Pathogenic role of HMGB1 in SARS?

Chen, Guoqian; Chen, Da-zhi; Li, Jianhua; Czura, Christopher J.; Tracey, Kevin J.; Sama, Andrew E.; Wang, Haichao

doi:10.1016/j.mehy.2004.01.037

« Previous Next »Medical Hypotheses
Volume 63, Issue 4 , Pages 691-695, 2004

Pathogenic role of HMGB1 in SARS?

Guoqian Chen
- Department of Emergency Medicine, North Shore University Hospital, New York University School of Medicine, Manhasset, NY 11030, USA
Da-zhi Chen
- North Shore – LIJ Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
Jianhua Li
- North Shore – LIJ Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
Christopher J. Czura
- North Shore – LIJ Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
Kevin J. Tracey
- North Shore – LIJ Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
Andrew E. Sama
- Department of Emergency Medicine, North Shore University Hospital, New York University School of Medicine, Manhasset, NY 11030, USA
Haichao Wang
- Department of Emergency Medicine, North Shore University Hospital, New York University School of Medicine, Manhasset, NY 11030, USA
- North Shore – LIJ Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
- Corresponding author. Tel.: +516-562-2823; fax: +516-562-3710

Received 29 January 2004; accepted 31 January 2004.

Abstract

High mobility group box 1 protein (HMGB1) is released by necrotic cells or activated macrophages/monocytes, and functions as a late mediator of lethal systemic and local pulmonary inflammation. Passive immunization with anti-HMGB1 antibodies confers significant protection against lethal endotoxemia, sepsis, and acute lung injury, even when antibodies are administered after the onset of these diseases. In light of observations that three Chinese herbal formulations recommended for treatment of severe acute respiratory syndrome (SARS) specifically inhibited the release of HMGB1 from innate immune cells, we hypothesize that HMGB1 might occupy a pathogenic role in SARS by mediating an injurious pulmonary inflammatory response.