[Cigarette smoking results in the number of CD8+Fas Ligand+ T cytotoxic lymphocytes in bronchoalveolar lavage (BAL) fluid of patients with idiopathic pulmonary fibrosis (IPF)].
Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease with unfavourable outcome. Tobacco consumption in IPF exacerbates the clinical manifestations and limits the time of patient survival. The cyto-immunological alterations caused by smoking in IPF patients need particular explanation. BAL was carried out in 21 non-treated patients with IPF, subdivided according to the smoking status (n=7 for smokers). BAL routine cytology was completed by; immunotyping, including T cell major subsets (CD4 and CD8) stained for Fas, Fas ligand (FasL) and TNFR-1, late apoptosis/cell cycle analyses (BAL cells were permeabilized and stained with PI) and TUNEL assay. BAL cytology in IPF, as compared with control group, was characterized by significantly higher total cell and macrophage number, increased lymphocyte, neutrophile and eosinophile percentage and relatively low CD4/CD8 ratio. Cigarette smoking in IPF resulted in enhanced BAL lymphocyte CD8 cell percentage and number, as compared with nonsmoking subgroup and further decline in CD4/CD8 ratio (0.41+/-0.15 vs 1.23+/-0.29 in nonsmokers, median +/- SEM, p<0.05). The percentage of CD8, but not CD4 cells carrying Fas Ligand was significantly increased in IPF smokers (12.0+/-3.1% vs 3.7+/-0.9% in nonsmokers, median +/- SEM, p<0.05). Apoptosis rate of BAL macrophages and lymphocytes was enhanced in IPF, as compared with controls (confirmed by both techniques), but without remarkable changes, if compared one IPF subgroup to another. The number and percentage of CD8+FasL+ was negatively correlated with vital capacity (VC) values in IPF patients, but not with BAL inflammatory cell apoptosis rate. Cigarette smoking enhanced a percentage as well as a total number of both BAL CD8 and BAL CD8+FasL+ cells in IPF patients. BAL cytotoxic cells (CD8+FasL+ lymphocytes) seem to have impact on impaired lung function in smoking IPF patients.
Kopiński
Piotr
P
Katedra Terapii Genowej, Collegium Medicum Uniwersytetu Mikołaja Kopemika w Bydgoszczy. kizgenoter@cm.umk.pl
Przybylski
Grzegorz
G
Balicka-Slusarczyk
Barbara
B
Chorostowska-Wynimko
Joanna
J
Pinis
Grazyna
G
Plato
Marta
M
Rozy
Adriana
A
Szczeklik
Jerzy
J
D000328:Adult; D017209:Apoptosis; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000276:immunology*; D016827:CD8 Antigens; D053222:Fas Ligand Protein; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011658:Pulmonary Fibrosis / Q000276:immunology*; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis; D012907:Smoking / Q000276:immunology* / Q000473:pathology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology / Q000473:pathology*
D016827:CD8 Antigens; D053222:Fas Ligand Protein; D018124:Receptors, Tumor Necrosis Factor