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Quantum Mechanics of Wound Healing: Nano-bio Interface of Wound Bed and Wound Dressing
Published in Cherry Bhargava, Amit Sachdeva, Pardeep Kumar Sharma, Smart Nanotechnology with Applications, 2020
Garima Shandilya, Kirtan Tarwadi, Sachin Chavan
Delayed healing and microbial aggregation are consequences of biofilm establishment and depend on the host response to it through innate and adaptive immunity. These biofilms are partially protected against the action of neutrophils, including phagocytosis, degranulation, and development of neutrophil extracellular traps [15]. Microbial virulence, microbial composition and diversity and composition of the extracellular matrix determine the efficiency of the immune defense. The physical and ecological stability of biofilms can contribute to the selection of more resistant or more virulent strains, which determine immune pressure to wound. Enzymes can also degrade collagen and other proteins as a result and cause harm to the host tissues and delay wound healing [16].
Experimental Results on Cellular and Subcellular Systems Exposed to Low-Frequency and Static Magnetic Fields
Published in Ben Greenebaum, Frank Barnes, Biological and Medical Aspects of Electromagnetic Fields, 2018
Myrtill Simkó, Mats-Olof Mattsson
Neutrophils are empowered with sophisticated machineries to perform migration (Nourshargh et al. 2010) and produce granules containing either chemokines and cytokines or other innate antimicrobial proteins to be released upon appropriate stimulus (Borregaard et al. 2007). Thus, in addition to the traditional phagocytic function, neutrophils may fight microbes by delivering granules with enzymatic functions (Reeves et al. 2002) and by what has been defined in 2004 as neutrophil extracellular traps (NETs) (Brinkmann et al. 2004). NETs are extracellular traps that capture and destroy extracellular microbes and are basically a backbone of nuclear decondensed chromatin mixed with neutrophil-derived antimicrobial proteins. The generation of NET results, for the neutrophil, in a unique form of cell death called NETosis followed by autophagy or phagocytosis by macrophages (Parker et al. 2012).
Osteoimmunomodulation with Biomaterials
Published in Nihal Engin Vrana, Biomaterials and Immune Response, 2018
Bengü Aktaş, Bora Garipcan, Zehra Betül Ahi, Kadriye Tuzlakoğlu, Emre Ergene, Pınar Yılgör Huri
All of these immune cells have distinct precursors and very specific roles in the inflammatory reaction. For example, monocytes are cells formed by precursor cells, called monoblasts, present in the bone marrow. These cells circulate via the bloodstream. During inflammation, monocytes leave the bloodstream and migrate to the tissues. Then, they differentiate into macrophages or dendritic cells under the influence of various growth factors and cytokines within tissues. Tissue macrophages are the first line of the body’s defence mechanism and their primary action is to perform phagocytosis to digest any foreign substance to the body [18]. Granulocytes are a group of white blood cells with small granules in their cytoplasm. There are three different types of granulocytes: neutrophils, eosinophils and basophils. Neutrophils kill the invaders in three different ways: phagocytosis, secretion of soluble antimicrobials and neutrophil extracellular traps (NETs). Eosinophils are very important for fighting against parasitic infections as their granules contain cathepsin, which is a unique toxic protein. Basophils are responsible for immune response during the formation of acute and chronic allergic diseases [19].
Short-term exposure of female BALB/cJ mice to e-cigarette aerosol promotes neutrophil recruitment and enhances neutrophil-platelet aggregation in pulmonary microvasculature
Published in Journal of Toxicology and Environmental Health, Part A, 2023
Hunter T. Snoderly, Hassan Alkhadrawi, Dhruvi M. Panchal, Kelly L. Weaver, Jenna N. Vito, Kasey A. Freshwater, Stell P. Santiago, I. Mark Olfert, Timothy R. Nurkiewicz, Margaret F. Bennewitz
Neutrophil-platelet aggregates produce downstream pro-inflammatory functionalities such as release of web-like DNA structures called neutrophil extracellular traps (NETs) (Etulain et al. 2015). Originally characterized as an anti-microbial response, NETosis is now considered a hallmark of inflammation in a variety of disease states including cystic fibrosis, sepsis, and cancer (Snoderly, Boone, and Bennewitz 2019). Once released, NETs provoke endothelial damage, platelet activation, and additional neutrophil recruitment, thereby forming a positive feedback loop that may result in vessel occlusion (Kim and Jenne 2016). However, existing investigations reported conflicting results regarding the influence of EC on NETosis and neutrophil recruitment. Reidel et al. (2018) noted no marked change in neutrophil % in the sputum of e-cigarette users; however, NETosis was elevated in user peripheral neutrophils upon treatment with phorbol 12-myristate 13-acetate (PMA), a NET-inducing stimulus, relative to NETosis induced by PMA in non-user neutrophils. Conversely, Corriden et al. (2020) reported a decrease in the number of neutrophils recovered from the peritoneal space of EC-exposed mice challenged with P. aeruginosa, as well as suppressed PMA-induced NETosis in non-e-cigarette user peripheral neutrophils treated with EC ex vivo compared to neutrophils treated with PMA alone. The impact of EC exposure on neutrophil-platelet aggregation and neutrophil recruitment specifically within the pulmonary microvasculature in vivo as well as persistence of this inflammatory response after cessation of exposure still needs to be defined.
Viburnum opulus fruit extract-capped gold nanoparticles attenuated oxidative stress and acute inflammation in carrageenan-induced paw edema model
Published in Green Chemistry Letters and Reviews, 2022
Cristina Bidian, Gabriela Adriana Filip, Luminița David, Bianca Moldovan, Ioana Baldea, Diana Olteanu, Mara Filip, Pompei Bolfa, Monica Potara, Alina Mihaela Toader, Simona Clichici
In inflammation, polymorphonuclear neutrophils (PMNs) play an important role because of their migration in inflamed tissues, attraction to chemokines, and due to their ability to eliminate pathogens by degranulation, phagocytosis, neutrophil extracellular traps, and cytokine release (8). Endogenous reactive oxygen species (ROS), released by NADPH-oxidase activity regulate pathways dependent on tyrosine phosphorylation, control phagocytosis, and modulate the expression of cytokines and chemokines involved in the inflammatory response (9).
Interleukin-6 in exhaustive exercises and its correlation to bacteremia: a pilot study
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Amr A. Elgharib, Dalia S. Khalifa, Salma A. Khodeer, Youstina Mohsen, Doaa T. Masallat
In the present study, a highly significant positive correlation was reported between duration of the exercise and infection (R = 0.4714). Susceptibility to infection was increased with IL6 level reduction. This was in agreement with Simpson et al. who reported that moderate exercise is immuno-enhancing but prolonged periods of intensive exercise training can depress immunity [27]. Also, Hume et al demonstrated that a lack of IL-6 resulted in a concomitant increase in bacterial load and severity of infection in eye. His findings imply that IL-6 may play a role in the activation of PMNs during infection [28]. IL-6 also correlates with neutrophil activation because it stimulates production of elastase and prime neutrophils for the production of oxygen-free radicals [29]. In a study conducted by Shi Y et al, they found that the increase of lactic acid during exhaustive exercises was related to the decrease in the production of neutrophil extracellular traps and reactive oxygen species released from neutrophils which protect the body from invasion of microorganisms [30]. This could be due to the decreased levels of IL-6 as found in this study. This can explain the transient immune suppression and increased susceptibility to infection. Clinical studies of IL-6 inhibitors reveal that their use is associated with an increased rate of both serious and opportunistic infections because IL-6 has a prominent role in the synthesis and secretion of acute-phase proteins [31]. IL-6 play an important role in the regulation of the innate and adaptive immune response and IL6 deficient mice showed higher mortality by weakened immune defense and higher bacterial burden [32]. This finding was not true in other studies which reported that exercise is a powerful behavioral intervention that improve immunity and health outcomes and the practice of physical activities strengthens the immune system, suggesting a benefit against infectious diseases [33,34].