Abstract
Background: Although immune cells, such as mast cell, is suggested to play a critical role in the pathogenesis of malignant pleural effusion (MPE), the role and underlying mechanism of non-classical in MPE has yet to be fully elucidated.
Objectives: To compare the distribution and phenotype of monocytes in MPE with transudate pleural effusion. To elucidate the possible role of inflammatory cytokines in non-classical monocytes in the pathogenesis of MPE.
Methods: Monocytes and its phenotype in both pleural effusion and blood was counted by flow cytometry. The express level of chemokines receptors and inflammatory cytokines in non-classical monocytes was detected by PCR and ELISA. The role of IL-1βin the proliferation, apoptosis, invasion, adhesion and EMT of A549 cells was measured by WB, flow cytometry, and wound healing test.
Measurements and Main Results: Human non-classical monocyte compartment was increased in MPE, compared to transudate pleural effusion patients. MPE expressed high level of chemokines (CCL2 and CX3CL1) and cytokines IL-1β. Non-classical monocytes isolated from MPE expressed high levels of CCR2, CX3CR1 and IL-1βcompared to classical monocytes. Recruitment of non-classical monocytes into MPE regulated by PMCs could suffer as a result of anti-CCL2 and anti-CX3CL1 mAbs. IL-1βpromote the pathogenesis of MPE by inducing the proliferation, immigration, invasion, and EMT, and inhibiting the apoptosis and adhesion of A549 cells, while utilizing IL-1RA weaken these effects.
Conclusions: Non-classical monocytes accumulates in the pleural cavity and promote the formation of MPE by secretion abundant IL-1β.
Footnotes
Cite this article as: European Respiratory Journal 2019; 54: Suppl. 63, PA3664.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2019