PMN apoptosis and its relationship with the lung injury after chest impact trauma

Ren Liu1, Shuang-ding Li, Jia-xin Min

  • 1Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China. liu0916@mail.china.com

Abstract

Insights

Delayed polymorphonuclear neutrophil (PMN) apoptosis after chest trauma contributes to lung injury. This PMN dysfunction, potentially driven by increased intracellular calcium, exacerbates inflammation and tissue damage.

Area of Science:

  • Immunology
  • Trauma Research
  • Cell Biology

Background:

  • Polymorphonuclear neutrophils (PMNs) are key inflammatory cells involved in all phases of inflammation.
  • Chest impact trauma can lead to significant inflammatory responses and tissue damage.

Purpose of the Study:

  • To investigate the relationship between PMN apoptosis and lung injury following chest impact trauma.
  • To understand the role of PMN behavior in the inflammatory process post-trauma.

Main Methods:

  • PMNs were isolated from rabbits experiencing chest impact trauma.
  • Apoptosis, necrosis, survival, and respiratory burst of PMNs were analyzed using flow cytometry.
  • Lactate dehydrogenase (LDH) levels and intracellular calcium ([Ca2+]i) were measured.

Main Results:

  • Delayed PMN apoptosis and increased viable cells were observed between 2 and 12 hours post-trauma.
  • PMN respiratory burst activity significantly increased from 2 hours, peaking at 8 hours.
  • Elevated LDH and transient increases in intracellular free Ca2+ in PMNs were noted post-trauma.

Conclusions:

  • Impaired PMN apoptosis and retention in tissues lead to sustained PMN activation and release of damaging substances.
  • The observed increase in intracellular free Ca2+ may be a key factor in the delayed PMN apoptosis.
  • These findings highlight PMN apoptosis as a critical determinant of lung injury severity after chest trauma.

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