Interaction Between the Central Nervous System and Immune System

Pneumonia is a common complication after experiencing a stroke with reports of 7-22% incidence in patients and accounts for 10% of stroke-related deaths. The literature suggests that injury to the CNS (like stroke) hinders the body’s ability to defend itself against bacterial assault. More specifically, it’s been observed that lymphocyte apoptosis and altered lymphocytic cytokine production result in impaired cellular immunity before stroke patients show symptoms of pneumonia.

A recent Science paper found that phenotypic changes in the invariant NK T (iNKT) cell population after stroke were responsible for the susceptibility to bacterial infection in mice. The iNKT cells produced high levels of IL10, which suppresses the Th1 response and shifts the immune system to a Th2-type response. They also found that blocking a noradrenergic neurotransmitter via administration of propranolol brought the iNKT cells back to an INF-gamma Th1 dominated phenotype and prevented bacterial infections after stroke. They suggest the use of alpha-galactosylceramide to activate invariant iNKT cells and increase production of IFN-gamma for immunomodulatory therapy instead of using antibiotics to reduce bacterial infection in stroke patients.

I thought these results provided a fascinating story on the cross talk between the CNS and the immune system as well as an interesting alternative to antibiotic treatment.

References:

Wong CHY, Jenne CN, Lee W-Y, Leger C, Kubes P (2011). Functional Innervation of Hepatic iNKT Cells is Immunosuppressive Following Stroke. Science; 334: 101-105.

Meisel C, Meisel A (2011) Suppressing Immunosuppression after Stroke. NEJM; 365(22): 2134-2136.

Hassan A, Khealani BA, Shafqat S, Aslam M, Salahuddin N, Syed NA, Baig SM, Wasay M (2006). Stroke-associated Pneumonia: Microbiological Data and Outcome. Singapore Med J; 47(3): 204-207