Smoking tobacco takes a heavy toll on the immune system --a toll that can be documented by PET scans with a radiopharmaceutical based on carbon-11, according to research presented at this week's Society of Nuclear Medicine and Molecular Imaging (SNMMI) meeting in Anaheim, CA.
Tobacco smoking is a leading cause of preventable death and can have complex effects on immune signaling. Nicotine suppresses the immune system, but other compounds in tobacco smoke can cause inflammation, according to a release issued by SNMMI.
Impaired signaling in the neuroimmune system can lead to compulsive drug use, so researchers from Yale University decided to use PET to examine neuroimmune responses between tobacco smokers and nonsmokers using a radiotracer called carbon-11 (C-11) PBR28.
Found on the outer mitochondrial membrane, peripheral benzodiazepine receptor (PBR) is overexpressed on some cancer cells and during inflammation. C-11 PBR28 targets and binds to cells expressing PBR, also known as 18 kDa translocator protein (TSPO), making it possible to use PET to detect inflammatory sites and cancer.
The research team, led by Ansel Hillmer, PhD, acquired baseline PET scans with C-11 PBR28 in 16 smokers and 19 nonsmokers. Next, a subset of eight smokers and nine nonsmokers received a second scan three hours after administration of lipopolysaccharide (LPS), a pro-inflammatory stimulus.
The team noted no significant differences between the smokers and nonsmokers with the baseline PET scans. But in the second set of scans, smokers had a much lower response to LPS compared with nonsmokers in some regions of the brain, like the striatum and cortex.
Hillmer and colleagues believe the preliminary results of this study indicate that tobacco smokers could have impaired neuroimmune function, compared with nonsmokers. The researchers hope to show how restoring the immune system could help smokers quit by improving cognitive function.
