RT Journal Article
SR Electronic
T1 Alveolar lymphocyte phenotype and respiratory distress syndrome
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP p4587
VO 38
IS Suppl 55
A1 Karine Risso
A1 Céline Sanfiorenzo
A1 Gaurav Kumar
A1 Francine de Salvador-Guillouet
A1 Alain Bernard
A1 Gilles Bernardin
A1 Pierre-Marie Roger
YR 2011
UL http://erj.ersjournals.com/content/38/Suppl_55/p4587.abstract
AB Introduction: The role played by adaptive immunity in the physiopathology of acute lung injury (ALI) and acute respiratory distress syndromes (ARDS) is largely unknown. We characterized lymphocytes phenotype in broncho-alveolar lavage (BAL) during respiratory distress syndromes.Patients and method: Analyses were carried out on BAL samples of three patients groups: ALI/ARDS patients (ARDS group), healthy patients (control group) and inflammatory pulmonary diseases patients (ID group). Lymphocyte and monocyte/macrophage phenotype determination used cytofluorometric technics. CD45RA+, CD45RA- and CD25FoxP3+ cells were respectively identified as naïve, memory and regulatory T cells. HLADR, KI67 and annexin V were used as markers for cell activation, proliferation and apoptosis respectively. CD4, CD8, CD80, CD86, CD28, CD40/CD40L and CTLA-4 were used as costimulatory cell markers.Results: 9 BAL were obtained from 8 ARDS patients, 8 BAL from 8 controls and 8 from ID patients. A significant increase of HLADR, KI67 and CTLA-4 on T CD4+ lymphocytes was observed in ARDS group compared to control. Concerning CTLA-4, the difference still persisted when comparing ID to ARDS group. KI67 expression was significantly increased on T CD8 T. HLA-DR and CD86 were significantly decreased on alveolar macrophages (AM) compared to others groups.Discussion: During ALI/ARDS activation and proliferation of T lymphocyte are noticeable, associated with alteration of the CD28/CTLA-4 costimulatory pathway and its ligand on AM.Conclusion: This is the first human study on adaptive immunity in ARDS/ALI identifying relevant modifications on T cell phenotype which may account for the dramatic alveolar inflammation observed in these syndromes.