@entity1981 ( @entity1981 ) is considered as a major etiological factor in the pathogenesis of @entity1030 . In this study we used A549 cells and THP-1 cells grown for 24 h in monoculture or in co-culture in @entity1981 -conditioned media and changes in their proliferation, viability, acetylated histone H3 levels and expression of extracellular antigens @entity5750 , HLA-DR, @entity1453 , and @entity9536 were assessed. @entity1981 was highly toxic to A549 cells but not to @entity1357 cells. In A549 cells, oxidative stress reached the highest values after 1 h of @entity1981 exposure and then decreased. In @entity1357 cells oxidative stress was lower and increased progressively with time. @entity1981 decreased proliferation of A549 and @entity1357 cells by about 80% and 21%, respectively. @entity1981 did not alter acetylated histone H3 levels in A549 cells, while in @entity1357 cells the levels were reduced by about 35%. @entity1981 significantly increased expression of @entity5750 , HLA-DR, @entity1453 , and @entity9536 in @entity1357 cells. In co-culture, na  ve or @entity1981 -pretreated @entity1357 cells significantly protected A549 cells against @entity1981 @entity137 but had higher death rates. These results show that epithelial cells are more fragile to @entity1981 than monocytes and that @entity1981 -activated monocytes may protect epithelial cells against @entity1981 -induced @entity137 .

Crosstalk Between Co-cultured A549 Cells and XXXX Cells Exposed to Cigarette Smoke.

@entity1357 :: ('2736', 'Gene') :: ['THP1'] @entity137 :: ('MESH:D064420', 'Disease') :: ['toxicity', 'cytotoxicity'] @entity5750 :: ('929', 'Gene') :: ['CD14'] @entity1030 :: ('MESH:D029424', 'Disease') :: ['chronic obstructive pulmonary disease'] @entity1453 :: ('3683', 'Gene') :: ['CD11a'] @entity9536 :: ('3684', 'Gene') :: ['CD11b'] @entity1981 :: ('OMIM:188890', 'Disease') :: ['Cigarette smoke', 'CS']
@entity1357 :: (2736,Gene) :: ['THP1']
