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Updated: Dec 20, 2025

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Requirement of Complement C6 for Intact Innate Immune Responses in Mice.

Fatemeh Fattahi1,2, Jamison J Grailer2, Michella Parlett2

  • 1Division of Allergy and Clinical Immunology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109.

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Complement protein 6 (C6) deficiency reduces innate immune responses, improving survival and decreasing organ damage in polymicrobial sepsis models. C6 knockout mice show attenuated cardiac dysfunction and lung injury.

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Area of Science:

  • Immunology
  • Sepsis Pathophysiology
  • Complement System

Background:

  • Polymicrobial sepsis triggers robust innate immune activation, releasing proinflammatory mediators and extracellular histones.
  • Extracellular histones are potent proinflammatory and prothrombotic factors contributing to sepsis severity.
  • The role of complement protein 6 (C6) in innate immune responses during sepsis is not fully understood.

Purpose of the Study:

  • To investigate the role of C6 in innate immune cell function during sepsis.
  • To evaluate the impact of C6 deficiency on sepsis outcomes, including survival and organ dysfunction.
  • To examine the effect of C6 knockout on NLRP3 inflammasome activation in immune cells.

Main Methods:

  • Generation and characterization of C6 knockout (C6-/-) mice.
  • Assessment of innate immune cell (PMNs, macrophages) function in C6-/- mice, including surface molecule expression, superoxide anion generation, reactive oxygen species, phagocytosis, and histone release.
  • Evaluation of NLRP3 inflammasome activation in C6-/- mice.
  • Induction of polymicrobial sepsis and LPS-induced acute lung injury in C6-/- and wild-type mice.
  • Measurement of plasma cytokine/chemokine levels, histone levels, cardiac function, and lung injury parameters.

Main Results:

  • C6-/- mice exhibited defective innate immune responses in polymorphonuclear neutrophils (PMNs), including impaired adhesion molecule expression, superoxide anion generation, reactive oxygen species production, histone release, and phagocytosis.
  • NLRP3 inflammasome activation was defective in both PMNs and macrophages of C6-/- mice.
  • C6-/- mice demonstrated significantly improved survival following polymicrobial sepsis, associated with reduced plasma levels of proinflammatory cytokines, chemokines, and extracellular histones.
  • Sepsis-induced cardiac dysfunction and LPS-induced acute lung injury (edema, hemorrhage) were attenuated in C6-/- mice, with reduced PMN infiltration in the lungs.

Conclusions:

  • C6 plays a critical role in mediating innate immune cell responses during sepsis.
  • Deficiency in C6 leads to dampened inflammatory responses, reduced extracellular histone levels, and consequently, less organ injury and improved survival in sepsis models.
  • Targeting C6 or its downstream pathways may represent a therapeutic strategy for mitigating sepsis-induced organ damage.