204 Cellular Immune Response After Hypoxic Ischemic Brain Injury in Neonatal Mice Persists for Months

Abstract

Background and aims: Hypoxic ischemia (HI) induces inflammation in the brain which can aggravate the damage. Immune cell infiltration into brain after hypoxic ischemia has previously been studied, but the timing and temporal interaction of these cells in the immature brain have not been investigated in detail before. Our aim was therefore to characterize the innate and adaptive (specific) immune response after HI. Methods: Using FACS and immunohistochemistry, innate (microglia, dendritic monocytes and neutrophils) and adaptive (B and T) cells in the brain parenchyma and spleen after brain injury were investigated. We used the Vannucci model to induce HI by unilateral electrocoagulation of the common carotid artery and subsequent hypoxia (10% O₂ for 60 min) in 10-day-old mice. We used a number of activation, innate and adaptive cell markers at 24, 48, 72h, 1, 2 weeks and 3 months after the insult.

Results: Activation of the innate immune cells was mainly seen up to one week after HI in the damaged brain hemisphere and in the spleen. However, in the spleen, a long term activation of CD11b+cells was also found. The adaptive (specific) immune response was activated mainly at later timepoints (72 hrs up to 3 months after HI) both in the brain and in the spleen.

Conclusions: The adaptive immune response sustained for months after brain ischemia. The functional consequences of this activation need to be studied further, but detrimental autoimmune effects or protective neuromodulation are two possible suggestions.

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