Human mesenchymal stem cells protect neutrophils from serum-deprived cell death

Maryam Maqbool1, Sharmili Vidyadaran, Elizabeth George

  • 1Immunology Laboratory, Department of Pathology, Universiti Putra Malaysia, Selangor, Malaysia.

Insights

Human mesenchymal stem cells (MSC) protect neutrophils from programmed cell death, especially in low-serum conditions. This finding highlights MSC

Area of Science:

  • Immunology
  • Cell Biology
  • Regenerative Medicine

Background:

  • Human mesenchymal stem cells (MSC) are known to inhibit the proliferation of many immune cells.
  • Neutrophils and other polymorphonuclear (PMN) cells are innate immune cells with effector functions not reliant on extensive proliferation.
  • The immunomodulatory effects of MSC on neutrophils, particularly under nutrient-limited conditions, remain less understood.

Purpose of the Study:

  • To investigate the impact of MSC on neutrophil viability and programmed cell death (PCD).
  • To assess MSC effects on neutrophils cultured in varying concentrations of fetal bovine serum (FBS).
  • To determine if MSC can rescue neutrophils from serum-deprived or nutrient-deprived cell death.

Main Methods:

  • Neutrophils were co-cultured with MSC in media with different FBS concentrations (0%, 1%, 5%, 10%).
  • Neutrophil viability was assessed after 24 hours of incubation.
  • Annexin V and propidium iodide (PI) staining were used to quantify apoptosis and necrosis, indicative of PCD.

Main Results:

  • MSC significantly increased neutrophil viability in the presence of 1%, 5%, and 10% FBS.
  • MSC treatment reduced the rate of programmed cell death (apoptosis) in neutrophils.
  • The proportion of viable neutrophils increased, while the proportion of dead cells decreased with MSC co-culture.

Conclusions:

  • Mesenchymal stem cells (MSC) demonstrate a protective effect on neutrophils against serum-deprived cell death.
  • MSC enhance neutrophil viability, likely by reducing apoptosis under nutrient-limited conditions.
  • Further research is needed to elucidate the specific signaling pathways or mechanisms involved in this MSC-mediated neutrophil rescue.

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