CD54 EXPRESSION IN CALU-6 IS DIFFERENTIALLY MODULATED BY HUMAN MACROPHAGES STIMULATED WITH OUTBREAK MDR STRAINS OF Mycobacterium tuberculosis

D KVIATCOVSKY; L BALBOA; P. SCHIERLOH; B.LOPEZ; MC SASIAIN; S. DE LA BARRERA

Congreso; LXI Reunion anual de la SAI; 2013

Mycobacterium tuberculosis (Mtb) which causes human and animal tuberculosis (TB) mainly infects the lung by interacting with airway epithelium and resident macrophages (Mac). The bronchial epithelium secretes cytokines (CKS) and chemokines upon interaction with Mtb or after interaction with infected resident Mac. As we have previously demonstrated that the outbreak multidrug-resistant strains of Mtb, M and Ra differentially modulate in vitro innate and adaptative immune response in humans, the aim of the present work was to evaluate the modulation of different pattern recognition receptors, adhesion and antigen presenting molecules in the bronchial cell line Calu-6. For this purpose, they were stimulated for 6 h with a) M, Ra and H37Rv strains (Mtb:Calu-6 ratio 10:1), b) Mac isolated from healthy donors (upon informed consent) and stimulated with Mtb (24 h, Mtb: Mac ratio 2:1 and 5.1) or c) supernatants from Mtb-stimulated Mac. Then CD11b, TLR2, Dectin-1, HLA-DR and CD54 expression was evaluated by flow cytometry. Results are expressed as median fluorescence intensity (MFI). Results: a) No modulation of CD11b, TLR2, dectin-1 or CD54 was observed by direct recognition, independent of the strain employed (n=8); this fact could be due to the low Mtb adhesion to Calu-6 (minor to 2 per cent); b) H37Rv and Ra-stimulated Mac enhanced CD54 MFI (p