD44 in the outcome of Listeria monocytogenes infection in murine bone marrow-derived macrophages (BMM). Surprisingly, a dramatically decreased intracellular survival of L. monocytogenes was observed in CD44^-/- BMM. CD44^-/- heart or lung fibroblast cultures also showed reduced bacterial levels. Moreover, livers from CD44^-/--infected mice showed diminished levels of L. monocytogenes. In contrast, intracellular growth of Salmonella enterica serovar Typhimurium was the same in CD44^-/- and control BMM. The CD44-mediated increased bacterial proliferation was not linked to altered BMM differentiation or to secretion of soluble factors. CD44 did not mediate listerial uptake, and it played no role in bacterial escape from the primary phagosome or formation of actin tails. Furthermore, CD44-enhanced listerial proliferation occurred in the absence of intracellular bacterial spreading. Interestingly, coincubation of BMM with hyaluronidase or anti-CD44 antibodies that selectively inhibit hyaluronan binding increased intracellular listerial proliferation. Treatment of cells with hyaluronan, in contrast, diminished listerial growth and induced proinflammatory transcript levels. We suggest that L. monocytogenes takes advantage of the CD44-mediated signaling to proliferate intracellularly, although binding of CD44 to certain ligands will inhibit such response.

Editor: B. B. Finlay

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