Synchronously in vivo real‐time monitoring bacterial load and temperature with evaluating immune response to decipher bacterial infection

Author:

Sheng Huaixuan1,Li Huizhu1,Li Shunyao1,Yu Chengxuan1,Wang Yueming2,Hu Haichen1,Fang Lu34,Chen Fuchun4,Lu Yanyan5,Xu Xiaogang5,Yang Xing6,Chen Shiyi1,Hao Yuefeng6,Li Yunxia1,Feng Sijia1,Chen Jun1ORCID

Affiliation:

1. Sports Medicine Institute of Fudan University, Department of Sports Medicine, Huashan Hospital Fudan University Shanghai China

2. Department of Anatomy and Physiology School of Medicine, Shanghai Jiao Tong University Shanghai China

3. University of Chinese Academy of Sciences Beijing China

4. Key Laboratory of Infrared System Detection and Imaging Technology, Shanghai Institute of Technical Physics, Chinese Academy of Sciences Shanghai China

5. Institute of Antibiotics, Huashan Hospital, Key Laboratory of Clinical Pharmacology of Antibiotics, National Health Commission, Fudan University Shanghai China

6. Department of Orthopedics Affiliated Suzhou Hospital of Nanjing Medical University Suzhou China

Abstract

AbstractDetermining the precise course of bacterial infection requires abundant in vivo real‐time data. Synchronous monitoring of the bacterial load, temperature, and immune response can satisfy the shortage of real‐time in vivo data. Here, we conducted a study in the joint‐infected mouse model to synchronously monitor the bacterial load, temperature, and immune response using the second near‐infrared (NIR‐II) fluorescence imaging, infrared thermography, and immune response analysis for 2 weeks. Staphylococcus aureus (S. aureus) was proved successfully labeled with glucose‐conjugated quantum dots in vitro and in subcutaneous‐infected model. The bacterial load indicated by NIR‐II fluorescence imaging underwent a sharp drop at 1 day postinfection. At the same time, the temperature gap detected through infrared thermography synchronously brought by infection reached lowest value. Meanwhile, the flow cytometry analysis demonstrated that immune response including macrophage, neutrophil, B lymphocyte, and T lymphocyte increased to the peak at 1 day postinfection. Moreover, both M1 macrophage and M2 macrophage in the blood have an obvious change at ~ 1 day postinfection, and the change was opposite. In summary, this study not only obtained real‐time and long‐time in vivo data on the bacterial load, temperature gap, and immune response in the mice model of S. aureus infection, but also found that 1 day postinfection was the key time point during immune response against S. aureus infection. Our study will contribute to synchronously and precisely studying the complicated complex dynamic relationship after bacterial infection at the animal level.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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