TY - JOUR
T1 - Mycobacterium tuberculosis catalase inhibits the formation of mast cell extracellular traps
AU - Campillo-Navarro, Marcia
AU - Leyva-Paredes, Kahiry
AU - Donis-Maturano, Luis
AU - Rodríguez-López, Gloria M.
AU - Soria-Castro, Rodolfo
AU - García-Pérez, Blanca Estela
AU - Puebla-Osorio, Nahum
AU - Ullrich, Stephen E.
AU - Luna-Herrera, Julieta
AU - Flores-Romo, Leopoldo
AU - Sumano-López, Héctor
AU - Pérez-Tapia, Sonia M.
AU - Estrada-Parra, Sergio
AU - Estrada-García, Iris
AU - Chacón-Salinas, Rommel
N1 - Publisher Copyright:
© 2018 Campillo-Navarro, Leyva-Paredes, Donis-Maturano, Rodríguez-López, Soria-Castro, García-Pérez, Puebla-Osorio, Ullrich, Luna-Herrera, Flores-Romo, Sumano-López, Pérez-Tapia, Estrada-Parra, Estrada-García and Chacón-Salinas.
PY - 2018/5/28
Y1 - 2018/5/28
N2 - Tuberculosis is one of the leading causes of human morbidity and mortality. Mycobacterium tuberculosis (Mtb) employs different strategies to evade and counterattack immune responses persisting for years. Mast cells are crucial during innate immune responses and help clear infections via inflammation or by direct antibacterial activity through extracellular traps (MCETs). Whether Mtb induce MCETs production is unknown. In this study, we report that viable Mtb did not induce DNA release by mast cells, but heat-killed Mtb (HK-Mtb) did. DNA released by mast cells after stimulation with HK-Mtb was complexed with histone and tryptase. MCETs induced with PMA and HK-Mtb were unable to kill live Mtb bacilli. Mast cells stimulated with HK-Mtb induced hydrogen peroxide production, whereas cells stimulated with viable Mtb did not. Moreover, MCETs induction by HK-Mtb was dependent of NADPH oxidase activity, because its blockade resulted in a diminished DNA release by mast cells. Interestingly, catalase-deficient Mtb induced a significant production of hydrogen peroxide and DNA release by mast cells, indicating that catalase produced by Mtb prevents MCETs release by degrading hydrogen peroxide. Our findings show a new strategy employed by Mtb to overcome the immune response through inhibiting MCETs formation, which could be relevant during early stages of infection.
AB - Tuberculosis is one of the leading causes of human morbidity and mortality. Mycobacterium tuberculosis (Mtb) employs different strategies to evade and counterattack immune responses persisting for years. Mast cells are crucial during innate immune responses and help clear infections via inflammation or by direct antibacterial activity through extracellular traps (MCETs). Whether Mtb induce MCETs production is unknown. In this study, we report that viable Mtb did not induce DNA release by mast cells, but heat-killed Mtb (HK-Mtb) did. DNA released by mast cells after stimulation with HK-Mtb was complexed with histone and tryptase. MCETs induced with PMA and HK-Mtb were unable to kill live Mtb bacilli. Mast cells stimulated with HK-Mtb induced hydrogen peroxide production, whereas cells stimulated with viable Mtb did not. Moreover, MCETs induction by HK-Mtb was dependent of NADPH oxidase activity, because its blockade resulted in a diminished DNA release by mast cells. Interestingly, catalase-deficient Mtb induced a significant production of hydrogen peroxide and DNA release by mast cells, indicating that catalase produced by Mtb prevents MCETs release by degrading hydrogen peroxide. Our findings show a new strategy employed by Mtb to overcome the immune response through inhibiting MCETs formation, which could be relevant during early stages of infection.
KW - Catalase
KW - Mast cell
KW - Mast cell extracellular trap
KW - Mycobacterium tuberculosis
KW - Tuberculosis
UR - http://www.scopus.com/inward/record.url?scp=85047667246&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85047667246&partnerID=8YFLogxK
U2 - 10.3389/fimmu.2018.01161
DO - 10.3389/fimmu.2018.01161
M3 - Article
C2 - 29892297
AN - SCOPUS:85047667246
SN - 1664-3224
VL - 9
JO - Frontiers in immunology
JF - Frontiers in immunology
IS - MAY
M1 - 1161
ER -