34 Phagocyte collaboration for the control of Pseudomonas aeruginosa

• Published in: Journal of cystic fibrosis 2015-06, Vol.14, p.S65-S65
• Main Authors: Muntaka, S, Asante, A, Cámara, M, Martínez-Pomares, L
• Format: Article
• Language: English
• Subjects: Pulmonary/Respiratory
• ISSN: 1569-1993; 1873-5010
• DOI: 10.1016/S1569-1993(15)30211-3

Pseudomonas aeruginosa (PA) is an opportunistic pathogen that causes infections in patients with compromised immunity. Several previous studies are animal based, but we have established a human neutrophil/macrophage PA infection model to investigate phagocyte collaboration in PA control. Objective i. to investigate the ability of human macrophage-neutrophil co-cultures to control Pseudomonas growth, promote inflammation and cause tissue damage, and ii. to determine how the presence of pro-inflammatory cytokines such as IFN-γ and IL-17A affect the outcome of the infection of macrophage-neutrophils co-cultures with PA. Methods A robust procedure has been established where, neutrophils or macrophages or both are infected with PA with or without cytokines under opsonic and or non-opsonic conditions, and the samples analysed for bacterial colony forming units (CFU) or Flow cytometry. Results The findings so far indicate: 1. macrophages have a minor effect on the control of PA but coordinate the immune response to PA infection; 2. phagocytosis of PA by neutrophils under non-opsonic conditions depends on cell density; 3. as expected, serum enhances neutrophil-mediated killing of PA; 4. IL-17A enhances neutrophil-mediated killing of PA under opsonic conditions and 5. neutrophils synergise with macrophages in clearing PA infection. Conclusion 1. Macrophages coordinate the immune response to PA by producing a number of cytokines. 2. Neutrophil control of PA infection is enhanced by human complement. 3. The cytokine IL-17A enhances the ability of human neutrophils to control PA infection. 4. Neutrophils and macrophages collaborate in clearing PA infections.