Interleukin 4 induces the apoptosis of mouse microglial cells by a 2 caspase-dependent mechanism

JAVIER A. SORIA; DANIELA S. ARROYO; EMILIA A. GAVIGLIO; MARIA CECILIA RODRIGUEZ GALAN; JI MING WANG; PABLO IRIBARREN

ACADEMIC PRESS INC ELSEVIER SCIENCE

Año: 2011 vol. 43 p. 616 - 616

Microglial cells are resident macrophages in the central nervous system (CNS) and become activated in manypathological conditions. Activation of microglial cells results in reactive microgliosis, manifested by anincrease in cell number in the affected CNS regions. The control of microgliosis may be important to preventpathological damage to the brain. The type 2 cytokine IL-4 has been reported to be protective in braininflammation. However, its effect on microglial cell survival was not well understood. In this study, we reporta dual effect of IL-4 on the survival of mouse microglial cells. In a 6 h short term culture, IL-4 reduced the deathof microglial cells induced by staurosporine. In contrast, in long term treatment (more than 48 h), IL-4increased the apoptotic death of both primary mouse microglial cells and a microglial cell line N9. Mechanisticstudies revealed that, in microglial cells, IL-4 increased the levels of cleaved cas