ORIGINAL RESEARCH article
Front. Immunol.
Sec. Microbial Immunology
The Protective Role of MDL-1 in Sepsis-Induced Lung Injury: Insights from a Murine CLP Model
Baoji Hu 1
Yunpeng Wang 2
Daoqin Gao 1
Mengzhi Pan 1
Yangliang Yang 1
Yuan Yuan 1
Lulong Bo 3
Yi Zhang 4
1. Shanghai Pudong Hospital, Shanghai, China
2. Chinese PLA 92493 Hospital, Hulu Island, China
3. Changhai Hospital, Shanghai, China
4. Shanghai Pudong New Area Gongli Hospital, Shanghai, China
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Abstract
The Myeloid DAP12-associating lectin-1 (MDL-1) serves as a pivotal pattern recognition receptor crucial for recognizing various pathogenic microorganisms and orchestrating immune responses during infections. In this study, we elucidate that MDL-1 exhibits predominant expression within the mononuclear phagocyte system and plays a significant role in modulating the severity of lung injury in sepsis. Notably, MDL-1-deficient (MDL-1-/-) mice subjected to cecal ligation and puncture (CLP) exhibited elevated levels of pro-inflammatory cytokines such as IL-6 and TNF-α, along with decreased production of IFN-γ. Moreover, the expression levels of chemokines like IP-10, KC, MCP-1, and MIP-1 were markedly upregulated in septic MDL-1-/- mice. Concurrently, enhanced levels of Syk and cleaved caspase 3 were detected in the lung tissues of MDL-1-/--CLP animals, underscoring an augmented inflammatory response. Collectively, our findings indicate that MDL-1 deficiency correlates with the exacerbation of lung inflammation in a murine model of CLP-induced sepsis, highlighting the critical immunomodulatory role of MDL-1 in safeguarding against excessive pulmonary inflammation.
Summary
Keywords
Inflammation, Lung Injury, MDL-1, murine, Sepsis
Received
09 October 2025
Accepted
20 February 2026
Copyright
© 2026 Hu, Wang, Gao, Pan, Yang, Yuan, Bo and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Baoji Hu
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