A recent study led by researchers at the Monell Chemical Sense Center delves into the intricate relationship between taste perception and the immune system, shedding light on the mechanisms involved in the complex interplay between taste perception and immune function. Published in iScience, the research not only uncovers these mechanisms but also highlights the potential of single-cell sequencing assay for transposase-accessible chromatin (scATAC-seq) for investigating epigenetic mechanisms that affect taste-cell gene expression.
Bitter taste is often associated with illnesses, causing loss of appetite and influencing patients' medication compliance. Bitter receptors, encoded by Tas2r genes, serve as a defense against oral and gut pathogens, but the process remains poorly understood.
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Using lipopolysaccharide (LPS) to induce inflammation akin to bacterial infections, the study demonstrated that mice exhibited a heightened aversion to bitter tastes, confirming the change originates in taste buds rather than the brain. This finding has implications for behavioral aspects of illness, such as appetite loss, even impacting preferences for sugary treats. Mice, like humans, show reduced preference for sweetness during illness.
Examining gene expression mechanisms underlying the bitter response, the team employed various analysis methods. Real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR) revealed heightened response across Tas2r taste-receptor genes during sickness periods. Additionally, using scATAC-seq, the researchers showed that LPS-induced inflammation increased the accessibility of many Tas2r genes, suggesting an epigenetic mechanism.
Moreover, the study highlighted how LPS-induced inflammation globally affected gene expression in taste stem cells, potentially leaving an epigenetic memory that influences future responses to infections. This insight into taste response alterations has implications for cancer treatments and chronic illnesses that lead to a lasting bitter taste.