Inhibition of neutrophil swarming by type I interferon promotes intracellular bacterial evasion

Shimin Li, Qi Yao, Jiajia Li, Haoxiang Yang, Rui Qian, Meijuan Zheng, Ning Wu, Hongyuan Jiang, Lu Li () and Zhutian Zeng ()
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Shimin Li: University of Science and Technology of China
Qi Yao: University of Science and Technology of China
Jiajia Li: University of Science and Technology of China
Haoxiang Yang: University of Science and Technology of China
Rui Qian: First Affiliated Hospital of Anhui Medical University
Meijuan Zheng: First Affiliated Hospital of Anhui Medical University
Ning Wu: The First Affiliated Hospital of Anhui Medical University and Institute of Clinical Immunology Anhui Medical University
Hongyuan Jiang: University of Science and Technology of China
Lu Li: University of Science and Technology of China
Zhutian Zeng: University of Science and Technology of China

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Listeria monocytogenes (LM) possesses the ability to breach multiple barriers and elicit intricate immune responses. However, there remains a lack of explicit understanding regarding how LM evades innate immune surveillance within the body. Here, we utilized liver intravital imaging to elucidate the dynamic process of LM during infection in the liver. We discovered that LM can rapidly escape from Kupffer cells (KCs) through listeriolysin O (LLO) and proliferate within hepatocytes. Upon LM exposure to the hepatic sinusoids, neutrophils rapidly aggregate at the site of infection. Subsequently, LM can induce type I interferon (IFN-I) production primarily in the spleen, which acts systemically on neutrophils to hamper their swarming by deactivating the ERK pathway, thus evading neutrophil-mediated eradication. Furthermore, our findings suggest that virus-induced IFN-I suppresses neutrophil swarming, and COVID-19 patients exhibit impaired neutrophil aggregation function. In conclusion, our findings provide compelling evidence demonstrating that intracellular bacteria represented by LM can hijack host defense mechanisms against viral infections to evade immune surveillance. Additionally, impaired neutrophil swarming caused by IFN-I is one of the significant factors contributing to the increased susceptibility to bacterial infections following viral infections.

Date: 2024
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DOI: 10.1038/s41467-024-53060-4

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