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Respiratory Pathophysiology
Published in Hyun Jung Kim, Biomimetic Microengineering, 2020
Brian F. Niemeyer, Alexander J. Kaiser, Kambez H. Benam
To recreate the human lung microvasculature on a platform that incorporates dynamic vascular flow, Seo et al. (2017) fabricated a microfluidic chip containing a single channel which they then lined with human endothelial cells. RBC transfusion was mimicked by perfusing the vascular channel with RBCs for four hours at physiologically relevant rates. As read out of vascular injury, the authors measured extracellular levels of the DNA-binding protein HMGB1, which were previously associated with necroptosis of cells, immune cell activation, and systemic inflammation (Pisetsky 2014). Although the endothelial cells remained adherent, the authors found that extracellular HMGB1 levels were significantly increased during transfusion of RBCs when compared with control samples perfused with media alone or the RBCs alone prior to transfusion (Seo et al. 2017). The authors then went on to measure the effects of shear stress on their system by repeating their experiments with considerably reduced shear stress. Interestingly, reduced shear stress lead to an exacerbation of HMGB1 release, suggesting that reduced shear force is associated with increased transfusion-associated vascular damage (Seo et al. 2017). These results were consistent with previous clinical findings that patients with increased susceptibility to transfusion-associated injuries exhibit reduced blood flow velocity (Donati et al. 2014).
Principles and Biological Pathways to Tissue Regeneration: The Tissue Regenerative Niche
Published in Claudio Migliaresi, Antonella Motta, Scaffolds for Tissue Engineering, 2014
Ranieri Cancedda, Claudia Lo Sicco
The polarization of macrophages, from M1 to M2, distorts the secretion of damage associated molecular patterns (DAMPS), such as high mobility group box 1 (HMGB1), TNF-alpha, VEGF, and metalloproteinase-9 (MMP-9), all molecules involved in the control of cell migration. The secreted DAMPS (HMGB1 and others), interacting with specific pattern recognition receptors, including RAGE and members of the Toll-like receptor (TLR) family, amplifies the inflammatory response, and enhances vasculogenesis and migration of specific progenitor cells [Pistoia and Raffaghello, 2011].
Glycyrrhizin and Omega-3 fatty acids have hepatoprotective roles through toll-like receptor-4
Published in Egyptian Journal of Basic and Applied Sciences, 2019
Nada F. Abo El-Magd, Amro El-Karef, Mamdouh M. El-Shishtawy, Laila A. Eissa
Toll-like receptor-4 (TLR-4) has a critical role in innate immunity as the first line of host defense. Dimerization of two receptor molecules precedes TLR-4 activation [4]. The TLR-4 pathway consists of two different signaling pathways, the myeloid differentiating primary response gene 88 (MyD88)-dependent and the MyD88-independent pathway. (MyD88)-dependent pathway results in the production of pro-inflammatory cytokines through activation of nuclear factor-κB (NF-κB), while the MyD88-independent pathway results in the production of type 1 interferons [5]. Innate immune responses are initiated when danger associated molecule patterns and pathogen-associated molecular patterns (PAMP) are recognized by pattern recognition receptors including TLR-4 [6]. A classical PAMP is a lipopolysaccharide (LPS) from gram-negative bacteria which activates high mobility group box1 (HMGB1). HMGB1 is a highly conserved protein released by injured or dying cells as a result of pathogenic products [7]. HMGB1 may trigger an inflammatory response via activation of TLR-4 pathway which activates NF-κB. This consequently causes an enhancement in the production of tumor necrosis factor α (TNF-α), interleukin-1b (IL-1b) and nitric oxide [8].
Evaluation of subchronic exposure to triclosan on hepatorenal and reproductive toxicities in prepubertal male rats
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Lee Ena, Jong Seung Lim, Ji Yeon Son, Yu Jin Park, Yong Hee Lee, Ji Yeong Kim, Seung Jun Kwack, Byung Mu Lee, Mee-Young Ahn, Hyung Sik Kim
The mechanism by which TCS produced changes in renal function is unknown. Through the use of serum biochemical parameters, histological examination, and protein expression of HMGB1, the nephrotoxic potential of TCS was determined. As noted by BUN and creatinine levels, data indicated that high doses of TCS induced renal toxicity in prepubertal male rats. Rodricks et al. (2010) found renal toxicity of TCS in subacute and chronic exposure conditions as evidenced by inflammation and tubular regeneration in rodent species. Indeed, the renal histopathological results showed that a high dose of TCS induced reduction of Bowman’s space, tubular necrosis, and occlusion of the tubular lumen. These results are consistent with marked alterations in kidney structure as noted by increased fibrous tissue and accumulation of collagen in the TCS-treated mice (Yueh et al. 2014). Several investigators reported that HMGB1 not only is a nuclear factor involved in transcriptional activation but also serves as an extracellular cytokine known to be a key mediator of innate immune responses to infection and injury in the kidney (Wu et al. 2010; Yang et al. 2015). In addition, HMGB1 is released from necrotic or damaged cells as a signal to trigger inflammation (Qing et al. 2008; Scaffidi, Misteli, and Bianchi 2002). To confirm the presence of inflammation in renal toxicity, protein expression of HMGB1 was examined. Data demonstrated that renal HMGB1 protein expression was detected at 0.25 mg/kg TCS and this response occurred in a dose-dependent manner. Overall, evidence indicates that subchronic exposure of TCS may induce inflammatory-mediated renal toxicity in prepubertal male rats.
Nanoprotection from SARS-COV-2: would nanotechnology help in Personal Protection Equipment (PPE) to control the transmission of COVID-19?
Published in International Journal of Environmental Health Research, 2023
Zhi Xin Phuna, Bibhu Prasad Panda, Naveen Kumar Hawala Shivashekaregowda, Priya Madhavan
Polymers and inorganic materials are excellent to be incorporated into facemasks, bio-based components can also be used to develop effective nanofilters. The use of natural product has always been the choice of interest for the pharmaceutical industry due to their relatively lower extend of adverse side effects. Since the potential therapy for COVID-19 are still under investigation with unknown side effects, natural products have attracted insightful attention. Bailly and Vergoten (2020) have recently reviewed the potential therapy of glycyrrhizic acid (GLR) against SARS-CoV-2 (Bailly and Vergoten 2020). GLR is a triterpenoid saponin that is mainly isolated from the root of the plants Glycyrrhiza glabra (also known as European licorice) (Pastorino et al. 2018). At a membrane level, GLR can stimulate cholesterol-dependent disorganization of lipid rafts that is essential for the entry of coronavirus. Whereas at subcellular level, GLR can trap the high mobility group box 1 (HMGB1) protein that play important roles in COVID-19 pathogenesis (Bailly and Vergoten 2020). As a damage-associated molecular pattern (DAMP) molecule, HMG1 can induce inflammation by triggering TLR4 to generate pro-inflammatory cytokines. HMGB1 also can form complexes with DNA, RNA, or other DAMP molecules, which are then endocytosed by receptor for advanced glycation end products (RAGE) that are only highly expressed in lungs. However, RAGE is disrupted by high levels of HMBG1. Thus, it is believed that SARS-CoV-2 may reach the cellular cytosol via HMGB1-assisted transfer with lysosome leakage (Andersson et al. 2020). Serum level of HMGBI was found to be elevated in COVID-19 patients, where it could induce the expression of SARS-CoV-2 entry receptor ACE2 (Chen et al. 2020). Targeting HMGB1 has emerged as one of the potential therapies against COVID-19.