interleukin-8 and Pleural-Diseases

The mechanisms underlying pleural inflammation and pleurodesis are poorly understood. We hypothesized that the cytokines transforming growth factor β (TGFβ1) and vascular endothelial growth factor (VEGF) play a major role in pleurodesis after intrapleural silver nitrate (SN) injection.. Forty rabbits received intrapleurally 0.5% SN alone or 0.5% SN + anti-TGFβ1, anti-IL-8, or anti-VEGF. After 28 days, the animals were euthanized and macroscopic pleural adhesions, microscopic pleural fibrosis, and collagen deposition were analyzed for characterization of the degree of pleurodesis (scores 0-4).. Scores of pleural adhesions, pleural fibrosis, total collagen, and thin collagen fibers deposition after 28 days were significantly lower for 0.5% SN + anti-TGFβ1 and 0.5% SN + anti-VEGF. Significant correlations were found between macroscopic adhesion and microscopic pleural fibrosis with total collagen and thin collagen fibers.. We conclude that both TGFβ1 and VEGF, but not IL-8, mediate the pleural inflammatory response and pleurodesis induced by SN.

Topics: Animals; Antibodies, Monoclonal; Fibrosis; Inflammation; Inflammation Mediators; Interleukin-8; Pleura; Pleural Diseases; Pleurodesis; Rabbits; Silver Nitrate; Tissue Adhesions; Transforming Growth Factor beta1; Vascular Endothelial Growth Factor A

In order to investigate the role of eotaxin in pleural diseases, we measured eotaxin in pleural effusions and studied the relationship between eotaxin levels and recruitment of inflammatory cells, particularly eosinophils. Interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) levels were also measured for comparison.. We evaluated 47 pleural effusion samples, 7 transudates and 40 exudates. The exudates consisted of 19 malignant, 11 tuberculous, and 5 parapneumonic effusions, and 5 effusions of other etiologies. Chemokine levels were measured by specific sandwich enzyme-linked immunosorbent assays.. Eotaxin was detected in all samples examined, but the levels did not differ significantly among the exudates. There was no significant correlation between the levels of eotaxin and MCP-1 or IL-8. The level of eotaxin but not the others was significantly higher in eosinophilic effusions (>10% eosinophils among white blood cells in the fluid) than in non-eosinophilic fluids. The number of eosinophils in pleural effusions was significantly correlated with the eotaxin levels, but not with the levels of other chemokines. The number of neutrophils was significantly correlated with IL-8 but not with the others.. Results suggest that eotaxin contributes to the migration of eosinophils in pleural inflammation. Taken together with the correlation between IL-8 and neutrophils, it appears that the predominant type of pleural inflammatory infiltrate is controlled, at least in part, by the subgroup of chemokines expressed in the pleural space.

Topics: Chemokine CCL11; Chemokine CCL2; Chemokines; Chemokines, CC; Chemotactic Factors, Eosinophil; Cytokines; Eosinophils; Humans; Interleukin-8; Monocytes; Pleural Diseases; Pleural Effusion