NONO regulates monocyte-macrophage lineage differentiation through a potential PI3K/AKT-dependent mechanism.

Non-POU domain containing octamer binding protein (NONO) is a multifunctional nuclear protein which plays important roles in regulating nuclear processes such as transcription and splicing. We aimed to delineate the effects and the underlying mechanisms of NONO on monocyte-macrophage lineage differentiation. By depolying a phorbol 12-myristate 13-acetate (PMA)-induced THP-1 cell differentiation model and a macrophage colony-stimulating factor (M-CSF)-induced mouse bone marrow cell differentiation model, we examined the expression pattern and the effects of NONO during monocyte-macrophage lineage differentiation.

Carbon monoxide inhibits human bronchial epithelial CCL5 and IL-6 secretion induced by SARS-CoV-2 spike RBD protein.

Carbon monoxide (CO) is a novel anti-inflammatory molecule, but the effects of CO on SARS-CoV-2 spike RBD (S-RBD)-induced human bronchial epithelial cytokines release remains unclear. CO was delivered using CO-releasing molecule 3 (CORM-3). The effects of S-RBD, ATPγS and CO on cytokines secretion were determined by enzyme-linked immunosorbent assay (ELISA) in 16HBE14o-human bronchial epithelial cell line.

SARS-CoV-2 spike protein receptor binding domain promotes IL-6 and IL-8 release via ATP/P2Y and ERK1/2 signaling pathways in human bronchial epithelia.

The spike protein of SARS-CoV-2 as well as its receptor binding domain (RBD) has been demonstrated to be capable of activating the release of pro-inflammatory mediators in endothelial cells and immune cells such as monocytes. However, the effects of spike protein or its RBD on airway epithelial cells and mechanisms underlying these effects have not been adequately characterized. Here, we show that the RBD of spike protein alone can induce bronchial epithelial inflammation in a manner of ATP/P2Y dependence.

Pro-inflammatory action of formoterol in human bronchial epithelia.

Despite the wide usage of β-adrenoceptor agonists in asthma treatment, they do have side effects such as aggravating inflammation. We previously reported that isoprenaline induced Cl secretion and IL-6 release via cAMP-dependent pathways in human bronchial epithelia, but the mechanisms underlying the inflammation-aggravation effects of β-adrenoceptor agonists remain pooly understood. In this study, we investigated formoterol, a more specific β-adrenoceptor agonist, -mediated signaling pathways involved in the production of IL-6 and IL-8 in 16HBE14o- human bronchial epithelia.

Cellular Mechanism Underlying the Facilitation of Contractile Response Induced by Tumor Necrosis Factor-α in Mouse Tracheal Smooth Muscle.

The proinflammatory cytokine tumor necrosis factor-α (TNF-α) augments intracellular Ca signaling and contractile responses of airway smooth muscles, leading to airway hyperresponsiveness. However, the underlying mechanism has not been fully elucidated. This study aimed to investigate the cellular mechanism of the potentiated contraction of mouse tracheal smooth muscle induced by TNF-α.

β-Adrenoceptor Activation Stimulates IL-6 Production via PKA, ERK1/2, Src, and Beta-Arrestin2 Signaling Pathways in Human Bronchial Epithelia.

Objective: β-Adrenoceptor agonists are widely used to treat asthma because of their bronchial-dilation effects. We previously reported that isoprenaline, via the apical and basolateral β-adrenoceptor, induced Cl secretion by activating cyclic AMP (cAMP)-dependent pathways in human bronchial epithelia. Despite these results, whether and how the β-adrenoceptor-mediated cAMP-dependent pathway contributes to pro-inflammatory cytokine release in human bronchial epithelia remains poorly understood.

Regulation of smooth muscle contractility by the epithelium in rat tracheas: role of prostaglandin E induced by the neurotransmitter acetylcholine.

Background: Previous studies have suggested the involvement of epithelium in modulating the contractility of neighboring smooth muscle cells. However, the mechanism underlying epithelium-derived relaxation in airways remains largely unclear. This study aimed to investigate the mechanism underlying epithelium-dependent smooth muscle relaxation mediated by neurotransmitters.

β adrenoceptor signaling regulates ion transport in 16HBE14o- human airway epithelial cells.

We investigated the regulation of Cl secretion by adrenoceptors in polarized 16HBE14o- human bronchial epithelial cells. Treatment with the nonselective β adrenoceptor agonist isoprenaline stimulated an increase in short-circuit current (I ), which was inhibited by the β adrenoceptor blocker propranolol. Treatment with procaterol, an agonist specific for the β adrenoceptor subtype, stimulated a similar increase in I , which was inhibited by the β adrenoceptor antagonist ICI 118551.

[Potential for Phosphorus Uptake by Bed Sediments and Its Response to Carbon Additions in the Shiwuli River, Chaohu Lake Basin].

Surficial sediments were collected from five sampling sites in the mainstream of the Shiwuli River along an urban-rural gradient in the Chaohu Lake basin during July 2017 (summer) and January 2018 (winter). The total uptake (SPU), abiotic uptake (SPU), and biotic uptake (SPU) of phosphorus by sediments were measured, and uptake responses to different carbon sources (i. e.

Anti-inflammatory action of HO-1/CO in human bronchial epithelium in response to cationic polypeptide challenge.

Carbon monoxide (CO) is an anti-inflammatory gaseous molecule produced endogenously by heme oxygenases (HOs) HO-1 and HO-2. However, the mechanisms underlying the anti-inflammatory effects of CO in the human bronchial epithelium are still not fully understood. In this study, the cationic peptide poly-l-arginine (PLA) was utilized to induce bronchial epithelial damage and subsequent pro-inflammatory cytokine release in the human bronchial epithelial cell line 16HBE14o-.

Carbon Monoxide Inhibits Cytokine and Chloride Secretion in Human Bronchial Epithelia.

Background/aims: Carbon monoxide (CO) is an important gas produced endogenously by heme oxygenase (HO) that functions as an anti-inflammatory and in ion channel modulation, but the effects of CO on airway inflammation and ion transport remains unclear.

Methods: The effect of CO on cell damage- and nucleotide-induced pro-inflammatory cytokine release in primary human bronchial epithelia cells (HBE) and in the 16HBE14o- human bronchial epithelial cell line were investigated. The effects of CO on calcium- and cAMP-dependent chloride (Cl-) secretion were examined using a technique that allowed the simultaneous measurement and quantification of real-time changes in signalling molecules (cAMP and Ca2+) and ion transport in a polarised epithelium.

Regulation of Intracellular Calcium by Carbon Monoxide in Human Bronchial Epithelial Cells.

Background/aims: Carbon monoxide (CO) is an important autocrine/paracrine messenger involved in a variety of physiological and pathological processes. This study aimed to investigate the regulatory role of CO released by CO-releasing molecule-2 (CORM-2) in a P2Y receptor-mediated calcium-signaling pathway in the human bronchial epithelial cell line, 16HBE14o-.

Methods: Intracellular calcium ([Ca2+]i) was measured by fura-2 microspectrofluorimetry.

[Pollution Characteristics and Nitrification and Denitrification Potential of Superficial Sediments from Streams in an Urban-Rural Fringe].

From May 2015 to June 2016, seasonal sediment samples were collected from three headwater streams in the urban-rural fringe of Hefei, Chaohu Lake basin, China. The nitrogen pollution characteristics of sediments were preliminarily investigated for the three streams. Three metrics, that is, potential nitrification rate (PNR), areal nitrification rate (ANR) and rate of denitrification were quantitatively determined, and their spatial and temporal variations were discussed subsequently.

[Soil Phosphorus Forms and Leaching Risk in a Typically Agricultural Catchment of Hefei Suburban].

To investigate the soil phosphorus forms and leaching risk in a typically agricultural catchment of Ershibu River in Hefei Suburban, Chaohu Lake basin, 132 surface soil samples were collected from the catchment area. The spatial distribution of total phosphorus (TP) and bio-available phosphorus (Bio-P), and the spatial variability of soil available phosphorus (Olsen-P) and easy desorption phosphorus (CaCl2-P) were analyzed using the Kriging technology of AreGIS after speciation analysis of soil phosphorus. Moreover, the enrichment level of soil phosphorus was studied, and the phosphorus leaching risk was evaluated through determining the leaching threshold value of soil phosphorus.