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= 0.07). Even though results suggest dietary oxidized protein did not induce oxidative stress during short-term feeding. Differences in performance, gut morphology, and digestibility are likely a result of reduced protein availability. © The Author(s) 2020. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.Central to the development of adipose tissue (AT) engineered models is the supporting vasculature. It is a key part of AT function and long-term maintenance, but the crosstalk between adipocytes and endothelial cells is not well understood. Here, we directly co-culture the two cell types at varying ratios in a 3D Type I collagen gel. Constructs were evaluated for adipocyte maturation and function and vascular network organization. Further, these constructs were treated with forskolin, a beta-adrenergic agonist, to stimulate lipolysis and browning. Adipocytes in co-cultures were found to be less mature than an adipocyte-only control, shown by smaller lipid droplets and downregulation of key adipocyte-related genes. The most extensive vascular network formation was found in the 11 co-culture, supported by vascular endothelial growth factor (VEGF) upregulation. After forskolin treatment, the presence of endothelial cells was shown to upregulate PPAR coactivator 1 alpha (PGC-1α) and leptin, but not uncoupling protein 1 (UCP1), suggesting a specific crosstalk that enhances early stages of browning. © The Author(s) 2020. https://www.selleckchem.com/products/CHIR-258.html Published by Oxford University Press. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.BACKGROUND Whooping cough is caused by infection of the airways with Bordetella pertussis (Bp). As IFN-γ is essential for protective immunity against Bp we investigated how IFN-γ is induced by Bp or the virulence antigens FHA, Prn or PT, and how IFN-γ contributes to local immune responses in humans. METHODS PBMCs from healthy donors and/or respiratory epithelial cells were stimulated with soluble antigens or inactivated intact Bp and the presence or absence of blocking antibodies or chemokines. Supernatants and cells were analyzed for IFN-γ and chemokine production and lymphocyte migration tested using epithelial supernatants. RESULTS The soluble antigens failed to induce IFN-γ production, whereas inactivated Bp induced IFN-γ production. NK cells were the main source of IFN-γ production, which was enhanced by IL-15. Epithelial-PBMC co-cultures showed robust IFN-γ-dependent CXCL9 and CXCL10 production by the epithelial cells following stimulation with IFN-γ and Bp. The epithelial-derived chemokines resulted in CXCR3-dependent recruitment of NK and T cells. CONCLUSIONS Inactivated Bp, but not antigens, induced potent IFN-γ production by NK cells, resulting in chemo-attraction of lymphocytes towards the respiratory epithelium. These data provide insight into the requirements for IFN-γ production and how IFN-γ enhances local immune responses to prevent Bp-mediated disease. © The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America.Chloride (Cl-) is pervasive in saline soils, and the existing research concerning the influence of Cl- on plants has mainly focused on its role as an essential micronutrient and its toxicity when massive accumulations occur. However, the possible functions of Cl- in plants adapting to abiotic stresses have not been well documented. Previous investigations have shown that the salt tolerance of the xerophytic species Pugionium cornutum might be related to high Cl- accumulation. Here, we further investigated the Cl--tolerant characteristics and possible physiological functions of Cl- in the salt tolerance and drought resistance of P. cornutum. The results showed that P. cornutum can accumulate a large amount of Cl- in its shoots, facilitating osmotic adjustment and turgor generation under saline conditions. The application of DIDS, a blocker of anion channels, significantly inhibited Cl- uptake, decreased both the Cl- content and the contribution of Cl- to leaf osmotic adjustment, and therefore exacerbated the NaCl-induced growth inhibition of P. cornutum. Unlike glycophytes, P. cornutum could maintain NO3- homeostasis in its shoots when large amounts of Cl- were absorbed and accumulated. The addition of NaCl mitigated the deleterious effects of osmotic stress on P. cornutum because Cl- accumulation elicited strong osmotic adjustment capacity. These findings suggest that P. cornutum is a Cl--tolerant species that can absorb and accumulate Cl- to improve growth under salt and drought stresses. © The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Experimental Biology.Phytoene synthase 1 (PSY1) and capsanthin-capsorubin synthase (CCS) are two major genes responsible for fruit color variation in pepper (Capsicum spp.) The role of PSY2 in fruit color development in pepper had been unknown. This is the first study showing the activity of PSY2 in Capsicum. We used a systemic approach to discover the genetic factors responsible for the yellow fruit color of C. annuum 'MicroPep Yellow' (MY) and to reveal the role of PSY2 in fruit color. We detected a complete deletion of PSY1 and a retrotransposon insertion in CCS in MY. Despite the loss of PSY1 and CCS function, the MY and mutant F2 plants from a cross between MY and the MicroPep Red (MR) accumulated basal levels of carotenoids, indicating that other PSY genes may complement the loss of PSY1. A qRT-PCR analysis demonstrated that PSY2 is constitutively expressed in both MR and MY fruits, and a color complementation assay using Escherichia coli revealed that PSY2 is capable of biosynthesizing a carotenoid. Virus-induced gene silencing of PSY2 in MY resulted in white fruits. These findings indicate that PSY2 can compensate for the absence of PSY1 in fruit, resulting in the yellow color of MY fruits. © The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email journals.permissions@oup.com.
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