Apoptosis in cells of bronchoalveolar lavage

A cellular reaction in patients who die with sepsis and respiratory failure

C. Liacos, S. Katsaragakis, M. M. Konstadoulakis, Evangelos Messaris, M. Papanicolaou, G. G. Georgiadis, E. Menenakos, A. Vasiliadi-Chioti, G. Androulakis

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Objective: Apoptosis represents a physiologic clearance mechanism in human tissues. The role of apoptosis has not been examined in lung cell populations, such as alveolar macrophages of septic patients, an organ frequently insulted in these patients. This study was designed to examine the effect of sepsis on the apoptosis of alveolar macrophages.Design: Prospective study. Setting: Intensive care unit and surgical intensive care and trauma unit of a large university hospital in Athens, Greece. Patients: Bronchoalveolar lavage was obtained from 20 consecutive patients who met the criteria for sepsis, admitted to two intensive care units. Bronchoalveolar lavage was obtained from nine volunteers without lung disease who served as controls. Interventions: None. Measurements and Main Results: The specimens were analyzed by using annexin V binding, terminal deoxynucleotidyl transfer-mediated deoxyuridine 5-triphosphate nick end labeling (TUNEL), DNA laddering, light microscopy, and immunohistochemistry. Spontaneous apoptosis of bronchoalveolar lavage cells and particularly of alveolar macrophages was significantly decreased in septic patients compared with nonseptic controls. This finding was confirmed by using morphologic criteria and the TUNEL method. Furthermore, gel electrophoresis of DNA obtained from bronchoalveolar cells revealed that DNA fragmentation was not necessarily associated with apoptotic cell death. The bcl-2 gene was minimally expressed in the control group. An inverse correlation was found between the percentage of apoptotic alveolar macrophages and the severity of sepsis. Conclusions: The prolonged survival of lung cells in septic patients and especially of alveolar macrophages may be attributable to the inhibition of apoptosis. This seems to represent an initial attempt of the host to increase the defense capacity to kill the invading microorganism, resulting in an unbalanced tissue load of cells and an uncontrolled release of toxic metabolites. Furthermore, the inhibition of apoptosis in septic patients may explain why lung function is impaired, leading to sepsis-induced acute respiratory distress syndrome and death.

Original languageEnglish (US)
Pages (from-to)2310-2317
Number of pages8
JournalCritical Care Medicine
Volume29
Issue number12
DOIs
StatePublished - Jan 1 2001

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Bronchoalveolar Lavage
Respiratory Insufficiency
Sepsis
Alveolar Macrophages
Apoptosis
Intensive Care Units
Lung
bcl-2 Genes
Trauma Centers
Poisons
Annexin A5
Greece
DNA
Adult Respiratory Distress Syndrome
DNA Fragmentation
Critical Care
Lung Diseases
Electrophoresis
Volunteers
Microscopy

All Science Journal Classification (ASJC) codes

  • Critical Care and Intensive Care Medicine

Cite this

Liacos, C., Katsaragakis, S., Konstadoulakis, M. M., Messaris, E., Papanicolaou, M., Georgiadis, G. G., ... Androulakis, G. (2001). Apoptosis in cells of bronchoalveolar lavage: A cellular reaction in patients who die with sepsis and respiratory failure. Critical Care Medicine, 29(12), 2310-2317. https://doi.org/10.1097/00003246-200112000-00013
Liacos, C. ; Katsaragakis, S. ; Konstadoulakis, M. M. ; Messaris, Evangelos ; Papanicolaou, M. ; Georgiadis, G. G. ; Menenakos, E. ; Vasiliadi-Chioti, A. ; Androulakis, G. / Apoptosis in cells of bronchoalveolar lavage : A cellular reaction in patients who die with sepsis and respiratory failure. In: Critical Care Medicine. 2001 ; Vol. 29, No. 12. pp. 2310-2317.
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abstract = "Objective: Apoptosis represents a physiologic clearance mechanism in human tissues. The role of apoptosis has not been examined in lung cell populations, such as alveolar macrophages of septic patients, an organ frequently insulted in these patients. This study was designed to examine the effect of sepsis on the apoptosis of alveolar macrophages.Design: Prospective study. Setting: Intensive care unit and surgical intensive care and trauma unit of a large university hospital in Athens, Greece. Patients: Bronchoalveolar lavage was obtained from 20 consecutive patients who met the criteria for sepsis, admitted to two intensive care units. Bronchoalveolar lavage was obtained from nine volunteers without lung disease who served as controls. Interventions: None. Measurements and Main Results: The specimens were analyzed by using annexin V binding, terminal deoxynucleotidyl transfer-mediated deoxyuridine 5-triphosphate nick end labeling (TUNEL), DNA laddering, light microscopy, and immunohistochemistry. Spontaneous apoptosis of bronchoalveolar lavage cells and particularly of alveolar macrophages was significantly decreased in septic patients compared with nonseptic controls. This finding was confirmed by using morphologic criteria and the TUNEL method. Furthermore, gel electrophoresis of DNA obtained from bronchoalveolar cells revealed that DNA fragmentation was not necessarily associated with apoptotic cell death. The bcl-2 gene was minimally expressed in the control group. An inverse correlation was found between the percentage of apoptotic alveolar macrophages and the severity of sepsis. Conclusions: The prolonged survival of lung cells in septic patients and especially of alveolar macrophages may be attributable to the inhibition of apoptosis. This seems to represent an initial attempt of the host to increase the defense capacity to kill the invading microorganism, resulting in an unbalanced tissue load of cells and an uncontrolled release of toxic metabolites. Furthermore, the inhibition of apoptosis in septic patients may explain why lung function is impaired, leading to sepsis-induced acute respiratory distress syndrome and death.",
author = "C. Liacos and S. Katsaragakis and Konstadoulakis, {M. M.} and Evangelos Messaris and M. Papanicolaou and Georgiadis, {G. G.} and E. Menenakos and A. Vasiliadi-Chioti and G. Androulakis",
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Liacos, C, Katsaragakis, S, Konstadoulakis, MM, Messaris, E, Papanicolaou, M, Georgiadis, GG, Menenakos, E, Vasiliadi-Chioti, A & Androulakis, G 2001, 'Apoptosis in cells of bronchoalveolar lavage: A cellular reaction in patients who die with sepsis and respiratory failure', Critical Care Medicine, vol. 29, no. 12, pp. 2310-2317. https://doi.org/10.1097/00003246-200112000-00013

Apoptosis in cells of bronchoalveolar lavage : A cellular reaction in patients who die with sepsis and respiratory failure. / Liacos, C.; Katsaragakis, S.; Konstadoulakis, M. M.; Messaris, Evangelos; Papanicolaou, M.; Georgiadis, G. G.; Menenakos, E.; Vasiliadi-Chioti, A.; Androulakis, G.

In: Critical Care Medicine, Vol. 29, No. 12, 01.01.2001, p. 2310-2317.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Apoptosis in cells of bronchoalveolar lavage

T2 - A cellular reaction in patients who die with sepsis and respiratory failure

AU - Liacos, C.

AU - Katsaragakis, S.

AU - Konstadoulakis, M. M.

AU - Messaris, Evangelos

AU - Papanicolaou, M.

AU - Georgiadis, G. G.

AU - Menenakos, E.

AU - Vasiliadi-Chioti, A.

AU - Androulakis, G.

PY - 2001/1/1

Y1 - 2001/1/1

N2 - Objective: Apoptosis represents a physiologic clearance mechanism in human tissues. The role of apoptosis has not been examined in lung cell populations, such as alveolar macrophages of septic patients, an organ frequently insulted in these patients. This study was designed to examine the effect of sepsis on the apoptosis of alveolar macrophages.Design: Prospective study. Setting: Intensive care unit and surgical intensive care and trauma unit of a large university hospital in Athens, Greece. Patients: Bronchoalveolar lavage was obtained from 20 consecutive patients who met the criteria for sepsis, admitted to two intensive care units. Bronchoalveolar lavage was obtained from nine volunteers without lung disease who served as controls. Interventions: None. Measurements and Main Results: The specimens were analyzed by using annexin V binding, terminal deoxynucleotidyl transfer-mediated deoxyuridine 5-triphosphate nick end labeling (TUNEL), DNA laddering, light microscopy, and immunohistochemistry. Spontaneous apoptosis of bronchoalveolar lavage cells and particularly of alveolar macrophages was significantly decreased in septic patients compared with nonseptic controls. This finding was confirmed by using morphologic criteria and the TUNEL method. Furthermore, gel electrophoresis of DNA obtained from bronchoalveolar cells revealed that DNA fragmentation was not necessarily associated with apoptotic cell death. The bcl-2 gene was minimally expressed in the control group. An inverse correlation was found between the percentage of apoptotic alveolar macrophages and the severity of sepsis. Conclusions: The prolonged survival of lung cells in septic patients and especially of alveolar macrophages may be attributable to the inhibition of apoptosis. This seems to represent an initial attempt of the host to increase the defense capacity to kill the invading microorganism, resulting in an unbalanced tissue load of cells and an uncontrolled release of toxic metabolites. Furthermore, the inhibition of apoptosis in septic patients may explain why lung function is impaired, leading to sepsis-induced acute respiratory distress syndrome and death.

AB - Objective: Apoptosis represents a physiologic clearance mechanism in human tissues. The role of apoptosis has not been examined in lung cell populations, such as alveolar macrophages of septic patients, an organ frequently insulted in these patients. This study was designed to examine the effect of sepsis on the apoptosis of alveolar macrophages.Design: Prospective study. Setting: Intensive care unit and surgical intensive care and trauma unit of a large university hospital in Athens, Greece. Patients: Bronchoalveolar lavage was obtained from 20 consecutive patients who met the criteria for sepsis, admitted to two intensive care units. Bronchoalveolar lavage was obtained from nine volunteers without lung disease who served as controls. Interventions: None. Measurements and Main Results: The specimens were analyzed by using annexin V binding, terminal deoxynucleotidyl transfer-mediated deoxyuridine 5-triphosphate nick end labeling (TUNEL), DNA laddering, light microscopy, and immunohistochemistry. Spontaneous apoptosis of bronchoalveolar lavage cells and particularly of alveolar macrophages was significantly decreased in septic patients compared with nonseptic controls. This finding was confirmed by using morphologic criteria and the TUNEL method. Furthermore, gel electrophoresis of DNA obtained from bronchoalveolar cells revealed that DNA fragmentation was not necessarily associated with apoptotic cell death. The bcl-2 gene was minimally expressed in the control group. An inverse correlation was found between the percentage of apoptotic alveolar macrophages and the severity of sepsis. Conclusions: The prolonged survival of lung cells in septic patients and especially of alveolar macrophages may be attributable to the inhibition of apoptosis. This seems to represent an initial attempt of the host to increase the defense capacity to kill the invading microorganism, resulting in an unbalanced tissue load of cells and an uncontrolled release of toxic metabolites. Furthermore, the inhibition of apoptosis in septic patients may explain why lung function is impaired, leading to sepsis-induced acute respiratory distress syndrome and death.

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