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

• We tested the effect of acute stress on key innate immune response in murine in vivo.
• Acute stress causes pro-oxidant and pro-inflammatory microenvironment.
• Acute stress dysregulates proper innate immunity.
• Post-stress mice show weaker clearance of microbial infection.
• This study gives a clue on stress-mediated immunoneurodegenerative diseases.

We examined the impact of acute restraint stress (ARS) with(out) intraperitoneal E. coli infection on TLR4 mRNA abundance in brain and spleen, clinical signs, cytokines and oxidative loads and peritoneal E. coli growth in balb/c mice. ARS exacerbated E. coli 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 While TLR4 stimulation in spleen of E. coli-infected mice was maximal, it superseded in brain of post-stressed E. coli-infected mice. ARS and E. coli infection elicited systemic pro-inflammatory and pro-oxidant status, with defective peritoneal E. coli clearance in post-ARS mice. Continuous TLR4 activation in post-stressed mice partially disarms innate immune response, and contributes to inappropriate host–E. coli 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.