Stressed (acute) mice display neuroimmunodysregulation and defective innate immune response against coliform infection

摘要

We examined the impact of acute restraint stress (ARS) with( out) intraperitoneal E. coil infection on TLR4 mRNA abundance in brain and spleen, clinical signs, cytokines and oxidative loads and peritoneal E. coil growth in balb/c mice. ARS exacerbated E. coil virulence and behavioral abnormality. At different post-stress hour the pattern and intensity of TLR4 activity differed in brain and spleen. While TLR4 stimulation in spleen of E. coil-infected mice was maximal, it superseded in brain of post-stressed E. con-infected mice. ARS and E. coil infection elicited systemic pro-inflammatory and pro-oxidant status, with defective peritoneal E. coil clearance in post-ARS mice. Continuous TLR4 activation in post-stressed mice partially disarms innate immune response, and contributes to inappropriate host-E. coil interactions and thus neuroimmune dysregulation/toxicity. The description of these observed novel effects induced by ARS will provide a basis for deeper investigations of the effects from increasingly stress-oriented rural/urban life upon neuroimmune system. (C) 2015 Elsevier B.V. All rights reserved.