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Infection and Immunity, May 2009, p. 2168-2176, Vol. 77, No. 5
0019-9567/09/$08.00+0     doi:10.1128/IAI.01350-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Stimulation of the Molecule 4-1BB Enhances Host Defense against Listeria monocytogenes Infection in Mice by Inducing Rapid Infiltration and Activation of Neutrophils and Monocytes{triangledown}

Sang-Chul Lee,1 Seong-A Ju,1 Boo-Hee Sung,2 Sook-Kyoung Heo,3 Hong Rae Cho,1 Eun A. Lee,1 Jung Dae Kim,1 In Hee Lee,4 Sang-Min Park,2 Quang Tam Nguyen,2 Jae-Hee Suh,1 and Byung-Sam Kim2*

Biomedical Research Center, Ulsan University Hospital, College of Medicine, University of Ulsan, Ulsan 682-714, Republic of Korea,1 Immunomodulation Research Center and Department of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea,2 Cardiovascular Medical Research Center and Department of Prescriptionology, University of Dongguk, Gyeongju City, Gyeongbuk 780-714, Republic of Korea,3 Department of Bio-Technology, Hoseo University, 29-1 Sechuli, Baebang-Myun, Asan City, Chungnam-Do 336-795, Republic of Korea4

Received 5 November 2008/ Returned for modification 4 January 2009/ Accepted 12 February 2009

The tumor necrosis factor receptor family molecule 4-1BB (CD137) has diverse roles in adaptive and innate immune responses. However, little is known of its role in bacterial infections. Previously, we showed that 4-1BB-deficient mice have enhanced susceptibility to Listeria monocytogenes infection, and mice pretreated with agonistic anti-4-1BB antibody (3E1) were much more resistant to L. monocytogenes infection than mice treated with control antibody. In this study, we report that stimulating 4-1BB by administering 3E1 in the early phase of L. monocytogenes infection is critical for promoting the survival of mice by inducing rapid infiltration of neutrophils and monocytes into L. monocytogenes-infected livers. The levels of tumor necrosis factor alpha, interleukin 6, and monocyte chemoattractant protein 1 in the livers of 3E1-treated mice increased as early as 30 min postinfection and peaked by 1 to 2 h, while those in mice treated with control antibody started to increase only at 16 h postinfection. Monocytes and neutrophils from the 3E1-treated mice had higher levels of activation markers, phagocytic activity, and reactive oxygen species than those from control mice. In vitro stimulation of 4-1BB induced the production of the inflammatory cytokines/chemokines of neutrophils, but not those of monocytes. These results suggest that 4-1BB stimulation of neutrophils in the early phase of L. monocytogenes infection causes rapid production of inflammatory cytokines/chemokines and that the subsequent infiltration of neutrophils and monocytes is crucial for eliminating the infecting L. monocytogenes.

* Corresponding author. Mailing address: Department of Biological Sciences, University of Ulsan, San 29, Mookeo-dong, Nam-Ku, Ulsan, Republic of Korea, 680-749. Phone: 82-52-259-1541. Fax: 82-52-259-2740. E-mail: bskim{at}mail.ulsan.ac.kr

{triangledown} Published ahead of print on 23 February 2009.

Editor: J. L. Flynn

Infection and Immunity, May 2009, p. 2168-2176, Vol. 77, No. 5
0019-9567/09/$08.00+0     doi:10.1128/IAI.01350-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Nguyen, Q.-T., Ju, S.-A, Park, S.-M., Lee, S.-C., Yagita, H., Lee, I. H., Kim, B.-S. (2009). Blockade of CD137 Signaling Counteracts Polymicrobial Sepsis Induced by Cecal Ligation and Puncture. Infect. Immun. 77: 3932-3938 [Abstract] [Full Text]  


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