Lipopolysaccharide-induced inflammation attenuates taste progenitor cell proliferation and shortens the life span of taste bud cells

Abstract

BackgroundThe mammalian taste bud, a complex collection of taste sensory cells, supporting cells, and immature basal cells, is the structural unit for detecting taste stimuli in the oral cavity. Even though the cells of the taste bud undergo constant turnover, the structural homeostasis of the bud is maintained by balancing cell proliferation and cell death. Compared with nongustatory lingual epithelial cells, taste cells express higher levels of several inflammatory receptors and signalling proteins. Whether inflammation, an underlying condition in some diseases associated with taste disorders, interferes with taste cell renewal and turnover is unknown. Here we report the effects of lipopolysaccharide (LPS)-induced inflammation on taste progenitor cell proliferation and taste bud cell turnover in mouse taste tissues.ResultsIntraperitoneal injection of LPS rapidly induced expression of several inflammatory cytokines, including tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6, in mouse circumvallate and foliate papillae. TNF-α and IFN-γ immunoreactivities were preferentially localized to subsets of cells in taste buds. LPS-induced inflammation significantly reduced the number of 5-bromo-2'-deoxyuridine (BrdU)-labeled newborn taste bud cells 1-3 days after LPS injection, suggesting an inhibition of taste bud cell renewal. BrdU pulse-chase experiments showed that BrdU-labeled taste cells had a shorter average life span in LPS-treated mice than in controls. To investigate whether LPS inhibits taste cell renewal by suppressing taste progenitor cell proliferation, we studied the expression of Ki67, a cell proliferation marker. Quantitative real-time RT-PCR revealed that LPS markedly reduced Ki67 mRNA levels in circumvallate and foliate epithelia. Immunofluorescent staining using anti-Ki67 antibodies showed that LPS decreased the number of Ki67-positive cells in the basal regions surrounding circumvallate taste buds, the niche for taste progenitor cells. PCR array experiments showed that the expression of cyclin B2 and E2F1, two key cell cycle regulators, was markedly downregulated by LPS in the circumvallate and foliate epithelia.ConclusionsOur results show that LPS-induced inflammation inhibits taste progenitor cell proliferation and interferes with taste cell renewal. LPS accelerates cell turnover and modestly shortens the average life span of taste cells. These effects of inflammation may contribute to the development of taste disorders associated with infections.

Taste of Fat: A Sixth Taste Modality?

“…This effect seems to be taste bud dependent because CB 1 R is found in a subset of type II cells expressing the sweet taste receptor T 1 R 3 , and a systemic administration of endocannabinoids increases the activity of gustatory nerves in the mouse (229 (LPS) can also affect TBC renewal. Indeed, LPS-mediated inflammation reduces the proliferation of taste progenitor cells and shortens the turnover of taste buds in mice (34). Whether an acute or chronic low-grade proinflammatory environment, as reported during obesity, modifies the taste perception, and hence eating preference, is presently unknown.…”

Regulation of bitter taste responses by tumor necrosis factor

“…persistent bitter or metallic taste in the mouth) (Brand, 2000; Bromley, 2000). In animal models, induced inflammation has been shown to affect taste responses and taste bud structure (Cavallin and McCluskey, 2005; Cohn et al, 2010; Phillips and Hill, 1996). How inflammation exerts its effects on taste reception or taste bud structure has not been fully elucidated.…”

Rocking Media Over Ex Vivo Corneas Improves This Model and Allows the Study of the Effect of Proinflammatory Cytokines on Wound Healing

“…22 Similarly, LPS has been shown to induce inflammation of the epithelium. 23,24 Accordingly, these cytokines and LPS were selected as potential proinflammatory cytokines for this study.…”