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Abstract <p>To elucidate the role of galectin-3 (Gal-3) in sepsis, bacterial sepsis models were established in wild-type infant mice and Gal-3 knockout (Gal-3⁻/⁻) mice. Macrophage phagocytic function and maturation were systematically compared between the two groups. Sepsis was induced by intraperitoneal injection of <i>Salmonella typhimurium</i> (2.5 × 10<sup>6</sup> colony-forming units [CFU]/mouse) into 2-week-old wild-type (<i>n</i> = 20) and Gal-3⁻/⁻ mice (<i>n</i> = 20). Macrophage cytokine production, including interleukin (IL)-8, tumor necrosis factor (TNF)-α, and IL-10, was quantified by enzyme-linked immunosorbent assay (ELISA). Bacterial clearance was evaluated by peripheral blood CFU enumeration, and intracellular bactericidal activity was assessed in macrophages co-incubated with <i>S. typhimurium</i>. To examine phagocytic maturation, bacteria labeled with pH-sensitive and pH-insensitive fluorescent probes were used, and phagosome acidification was analyzed by flow cytometry. Compared with wild-type controls, Gal-3⁻/⁻ macrophages exhibited no significant changes in IL-8 or TNF-α expression (<i>P</i> &gt; 0.05) but showed a marked reduction in IL-10 levels (<i>P</i> &lt; 0.05). In parallel, Gal-3⁻/⁻ mice displayed significantly impaired bacterial clearance and intracellular killing capacity (<i>P</i> &lt; 0.05). Defective phagosome acidification and reduced phagosome-lysosome fusion were observed in Gal-3-deficient macrophages, rendering Gal-3⁻/⁻ mice more susceptible to bacterial sepsis. Collectively, these results indicate that Gal-3 is a key regulator of macrophage phagocytic maturation and antimicrobial defense during sepsis.</p> Impact Statement <p>This study identifies galectin-3 as a critical regulator of phagosome acidification and bacterial clearance during sepsis. Loss of galectin-3 disrupts immune homeostasis, characterized by impaired intracellular bacterial killing and reduced IL-10 production, rather than a global increase in pro-inflammatory cytokines. These findings suggest that galectin-3 contributes to sepsis progression by modulating immunoregulatory balance and highlight its potential value for immune endotype stratification and therapeutic targeting.</p> Graphical Abstract <p></p>

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Study on the Role of Galectin-3 in Sepsis

  • 期刊论文

  • 发表日期：

    2026年3月25日

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  • Wen Pan,
  • Jungang Zhao,
  • Feng Liu,
  • Qian Liu,
  • Qin Chen,
  • Guoji Zhu,
  • Yong Cheng

摘要

Abstract

To elucidate the role of galectin-3 (Gal-3) in sepsis, bacterial sepsis models were established in wild-type infant mice and Gal-3 knockout (Gal-3⁻/⁻) mice. Macrophage phagocytic function and maturation were systematically compared between the two groups. Sepsis was induced by intraperitoneal injection of Salmonella typhimurium (2.5 × 106 colony-forming units [CFU]/mouse) into 2-week-old wild-type (n = 20) and Gal-3⁻/⁻ mice (n = 20). Macrophage cytokine production, including interleukin (IL)-8, tumor necrosis factor (TNF)-α, and IL-10, was quantified by enzyme-linked immunosorbent assay (ELISA). Bacterial clearance was evaluated by peripheral blood CFU enumeration, and intracellular bactericidal activity was assessed in macrophages co-incubated with S. typhimurium. To examine phagocytic maturation, bacteria labeled with pH-sensitive and pH-insensitive fluorescent probes were used, and phagosome acidification was analyzed by flow cytometry. Compared with wild-type controls, Gal-3⁻/⁻ macrophages exhibited no significant changes in IL-8 or TNF-α expression (P > 0.05) but showed a marked reduction in IL-10 levels (P < 0.05). In parallel, Gal-3⁻/⁻ mice displayed significantly impaired bacterial clearance and intracellular killing capacity (P < 0.05). Defective phagosome acidification and reduced phagosome-lysosome fusion were observed in Gal-3-deficient macrophages, rendering Gal-3⁻/⁻ mice more susceptible to bacterial sepsis. Collectively, these results indicate that Gal-3 is a key regulator of macrophage phagocytic maturation and antimicrobial defense during sepsis.

Impact Statement

This study identifies galectin-3 as a critical regulator of phagosome acidification and bacterial clearance during sepsis. Loss of galectin-3 disrupts immune homeostasis, characterized by impaired intracellular bacterial killing and reduced IL-10 production, rather than a global increase in pro-inflammatory cytokines. These findings suggest that galectin-3 contributes to sepsis progression by modulating immunoregulatory balance and highlight its potential value for immune endotype stratification and therapeutic targeting.

Graphical Abstract