Daphnia magna's sense of competition: intra-specific interactions (ISI) alter life history strategies and increase metals toxicity.

Daphnia magna's sense of competition: intra-specific interactions (ISI) alter life history strategies and increase metals toxicity.

Ecotoxicology. 2016 May 5;

Authors: Gust KA, Kennedy AJ, Melby NL, Wilbanks MS, Laird J, Meeks B, Muller EB, Nisbet RM, Perkins EJ

Abstract
This work investigates whether the scale-up to multi-animal exposures that is commonly applied in genomics studies provides equivalent toxicity outcomes to single-animal experiments of standard Daphnia magna toxicity assays. Specifically, we tested the null hypothesis that intraspecific interactions (ISI) among D. magna have neither effect on the life history strategies of this species, nor impact toxicological outcomes in exposure experiments with Cu and Pb. The results show that ISI significantly increased mortality of D. magna in both Cu and Pb exposure experiments, decreasing 14 day LC50 s and 95 % confidence intervals from 14.5 (10.9-148.3) to 8.4 (8.2-8.7) µg Cu/L and from 232 (156-4810) to 68 (63-73) µg Pb/L. Additionally, ISI potentiated Pb impacts on reproduction eliciting a nearly 10-fold decrease in the no-observed effect concentration (from 236 to 25 µg/L). As an indication of environmental relevance, the effects of ISI on both mortality and reproduction in Pb exposures were sustained at both high and low food rations. Furthermore, even with a single pair of Daphnia, ISI significantly increased (p < 0.05) neonate production in control conditions, demonstrating that ISI can affect life history strategy. Given these results we reject the null hypothesis and conclude that results from scale-up assays cannot be directly applied to observations from single-animal assessments in D. magna. We postulate that D. magna senses chemical signatures of conspecifics which elicits changes in life history strategies that ultimately increase susceptibility to metal toxicity.

PMID: 27151402 [PubMed - as supplied by publisher]

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Formaldehyde Induces Rho-associated Kinase Activity to Evoke Airway Hyperresponsiveness.

Formaldehyde Induces Rho-associated Kinase Activity to Evoke Airway Hyperresponsiveness.

Am J Respir Cell Mol Biol. 2016 May 5;

Authors: Jude J, Koziol-White C, Scala J, Yoo E, Jester W, Maute C, Dalton P, Panettieri R

Abstract
BACKGROUND: Formaldehyde, a common indoor air pollutant, exacerbates asthma and synergizes with allergen to induce airway hyperresponsiveness (AHR) in animal models. The mechanisms mediating formaldehyde-induced AHR remain poorly understood. We posit that formaldehyde modulates agonist-induced contractile response of human airway smooth muscle (HASM) cells to elicit AHR.
METHODS: HASM cells were exposed to formaldehyde or vehicle and agonist-induced intracellular Ca(2+) ([Ca2+]i), and myosin light chain phosphatase (MYPT1) phosphorylation were determined. Air-liquid interface (ALI)-differentiated human bronchial epithelial (HBE) cells were exposed to formaldehyde or vehicle and co-cultured with HASM cells. Agonist-induced [Ca(2+)]i and MYPT1 phosphorylation were determined in the co-cultured HASM cells. Precision-cut human lung slices (PCLS) were exposed to PBS or varying concentrations of formaldehyde and then carbachol (cch) -induced airway narrowing was determined 24 h post-exposure. HASM cells were transfected with non-targeting (NT) or Nrf-2-targeting (Nrf-2) siRNA, exposed to formaldehyde or vehicle, followed by determination of anti-oxidant response (NQO1 and Trx1) and basal and agonist-induced MYPT1 phosphorylation.
RESULTS: Formaldehyde enhanced the basal Rho-kinase activity and MYPT1 phosphorylation with little effect on agonist-induced [Ca(2+)]i in HASM cells. Formaldehyde induced Nrf-2-dependent anti-oxidant response in HASM cells although the MYPT1 phosphorylation was independent of Nrf-2 induction. Although HBE cells exposed to formaldehyde had little effect on agonist-induced [Ca(2+)]i or MYPT1 phosphorylation in co-cultured HASM cells, formaldehyde enhanced cch-induced airway responsiveness in PCLS.
CONCLUSIONS: Formaldehyde induces phosphorylation of the regulatory subunit of myosin light chain phosphatase (MYPT1), independent of formaldehyde-induced Nrf-2 activation in HASM cells. The findings suggest that Rho kinase-dependent Ca(2+) sensitization pathway plays a role in in formaldehyde-induced AHR.

PMID: 27149505 [PubMed - as supplied by publisher]

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Formaldehyde Induces Rho-associated Kinase Activity to Evoke Airway Hyperresponsiveness.

Formaldehyde Induces Rho-associated Kinase Activity to Evoke Airway Hyperresponsiveness.

Am J Respir Cell Mol Biol. 2016 May 5;

Authors: Jude J, Koziol-White C, Scala J, Yoo E, Jester W, Maute C, Dalton P, Panettieri R

Abstract
BACKGROUND: Formaldehyde, a common indoor air pollutant, exacerbates asthma and synergizes with allergen to induce airway hyperresponsiveness (AHR) in animal models. The mechanisms mediating formaldehyde-induced AHR remain poorly understood. We posit that formaldehyde modulates agonist-induced contractile response of human airway smooth muscle (HASM) cells to elicit AHR.
METHODS: HASM cells were exposed to formaldehyde or vehicle and agonist-induced intracellular Ca(2+) ([Ca2+]i), and myosin light chain phosphatase (MYPT1) phosphorylation were determined. Air-liquid interface (ALI)-differentiated human bronchial epithelial (HBE) cells were exposed to formaldehyde or vehicle and co-cultured with HASM cells. Agonist-induced [Ca(2+)]i and MYPT1 phosphorylation were determined in the co-cultured HASM cells. Precision-cut human lung slices (PCLS) were exposed to PBS or varying concentrations of formaldehyde and then carbachol (cch) -induced airway narrowing was determined 24 h post-exposure. HASM cells were transfected with non-targeting (NT) or Nrf-2-targeting (Nrf-2) siRNA, exposed to formaldehyde or vehicle, followed by determination of anti-oxidant response (NQO1 and Trx1) and basal and agonist-induced MYPT1 phosphorylation.
RESULTS: Formaldehyde enhanced the basal Rho-kinase activity and MYPT1 phosphorylation with little effect on agonist-induced [Ca(2+)]i in HASM cells. Formaldehyde induced Nrf-2-dependent anti-oxidant response in HASM cells although the MYPT1 phosphorylation was independent of Nrf-2 induction. Although HBE cells exposed to formaldehyde had little effect on agonist-induced [Ca(2+)]i or MYPT1 phosphorylation in co-cultured HASM cells, formaldehyde enhanced cch-induced airway responsiveness in PCLS.
CONCLUSIONS: Formaldehyde induces phosphorylation of the regulatory subunit of myosin light chain phosphatase (MYPT1), independent of formaldehyde-induced Nrf-2 activation in HASM cells. The findings suggest that Rho kinase-dependent Ca(2+) sensitization pathway plays a role in in formaldehyde-induced AHR.

PMID: 27149505 [PubMed - as supplied by publisher]

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Formaldehyde Induces Rho-associated Kinase Activity to Evoke Airway Hyperresponsiveness.

Formaldehyde Induces Rho-associated Kinase Activity to Evoke Airway Hyperresponsiveness.

Am J Respir Cell Mol Biol. 2016 May 5;

Authors: Jude J, Koziol-White C, Scala J, Yoo E, Jester W, Maute C, Dalton P, Panettieri R

Abstract
BACKGROUND: Formaldehyde, a common indoor air pollutant, exacerbates asthma and synergizes with allergen to induce airway hyperresponsiveness (AHR) in animal models. The mechanisms mediating formaldehyde-induced AHR remain poorly understood. We posit that formaldehyde modulates agonist-induced contractile response of human airway smooth muscle (HASM) cells to elicit AHR.
METHODS: HASM cells were exposed to formaldehyde or vehicle and agonist-induced intracellular Ca(2+) ([Ca2+]i), and myosin light chain phosphatase (MYPT1) phosphorylation were determined. Air-liquid interface (ALI)-differentiated human bronchial epithelial (HBE) cells were exposed to formaldehyde or vehicle and co-cultured with HASM cells. Agonist-induced [Ca(2+)]i and MYPT1 phosphorylation were determined in the co-cultured HASM cells. Precision-cut human lung slices (PCLS) were exposed to PBS or varying concentrations of formaldehyde and then carbachol (cch) -induced airway narrowing was determined 24 h post-exposure. HASM cells were transfected with non-targeting (NT) or Nrf-2-targeting (Nrf-2) siRNA, exposed to formaldehyde or vehicle, followed by determination of anti-oxidant response (NQO1 and Trx1) and basal and agonist-induced MYPT1 phosphorylation.
RESULTS: Formaldehyde enhanced the basal Rho-kinase activity and MYPT1 phosphorylation with little effect on agonist-induced [Ca(2+)]i in HASM cells. Formaldehyde induced Nrf-2-dependent anti-oxidant response in HASM cells although the MYPT1 phosphorylation was independent of Nrf-2 induction. Although HBE cells exposed to formaldehyde had little effect on agonist-induced [Ca(2+)]i or MYPT1 phosphorylation in co-cultured HASM cells, formaldehyde enhanced cch-induced airway responsiveness in PCLS.
CONCLUSIONS: Formaldehyde induces phosphorylation of the regulatory subunit of myosin light chain phosphatase (MYPT1), independent of formaldehyde-induced Nrf-2 activation in HASM cells. The findings suggest that Rho kinase-dependent Ca(2+) sensitization pathway plays a role in in formaldehyde-induced AHR.

PMID: 27149505 [PubMed - as supplied by publisher]

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The Effects of Odor Quality and Temporal Asynchrony on Modulation of Taste Intensity by Retronasal Odor.

Related Articles

The Effects of Odor Quality and Temporal Asynchrony on Modulation of Taste Intensity by Retronasal Odor.

Chem Senses. 2016 May 3;

Authors: Isogai T, Wise PM

Abstract
The experiments had 2 main goals: 1) to add to the sparse literature on how retronasal aromas interact with bitter tastes, and 2) to determine whether modulation of taste intensity by aroma depends on temporal contiguity, as one might expect if flavor interactions depend on cross-modal binding (similar to object perception in other modalities). An olfactometer-gustometer allowed independent oral presentation of odorized air and liquid samples. First, using simultaneous presentation of odors and tastes (Experiments 1a-d) we found that a "sweet-smelling" aroma enhanced the rated sweetness of sucrose and decreased the rated bitterness of sucrose octaacetate (SOA), and that a "bitter-smelling" aroma enhanced the bitterness of SOA and decreased the sweetness of sucrose. Thus, with respect to effects on taste intensity, sweet and bitter aromas mimicked mixture-interactions between sweet and bitter tastes under current conditions. Next (Experiment 2), both odors were again paired with both tastes, with a parametric manipulation of odor onset. Odor presentation ranged from before taste delivery to after taste delivery. Enhancement of taste intensity was greatest with simultaneous onset, and greatly attenuated with offsets of 1s. These results are consistent with the idea that enhancement of taste by retronasal aroma depends on a temporal binding window like many other cross-modal interactions. The effects of temporal offsets on suppression of taste were inconclusive. These findings are discussed within the context of past work on odor-taste interactions.

PMID: 27143280 [PubMed - as supplied by publisher]

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Mouse nasal epithelial innate immune responses to Pseudomonas aeruginosa quorum-sensing molecules require taste signaling components.

Related Articles

Mouse nasal epithelial innate immune responses to Pseudomonas aeruginosa quorum-sensing molecules require taste signaling components.

Innate Immun. 2014 Aug;20(6):606-17

Authors: Lee RJ, Chen B, Redding KM, Margolskee RF, Cohen NA

Abstract
We previously observed that the human bitter taste receptor T2R38 is an important component of upper respiratory innate defense because it detects acyl homoserine lactone (AHL) quorum-sensing molecules secreted by Gram-negative bacteria. T2R38 activation in human sinonasal epithelial cells stimulates calcium and NO signals that increase mucociliary clearance, the major physical respiratory defense against inhaled pathogens. While mice do not have a clear T2R38 ortholog, they do have bitter taste receptors capable of responding to T2R38 agonists, suggesting that T2R-mediated innate immune mechanisms may be conserved in mice. We examined whether AHLs activate calcium and NO signaling in mouse nasal epithelial cells, and utilized pharmacology, as well as cells from knockout mice lacking important components of canonical taste signal transduction pathways, to determine if AHL-stimulated responses require taste signaling molecules. We found that AHLs stimulate calcium-dependent NO production that increases mucociliary clearance and thus likely serves an innate immune role against Gram-negative bacteria. These responses require PLCβ2 and TRPM5 taste signaling components, but not α-gustducin. These data suggest the mouse may be a useful model for further studies of T2R-mediated innate immunity.

PMID: 24045336 [PubMed - indexed for MEDLINE]

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The Effects of Odor Quality and Temporal Asynchrony on Modulation of Taste Intensity by Retronasal Odor.

The Effects of Odor Quality and Temporal Asynchrony on Modulation of Taste Intensity by Retronasal Odor.

Chem Senses. 2016 May 3;

Authors: Isogai T, Wise PM

Abstract
The experiments had 2 main goals: 1) to add to the sparse literature on how retronasal aromas interact with bitter tastes, and 2) to determine whether modulation of taste intensity by aroma depends on temporal contiguity, as one might expect if flavor interactions depend on cross-modal binding (similar to object perception in other modalities). An olfactometer-gustometer allowed independent oral presentation of odorized air and liquid samples. First, using simultaneous presentation of odors and tastes (Experiments 1a-d) we found that a "sweet-smelling" aroma enhanced the rated sweetness of sucrose and decreased the rated bitterness of sucrose octaacetate (SOA), and that a "bitter-smelling" aroma enhanced the bitterness of SOA and decreased the sweetness of sucrose. Thus, with respect to effects on taste intensity, sweet and bitter aromas mimicked mixture-interactions between sweet and bitter tastes under current conditions. Next (Experiment 2), both odors were again paired with both tastes, with a parametric manipulation of odor onset. Odor presentation ranged from before taste delivery to after taste delivery. Enhancement of taste intensity was greatest with simultaneous onset, and greatly attenuated with offsets of 1s. These results are consistent with the idea that enhancement of taste by retronasal aroma depends on a temporal binding window like many other cross-modal interactions. The effects of temporal offsets on suppression of taste were inconclusive. These findings are discussed within the context of past work on odor-taste interactions.

PMID: 27143280 [PubMed - as supplied by publisher]

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