Odor Signals of Immune Activation and CNS Inflammation
Final rept. 15 Sep 2012-14 Dec 2014
MONELL CHEMICAL SENSES CENTER PHILADELPHIA PA
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We hypothesized that inflammation results in detectable alteration of body odor and that traumatic brain injury TBI might similarly produce volatile metabolites specific to injury. Using an animal model, we first trained biosensor mice to distinguish between urine odors from lipopolysaccharide-treated and control mice. Lipopolysaccharide LPS is a general elicitor of inflammation. Trained biosensors could distinguish between the odors of LPS-treated and control mouse urine. Chemical analyses further demonstrated that LPS-induced inflammation results in alteration of urine volatiles. Importantly, urine samples collected many days following LPS-administration were discriminable. Thus, odor differences were not produced by acute effects of LPS-treatment e.g. dehydration nor were they likely related to changes in cytokines which typically occur within hours of LPS exposure and return to normal within 24 hours. We similarly demonstrated odor alteration due to treatment with LPS in humans. Urine samples collected from humans receiving a small dose of LPS or control were subjected to discrimination tasks by a human sensory panel as well as chemical analyses. Both assays suggested that treatment with LPS results in a detectable alteration of urine volatiles. Odor changes resulting from TBI were also evaluated using an animal model. Because both LPS and TBI elicit inflammatory processes and LPS-induced inflammation induces body odor changes, we hypothesized that 1 TBI would induce a distinct change in body odor and 2 this change would resemble the change induced by LPS. Mice receiving surgery and lateral fluid percussion injury LFPI or surgery without brain injury were employed as urine donors. Biosensors trained to discriminate LPS-treated mouse odors from control odors did not generalize this learned response to LFPI TBI urine.
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