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Updated: Feb 21, 2026
Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages
Published on: October 25, 2017
Macrophage C-type lectin is essential for phagosome maturation and acidification during Escherichia coli-induced
Wook-Bin Lee1, Ji-Jing Yan2, Ji-Seon Kang3
1Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Republic of Korea.
Abstract:
Sepsis is a life-threatening condition caused by an uncontrolled response to bacterial infection. Impaired bactericidal activity in the host is directly associated with severe sepsis; however, the underlying regulatory mechanism(s) is largely unknown. Here, we show that MCL (macrophage C-type lectin) plays a crucial role in killing bacteria during Escherichia coli-induced peritonitis. MCL-deficient mice with E. coli-induced sepsis showed lower survival rates and reduced bacterial clearance when compared with control mice, despite similar levels of proinflammatory cytokine production. Although the ability of macrophages from MCL-deficient mice to kill bacteria was impaired, they showed normal phagocytic activity and production of reactive oxygen species. In addition, MCL-deficient macrophages showed defective phagosome maturation and phagosomal acidification after E. coli infection. Taken together, these results indicate that MCL plays an important role in host defense against E. coli infection by promoting phagosome maturation and acidification, thereby providing new insight into the role of MCL during pathogenesis of sepsis and offering new therapeutic options.
Insights
Macrophage C-type lectin (MCL) is crucial for fighting bacterial infections in sepsis. MCL deficiency impairs bacterial clearance by hindering phagosome maturation and acidification, impacting host defense against E. coli.
Area of Science:
- Immunology
- Microbiology
- Pathogenesis
Background:
- Sepsis, a life-threatening response to bacterial infection, involves impaired host bactericidal activity.
- The regulatory mechanisms behind this impaired activity in severe sepsis remain largely unknown.
Purpose of the Study:
- To investigate the role of Macrophate C-type lectin (MCL) in host defense during Escherichia coli-induced sepsis.
- To elucidate the mechanisms by which MCL influences bacterial clearance and macrophage function.
Main Methods:
- Utilized MCL-deficient mice and wild-type controls to study E. coli-induced peritonitis.
- Assessed survival rates, bacterial clearance, proinflammatory cytokine production, phagocytic activity, reactive oxygen species production, phagosome maturation, and phagosomal acidification.
Main Results:
- MCL-deficient mice exhibited lower survival rates and reduced bacterial clearance compared to controls.
- Macrophage phagocytic activity and reactive oxygen species production were normal in MCL-deficient mice.
- MCL deficiency led to defective phagosome maturation and acidification in macrophages following E. coli infection.
Conclusions:
- Macrophate C-type lectin (MCL) plays a critical role in host defense against E. coli infection.
- MCL promotes bacterial clearance by enhancing phagosome maturation and acidification within macrophages.
- These findings offer new insights into sepsis pathogenesis and potential therapeutic targets.
