Neutrophil responses to injury or inflammation impair peripheral gustatory function

Steen, Pamela Wall; Shi, Liqiao; He, Lin; McCluskey, Lynnette Phillips

doi:10.1016/j.neuroscience.2010.02.056

Cited by 21 publications

(21 citation statements)

References 56 publications

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“…Pilot studies revealed no consistent differences in CT responses from male vs. female B6 control mice. Thus, we chose to use females to be consistent with previous work in our laboratory (McCluskey, 2004, Steen et al, 2010). Mice were group-housed in polyurethane shoebox cages for at least one week before experiments began, when they were moved to single housing.…”

Section: Methodsmentioning

confidence: 99%

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Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice

Zhu

McCluskey

2014

Neuroscience

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A fundamental role of the taste system is to discriminate between nutritive and toxic foods. However, it is unknown whether bacterial pathogens that might contaminate food and water modulate the transmission of taste input to the brain. We hypothesized that exogenous, bacterially-derived lipopolysaccharide (LPS), modulates neural responses to taste stimuli. Neurophysiological responses from the chorda tympani nerve, which innervates taste cells on the anterior tongue, were unchanged by acute exposure to LPS. Instead, neural responses to sucrose were selectively inhibited in mice that drank LPS during a single overnight period. Decreased sucrose sensitivity appeared 7 days after LPS ingestion, in parallel with decreased lingual expression of Tas1r2 and Tas1r3 transcripts, which are translated to T1R2+T1R3 subunits forming the sweet taste receptor. Tas1r2 and Tas1r3 mRNA expression levels and neural responses to sucrose were restored by 14 days after LPS consumption. Ingestion of LPS, rather than contact with taste receptor cells, appears to be necessary to suppress sucrose responses. Furthermore, mice lacking the Toll-like receptor (TLR) 4 for LPS were resistant to neurophysiological changes following LPS consumption. These findings demonstrate that ingestion of LPS during a single period specifically and transiently inhibits neural responses to sucrose. We suggest that LPS drinking initiates TLR4-dependent hormonal signals that downregulate sweet taste receptor genes in taste buds. Delayed inhibition of sweet taste signaling may influence food selection and the complex interplay between gastrointestinal bacteria and obesity.

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Section: Methodsmentioning

confidence: 99%

“…In the absence of neural injury, LPS inhibits taste receptor cell proliferation and stimulates the expression of proinflammatory genes in taste buds (Wang et al, 2007, Wang et al, 2009, Cohn et al, 2010). Subcutaneous, lingual injections of LPS impair sodium taste function by stimulatng neutrophil infiltration of the sensory field (Steen et al, 2010). …”

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confidence: 99%

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice

Zhu

McCluskey

2014

Neuroscience

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“…Old and young rats received unilateral CT section or sham sectioning as previously described (Hill and Phillips, 1994, McCluskey, 2004, Steen et al, 2010). Rats were injected with atropine sulfate [0.054 mg/kg; intraperitoneal (i.p.)]…”

Section: Methodsmentioning

confidence: 99%

“…Separate groups of young (3 month old; n=4) and old (24 month old; n=4) rats received an injection of lipopolysaccharide (s.c.; E. coli 026:B6; Sigma, St. Louis, MO) to the ventral tongue to stimulate neutrophil invasion. Injections consisted of 10 μg of LPS in 10 μl sterile PBS as in previous work (Steen et al, 2010). …”

Section: Methodsmentioning

confidence: 99%

Aging profoundly delays functional recovery from gustatory nerve injury

Yadgarov

Sharif

et al. 2012

Neuroscience

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The peripheral taste system remains plastic during adulthood. Sectioning the chorda tympani (CT) nerve, which sends sensory information from the anterior tongue to the CNS, causes degeneration of distal fibers and target taste buds. However, taste function is restored after about 40 days in young adult rodents. We tested whether aging impacts the reappearance of neural responses after unilateral CT nerve injury. Taste bud regeneration was minimal at day 50–65 after denervation, and most aged animals died before functional recovery could be assessed. A subset (n=3/5) of old rats exhibited normal CT responses at day 85 post-sectioning, suggesting the potential for efficient recovery. The aged taste system is fairly resilient to sensory receptor loss and major functional changes in normal aging. However, injury to the taste system reveals a surprising vulnerability in old rodents. The gustatory system provides an excellent model to study mechanisms underlying delayed recovery from peripheral nerve injury. Strategies to accelerate recovery and restore normal function will be of interest as the elderly population continues to grow.

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“…It is clearly evident that the taste system is less vulnerable to disruption after system maturation, regardless of injury type. The mechanism for this variation in plasticity across development is unknown, though differences in peripheral immune response are a strong potential candidate (Steen et al, 2010; He et al, 2012). …”

Section: Discussionmentioning

confidence: 99%

Chronic Oral Capsaicin Exposure During Development Leads to Adult Rats with Reduced Taste Bud Volumes

2016

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Introduction Cross-sensory interaction between gustatory and trigeminal nerves occurs in the anterior tongue. Surgical manipulations have demonstrated that the strength of this relationship varies across development. Capsaicin is a neurotoxin that affects fibers of the somatosensory lingual nerve surrounding taste buds, but not fibers of the gustatory chorda tympani nerve which synapse with taste receptor cells. Since capsaicin is commonly consumed by many species, including humans, experimental use of this neurotoxin provides a naturalistic perturbation of the lingual trigeminal system. Neonatal or adults rats consumed oral capsaicin for 40 days and we examined the cross-sensory effect on the morphology of taste buds across development. Methods Rats received moderate doses of oral capsaicin, with chronic treatments occurring either before or after taste system maturation. Tongue morphology was examined either 2 or 50 days after treatment cessation. Edema, which has been previously suggested as a cause of changes in capsaicin-related gustatory function, was also assessed. Results Reductions in taste bud volume occurred 50 days, but not 2 days post-treatment for rats treated as neonates. Adult rats at either time post-treatment were unaffected. Edema was not found to occur with the 5 ppm concentration of capsaicin we used. Conclusions Results further elucidate the cooperative relationship between these discrete sensory systems and highlight the developmentally mediated aspect of this interaction. Implications Chronic exposure to even moderate levels of noxious stimuli during development has the ability to impact the orosensory environment, and these changes may not be evident until long after exposure has ceased.

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Neutrophil responses to injury or inflammation impair peripheral gustatory function

Cited by 21 publications

References 56 publications

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice

Aging profoundly delays functional recovery from gustatory nerve injury

Chronic Oral Capsaicin Exposure During Development Leads to Adult Rats with Reduced Taste Bud Volumes

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