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Journal articles on the topic 'Balance inflammatoire'

Author: Grafiati

Published: 21 December 2024

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1

Buron, F., P. Malvezzi, E. Villar, C. Chauvet, B. Janbon, L. Denis, R. Cahen, et al. "Effet du sirolimus sur la balance inflammatoire en transplantation rénale : étude sirilygre." Néphrologie & Thérapeutique 8, no. 5 (September 2012): 268. http://dx.doi.org/10.1016/j.nephro.2012.07.305.

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2

SAUVET, F., M. CHENNAOUI, S. BANZET, C. BOURRILHON, F. CANINI, L. BOURDON, and N. KOULMANN. "Coup de chaleur d’exercice, système cardiovasculaire et vulnérabilité systémique." Médecine et Armées Vol. 40 No. 3, Volume 40, Numéro 3 (June 1, 2012): 231–40. http://dx.doi.org/10.17184/eac.6611.

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L’un des problèmes posés par le coup de chaleur d’exercice réside dans la précocité des troubles neurologiques qui sont la conséquence de mécanismes pernicieux généraux et cérébraux aboutissant à un déficit de perfusion tissulaire et à une ischémie cérébrale. Au niveau général, la redistribution vasculaire et les modifications de la vasomotricité d’origine inflammatoire, favorisent l’apparition d’un collapsus vasculaire. L'ischémie cérébrale, liée à l’oedème cérébral et à l’hypoperfusion, favorise un état de déséquilibre énergétique qui s'accompagne d'une cytotoxicité, d’une inflammation locale et d'une augmentation de la production de radicaux libres qui majorent la diminution des débits sanguins. Ainsi, les modifications vasculaires observées sont liées à des réponses physiopathologies locales et générales, parfois contradictoires et complexes, qui entrent en compétition et déséquilibrent dans un sens ou dans l’autre la balance vasoconstriction/vasodilatation. Ces déséquilibres modifient les résistances vasculaires, créant des mécanismes vicieux qui favorisent la diminution de la tolérance à la chaleur. Dans ce travail, nous décrierons l’implication du système cardiovasculaire dans la diminution de la tolérance à la chaleur et la survenue d’un coup de chaleur d’exercice. Nous aborderons également les mécanismes qui augmentent la vulnérabilité individuelle et les effets des contremesures protectrices.

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3

Horiuchi, I., Y. Kawano, M. Minohara, and J. Kira. "Th1Th2 balance in inflammatory neurologic diseases." Journal of Neuroimmunology 90, no. 1 (September 1998): 81. http://dx.doi.org/10.1016/s0165-5728(98)91665-4.

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4

Adrie, Ch, and M. R. Pinsky. "The inflammatory balance in human sepsis." Intensivmedizin und Notfallmedizin 36, no. 5 (June 25, 1999): 419–28. http://dx.doi.org/10.1007/s003900050260.

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5

Adrie, C., and M. R. Pinsky. "The inflammatory balance in human sepsis." Intensive Care Medicine 26, no. 4 (April 26, 2000): 364–75. http://dx.doi.org/10.1007/s001340051169.

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6

Tedgui, A., and Z. Mallat. "Pro- and anti-inflammatory balance and atherosclerosis." Atherosclerosis 151, no. 1 (July 2000): 165. http://dx.doi.org/10.1016/s0021-9150(00)80751-0.

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7

Hutcheson, Jack. "Adipokines influence the inflammatory balance in autoimmunity." Cytokine 75, no. 2 (October 2015): 272–79. http://dx.doi.org/10.1016/j.cyto.2015.04.004.

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8

Ferrarelli, Leslie K. "New connections: Restoring immune balance." Science Signaling 13, no. 661 (December 8, 2020): eabf9854. http://dx.doi.org/10.1126/scisignal.abf9854.

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9

Wagener, Frank, Carine Carels, and Ditte Lundvig. "Targeting the Redox Balance in Inflammatory Skin Conditions." International Journal of Molecular Sciences 14, no. 5 (April 26, 2013): 9126–67. http://dx.doi.org/10.3390/ijms14059126.

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10

Esmaelzadeh, Abbas, Hassan Vosooghinia, Mohammad Reza Sheikhian, Hadi Bagheri Hosseini, Daryoush Hamidi Alamdari, Fatemeh Ahmadi, Maryam Emadzadeh, and Seyed Mahdi Pakdaman Shahri. "Pro-Oxidant Antioxidant Balance in Inflammatory Bowel Disease." International Journal of Clinical Medicine 07, no. 05 (2016): 334–41. http://dx.doi.org/10.4236/ijcm.2016.75035.

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11

Müller, B., U. Gimsa, N. A. Mitchison, and A. Radbruch. "Modulating the Th1/Th2 balance in inflammatory arthritis." Springer Seminars in Immunopathology 20, no. 1-2 (October 27, 1998): 181–96. http://dx.doi.org/10.1007/s002810050029.

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12

Goetzl, Laura, Susan Raine, Jose Rivers, Mary Ann Mastrangelo, David J. Tweardy, and Maya S. Suresh. "Maternal inflammatory balance and fetal exposure to hyperthermia." American Journal of Obstetrics and Gynecology 191, no. 6 (December 2004): S167. http://dx.doi.org/10.1016/j.ajog.2004.10.495.

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13

M�ller, B., U. Gimsa, N. A. Mitchison, A. Radbruch, J. Sieper, and Z. Yin. "Modulating the Th1/Th2 balance in inflammatory arthritis." Springer Seminars in Immunopathology 20, no. 1-2 (1998): 181–96. http://dx.doi.org/10.1007/bf00832006.

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14

Guenin, Sophie, Abrahem Kazemi, Abigail Cline, Steven R. Feldman, and Bijan Safai. "Rethinking the Inflammatory Balance in Psoriasis and Atherosclerosis." Journal of Drugs in Dermatology 22, no. 8 (July 1, 2023): 832–34. http://dx.doi.org/10.36849/jdd.7082.

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15

Myers, Jay L., and Jorie C. Allen. "Nutrition and Inflammation." American Journal of Lifestyle Medicine 6, no. 1 (October 13, 2011): 14–17. http://dx.doi.org/10.1177/1559827611424259.

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Evidence indicates that chronic diseases, such as cardiovascular disease, obesity, and asthma are part of a group of conditions linked by inflammatory dysregulation. One explanation for these associations is that the Western diet is obeseogenic and promotes the secretion of inflammatory biochemical signals. Weight gain results in lipid accumulation and adipocyte stress—factors known to disrupt the balance of systemic cell signaling (adipokines and cytokines) that favors inflammation. Markers are used as indicators of the inflammatory milieu and include the measurement of proinflammatory (C-reactive protein, interleukin-6, tumor necrosis factor-a) and anti-inflammatory (adiponectin) signaling molecules. Consumption of a high ratio of omega-6 to omega-3 fatty acids is also an important indicator for a potentially inflammatory profile. This ratio may determine the direction of biological pathways for another family of inflammatory mediators—eicosanoids—which vary according to the omega fatty acid precursor. An improved dietary pattern that emphasizes balanced energy and nutrient intake resulting in a reduced ratio of omega-6 to omega-3 fatty acids plays a particularly important role in inflammation management.

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16

Guan, Yulong, Caihong Wan, Shigang Wang, Peng Sun, and Cun Long. "Balanced Ultrafiltration: Inflammatory Mediator Removal Capacity." Artificial Organs 36, no. 10 (July 23, 2012): 894–900. http://dx.doi.org/10.1111/j.1525-1594.2012.01471.x.

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17

Kunst, Claudia, Stephan Schmid, Marlen Michalski, Deniz Tümen, Jonas Buttenschön, Martina Müller, and Karsten Gülow. "The Influence of Gut Microbiota on Oxidative Stress and the Immune System." Biomedicines 11, no. 5 (May 8, 2023): 1388. http://dx.doi.org/10.3390/biomedicines11051388.

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The human gastrointestinal tract is home to a complex microbial community that plays an important role in the general well-being of the entire organism. The gut microbiota generates a variety of metabolites and thereby regulates many biological processes, such as the regulation of the immune system. In the gut, bacteria are in direct contact with the host. The major challenge here is to prevent unwanted inflammatory reactions on one hand and on the other hand to ensure that the immune system can be activated when pathogens invade. Here the REDOX equilibrium is of utmost importance. This REDOX equilibrium is controlled by the microbiota either directly or indirectly via bacterial-derived metabolites. A balanced microbiome sorts for a stable REDOX balance, whereas dysbiosis destabilizes this equilibrium. An imbalanced REDOX status directly affects the immune system by disrupting intracellular signaling and promoting inflammatory responses. Here we (i) focus on the most common reactive oxygen species (ROS) and (ii) define the transition from a balanced REDOX state to oxidative stress. Further, we (iii) describe the role of ROS in regulating the immune system and inflammatory responses. Thereafter, we (iv) examine the influence of microbiota on REDOX homeostasis and how shifts in pro- and anti-oxidative cellular conditions can suppress or promote immune responses or inflammation.

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18

Rodrigues, Denise, Juliana Romanelli Marçal, Renata Samuel, Danielle Fernandes, Marcelo Araujo, Marcelo Napimoga, Sanivia Lima-Pereira, et al. "Th17/Treg immunoregulatory balance in human periapical lesions (47.5)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 47.5. http://dx.doi.org/10.4049/jimmunol.184.supp.47.5.

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Abstract Cysts and granulomas are chronic periapical lesions mediated by a set of inflammatory mediators that develop in order to contain a periapical infection. This study analyzed the inflammatory infiltrate, mast cells and in situ expression of cytokines, chemokines and FoxP3 in human periapical granulomas and cysts compared to controls. Fifty-five lesions (25 cysts, 25 granulomas and 5 controls) were analyzed. The type of inflammatory infiltrate was evaluated by HE staining and the presence of mast cells was analyzed by toluidine blue staining. Indirect immunohistochemistry was used to evaluate the expression of cytokines, chemokines and FoxP3. The inflammatory infiltrate mainly consisted of mononuclear cells. In cysts, mononuclear infiltrates were significantly more frequent than mixed (polymorphonuclear/mononuclear) infiltrates (p=0.04). Mixed inflammatory infiltrates were significantly more frequent in patients presenting fistulae (p=0.0001). The number of mast cells was significantly higher in granulomas than in cystic lesions (p=0.02). A significant difference in the expression of IL-17 (p=0.001) and TGF-β (p=0.003) was observed between cysts and granulomas and the control group. Significantly higher IL-17 levels were also observed in cases of patients with fistulae (p=0.03). Mast cells, TGF-β and IL-17 probably participate in the modulation of the inflammatory process in established periapical lesions, especially in granulomas.

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19

Proudfoot, Lorna. "Parasitic helminths tip the balance: potential anti-inflammatory therapies." Immunology 113, no. 4 (December 2004): 438–40. http://dx.doi.org/10.1111/j.1365-2567.2004.01996.x.

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20

SOMERVILLE, KEVIN, and GEORGE NOBLE. "Non-steroidal anti-inflammatory drugs: is the balance shifting?" Age and Ageing 26, no. 6 (1997): 417–22. http://dx.doi.org/10.1093/ageing/26.6.417.

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21

Sheikh, Amania A., and Daniel T. Utzschneider. "IRF2 integrates inflammatory signals to balance T cell exhaustion." Immunity 55, no. 12 (December 2022): 2225–27. http://dx.doi.org/10.1016/j.immuni.2022.11.010.

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22

Zhou, Yang, and Sabrina Bréchard. "Neutrophil Extracellular Vesicles: A Delicate Balance between Pro-Inflammatory Responses and Anti-Inflammatory Therapies." Cells 11, no. 20 (October 21, 2022): 3318. http://dx.doi.org/10.3390/cells11203318.

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Extracellular vesicles (EVs) are released in the extracellular environment during cell activation or apoptosis. Working as signal transducers, EVs are important mediators of intercellular communication through the convoying of proteins, nucleic acids, lipids, and metabolites. Neutrophil extracellular vesicles (nEVs) contain molecules acting as key modulators of inflammation and immune responses. Due to their potential as therapeutic tools, studies about nEVs have been increasing in recent years. However, our knowledge about nEVs is still in its infancy. In this review, we summarize the current understanding of the role of nEVs in the framework of neutrophil inflammation functions and disease development. The therapeutic potential of nEVs as clinical treatment strategies is deeply discussed. Moreover, the promising research landscape of nEVs in the near future is also examined.

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23

Rupali Kapoor, Rupali, Sakshi Chauhan, and Swapnil Saini. "Comparative study of Vatarakta w.s.r. to Gouty Arthritis." Journal of Ayurveda and Integrated Medical Sciences 8, no. 12 (February 1, 2024): 204–11. http://dx.doi.org/10.21760/jaims.8.12.30.

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A healthy lifestyle isn’t just diet and exercise. Today we go over the components of leading a healthy lifestyle and how it’s important to lead a balanced life. In general, most would agree that a healthy person doesn’t smoke, is at a healthy weight, eats a balanced healthy diet, thinks positively, feels relaxed, exercises regularly, has good relationships, and benefits from a good life balance. The World Health Organization in 1946 defined health as ‘A complete state of mental, physical and social well-being not merely the absence of disease’ Vatarakta is a metabolic condition where the most common symptom is pain, which interferes with the patients' daily lives. Vatarakta is named on the basis of the Vata dosha & Rakta dosha which have their own independent derivation & are the main Samprapti Ghatak involved in the Vatarakta. Gouty arthritis is a purine metabolic condition and an inflammatory reaction to the MSUM (Monosodium Urate Monohydrate) crystals that are produced as a result of hyperuricemia.

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24

Moutusy, Salvinaz Islam, and Seiichiroh Ohsako. "Gut Microbiome-Related Anti-Inflammatory Effects of Aryl Hydrocarbon Receptor Activation on Inflammatory Bowel Disease." International Journal of Molecular Sciences 25, no. 6 (March 16, 2024): 3372. http://dx.doi.org/10.3390/ijms25063372.

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Inflammatory bowel disease (IBD) is one of the most prevalent chronic inflammations of the gastrointestinal tract (GIT). The gut microbial population, the cytokine milieu, the aryl hydrocarbon receptor (AHR) expressed by immune and nonimmune cells and the intrinsic pathway of Th-cell differentiation are implicated in the immunopathology of IBD. AHR activation requires a delicate balance between regulatory and effector T-cells; loss of this balance can cause local gut microbial dysbiosis and intestinal inflammation. Thus, the study of the gut microbiome in association with AHR provides critical insights into IBD pathogenesis and interventions. This review will focus on the recent advancements to form conceptional frameworks on the benefits of AHR activation by commensal gut bacteria in IBD.

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25

Tsvinger, S. M., A. V. Govorin, and A. M. Karachenova. "Features of cytokine balance in patients with osteoarthrosis and atherosclerosis." Siberian Medical Review, no. 6 (2020): 70–74. http://dx.doi.org/10.20333/2500136-2020-6-70-74.

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The aim of the research is to study the content of some key pro / anti-inflammatory cytokines in patients with osteoarthritis and to evaluate their role in predicting atherogenesis in this category of patients. Material and methods. Patients with primary osteoarthritis of I-III radiological stages were examined. Doppler vessels ultrasound (Doppler ultrasound) of the neck, upper and lower extremities was performed; blood levels of pro / anti-inflammatory cytokines were examined: IL-1β, TNF-α, IL-6, IL- 8, IL-18, MCP-1, IL-17, IL-10, IL-33 by flow cytometry. Results. According to the thickness of intima - media complex, the patients were divided into 2 groups: with a normal thickness of intima - media complex and with atherosclerotic plaque. A significant increase in pro-inflammatory cytokines was revealed in patients with osteoarthritis associated with atherosclerosis compared with those having osteoarthritis with normal thickness of intima-media complex. The level of pro / anti-inflammatory cytokines along with atherosclerosis are closely interconnected. Conclusion. According to the results of the studies obtained, it was found that a long-term subclinical inflammatory process leads to multidirectional disturbances in cytokine balance in patients with osteoarthritis, which probably contributes to the progression of both osteoarthritis and atherosclerosis. A possible factor of early atherosclerosis development in patients with osteoarthritis was also identified.

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26

Tamburini, Bartolo, Marco Pio La Manna, Lidia La Barbera, Leila Mohammadnezhad, Giusto Davide Badami, Mojtaba Shekarkar Azgomi, Francesco Dieli, and Nadia Caccamo. "Immunity and Nutrition: The Right Balance in Inflammatory Bowel Disease." Cells 11, no. 3 (January 28, 2022): 455. http://dx.doi.org/10.3390/cells11030455.

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Inflammatory bowel disease (IBD) is an increasingly urgent medical problem that strongly impairs quality of life for patients. A global rise in incidence has been observed over the last few decades, with the highest incidence rates recorded in North America and Europe. Still, an increased incidence has been reported in the last ten years in newly industrialized countries in Asia, including China and India, both with more than one billion inhabitants. These data underline that IBD is an urgent global health problem. In addition, it is estimated that between 20% and 30% of IBD patients will develop colorectal cancer (CRC) within their lifetime and CRC mortality is approximately 50% amongst IBD patients. Although the exact etiology of IBD is still being defined, it is thought to be due to a complex interaction between many factors, including defects in the innate and adaptive immune system; microbial dysbiosis, i.e., abnormal levels of, or abnormal response to, the gastrointestinal microbiome; a genetic predisposition; and several environmental factors. At present, however, it is not fully understood which of these factors are the initiators of inflammation and which are compounders. The purpose of this review is to analyze the complex balance that exists between these elements to maintain intestinal homeostasis and prevent IBD or limit adverse effects on people’s health.

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LIAN, ZEQIN, XIAOYUAN PERRARD, CHRISTIE M. BALLANTYNE, and HUAIZHU WU. "1941-P: Aging Disturbs the Inflammatory Balance in Adipose Tissue." Diabetes 69, Supplement 1 (June 2020): 1941—P. http://dx.doi.org/10.2337/db20-1941-p.

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28

Mohamadzadeh, Mansour, Lieping Chen, Gene G. Olinger, William D. Pratt, and Alan L. Schmaljohn. "Filoviruses and the Balance of Innate, Adaptive, and Inflammatory Responses." Viral Immunology 19, no. 4 (December 2006): 602–12. http://dx.doi.org/10.1089/vim.2006.19.602.

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29

Lawrence, Catherine B. "Galanin-like peptide modulates energy balance by affecting inflammatory mediators?" Physiology & Behavior 97, no. 5 (July 2009): 515–19. http://dx.doi.org/10.1016/j.physbeh.2009.02.041.

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30

Fett, James D., and Aftab A. Ansari. "Inflammatory markers and cytokines in peripartum cardiomyopathy: a delicate balance." Expert Opinion on Therapeutic Targets 14, no. 9 (July 29, 2010): 895–98. http://dx.doi.org/10.1517/14728222.2010.511181.

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31

Bisschops, Laurens L. A., Cornelia W. E. Hoedemaekers, Tom E. Mollnes, and Johannes G. van der Hoeven. "Rewarming after hypothermia after cardiac arrest shifts the inflammatory balance*." Critical Care Medicine 40, no. 4 (April 2012): 1136–42. http://dx.doi.org/10.1097/ccm.0b013e3182377050.

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Tallman, Richard D., Mark Dumond, and David Brown. "Inflammatory mediator removal by zero-balance ultrafiltration during cardiopulmonary bypass." Perfusion 17, no. 2 (March 2002): 111–15. http://dx.doi.org/10.1191/0267659102pf540oa.

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The abnormal conditions to which blood is subjected during cardiopulmonary bypass (CPB) trigger an activation of the inflammatory response in all patients to varying degrees. Both complement activation and the release of cytokines characterize this response. Most inflammatory mediators have a molecular weight that is below the membrane pore size of commonly used ultrafilters, which should allow them to be freely filtered. However, some mediators have been shown to fail to cross through the membrane even though they are small enough to cross. The purpose of the present study was to determine whether certain inflammatory mediators could be removed by ultrafiltration when performed during the rewarming phase of CPB. Thirty adult patients undergoing a single, open-heart procedure were randomized to either control (no ultrafiltration) or to the zero-balance ultrafiltration (ZBUF) group. ZBUF was performed by removing 3 l/m2 blood using a 65-kDa ultrafilter with 1.3-m2 surface area. A volume of a balanced salt crystalloid solution (Plasmalyte) equal to the filtered blood volume was given to replace the fluid removed. Patient data was taken before CPB (T1), immediately following CPB (T2), and 12 h following the procedure (T3). The average volume of filtrate removed during ZBUF was 6405 ml, which was analyzed for the presence of interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TNF-α), C3a, and C5a. The average concentrations of the mediators measured in the effluent were: IL-1, 0.17 pg/ml; IL-6, 0.64 pg/ml; TNF-α, 1.25 ng/ml; C3a, 782.6 ng/ml; C5a, 25.6 ng/ml. In every case except for IL-1, the amounts of mediators removed were significantly greater than zero. This study demonstrates that ultrafiltration is a strategy that can be used during CPB in the adult to remove significant amounts of inflammatory mediators.

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33

Warner, Fiona J., John S. Lubel, Geoffrey W. McCaughan, and Peter W. Angus. "Liver fibrosis: a balance of ACEs?" Clinical Science 113, no. 3 (July 2, 2007): 109–18. http://dx.doi.org/10.1042/cs20070026.

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There is an increasing body of evidence to suggest that the RAS (renin–angiotensin system) contributes to tissue injury and fibrosis in chronic liver disease. A number of studies have shown that components of a local hepatic RAS are up-regulated in fibrotic livers of humans and in experimental animal models. Angiotensin II, the main physiological effector molecule of this system, mediates liver fibrosis by stimulating fibroblast proliferation (myofibroblast and hepatic stellate cells), infiltration of inflammatory cells, and the release of inflammatory cytokines and growth factors such as TGF (transforming growth factor)-β1, IL (interleukin)-1β, MCP (monocyte chemoattractant protein)-1 and connective tissue growth factor. Furthermore, blockade of the RAS by ACE (angiotensin-converting enzyme) inhibitors and angiotensin type 1 receptor antagonists significantly attenuate liver fibrosis in experimental models of chronic liver injury. In 2000 ACE2 (angiotensin-converting enzyme 2), a human homologue of ACE, was identified. ACE2 efficiently degrades angiotensin II to angiotensin-(1–7), a peptide which has recently been shown to have both vasodilatory and tissue protective effects. This suggests that ACE2 and its products may be part of an alternate enzymatic pathway in the RAS, which counterbalances the generation and actions of angiotensin II, the ACE2–angiotensin-(1–7)–Mas axis. This review focuses on the potential roles of the RAS, angiotensin II and ACE2 in chronic liver injury and fibrogenesis.

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Chebotareva, Natalya V., Anatoly A. Vinogradov, Alla A. Gindis, Irina N. Bobkova, Wenjing Cao, and Lidia V. Lysenko. "The balance of proinflammatory cytokines and Treg cells in chronic glomerulonephritis." Terapevticheskii arkhiv 92, no. 6 (July 9, 2020): 46–52. http://dx.doi.org/10.26442/00403660.2020.06.000671.

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Chronic glomerulonephritis (CGN) is a disease with a steadily progressing course, which is based on inflammation with the activation of immune cells. The severity of the inflammatory reaction in the kidney tissue is determined by the balance of locally pro-inflammatory factors and protective mechanisms, which include anti-inflammatory cytokines and T-regulatory lymphocytes (Treg). The study of processes that can modulate the severity of inflammation in the kidney is of particular interest for understanding the basic patterns of CGN progression. Aim. To determine the clinical significance of the Th17, Th1, and Treg cytokines in urine to assess the activity and progression of chronic glomerulonephritis with nephrotic syndrome (NS). Materials and methods. The study included 98 patients with CGN 37 women and 61 men. Patients were divided into two groups according to the degree of CGN activity. Group I consisted of 51 patients with NS. In 21 subjects, a decrease in GFR60 ml/min was revealed. Group II included 47 patients with proteinuria from 1 to 3 g/day without NS. GFR60 ml/min/1.73 m2 was observed in 26 patients. A kidney biopsy was performed in 65 patients and the hystological diagnosis was verified: 20 had mesangioproliferative GN, 16 had membranous nephropathy, 18 had focal segmental glomerulosclerosis, and 11 had membranoproliferative GN. The control group consisted of 15 healthy people. The levels of IL-6, IL-10, IL-17, tumor necrosis factor a (TNF-a) in the urine were determined using enzyme-linked immunosorbent assay. The number of FoxP3-positive cells in the inflammatory interstitial infiltrate of the cortical layer was determined in 39 patients (in a biopsy sample in a 1.5 mm2 area). Results. In group of patients with CGN, there was an increase in the levels of Th17, Th1, and Treg cytokines in urine TNF-a and IL-10 compared with healthy individuals. An increase in the levels of IL-6 in the urine of patients with high clinical activity of CGN (with NS and renal dysfunction) was more pronounced than in patients with NS and normal renal function. There was a decrease in the number of Treg cells in the interstitium of the kidney and a decrease in the production of anti-inflammatory IL-10 in CGN patients with NS, compared with patients without NS. The most pronounced changes in the cytokine profile were observed in patients with FSGS with an increase in pro-inflammatory cytokines and a decrease in Treg in the kidney tissue/anti-inflammatory IL-10 in the urine. Conclusion. An imbalance of cytokines characterized by an increased levels of pro-inflammatory IL-17, IL-6, TNF-a, and a reduced levels of anti-inflammatory IL-10 and T-regulatory cells in the kidney tissue is noted in patients with NS, especially with FSGS. Imbalance of cytokines reflects the high activity of CGN and the risk of the progression of the disease.

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35

Musolino, Caterina, Alessandro Allegra, Vanessa Innao, Andrea Gaetano Allegra, Giovanni Pioggia, and Sebastiano Gangemi. "Inflammatory and Anti-Inflammatory Equilibrium, Proliferative and Antiproliferative Balance: The Role of Cytokines in Multiple Myeloma." Mediators of Inflammation 2017 (2017): 1–24. http://dx.doi.org/10.1155/2017/1852517.

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Multiple myeloma (MM) is typically exemplified by a desynchronized cytokine system with increased levels of inflammatory cytokines. We focused on the contrast between inflammatory and anti-inflammatory systems by assessing the role of cytokines and their influence on MM. The aim of this review is to summarize the available information to date concerning this equilibrium to provide an overview of the research exploring the roles of serum cytokines in MM. However, the association between MM and inflammatory cytokines appears to be inadequate, and other functions, such as pro-proliferative or antiproliferative effects, can assume the role of cytokines in the genesis and progression of MM. It is possible that inflammation, when guided by cancer-specific Th1 cells, may inhibit tumour onset and progression. In a Th1 microenvironment, proinflammatory cytokines (e.g., IL-6 and IL-1) may contribute to tumour eradication by attracting leucocytes from the circulation and by increasing CD4+T cell activity. Hence, caution should be used when considering therapies that target factors with pro- or anti-inflammatory activity. Drugs that may reduce the tumour-suppressive Th1-driven inflammatory immune response should be avoided. A better understanding of the relationship between inflammation and myeloma will ensure more effective therapeutic interventions.

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36

Rosa, Luciana, Giselli Scaini, Camila B. Furlanetto, Leticia S. Galant, Francieli Vuolo, Dhébora M. Dall'Igna, Patrícia F. Schuck, Gustavo C. Ferreira, Felipe Dal‐Pizzol, and Emilio L. Streck. "Administration of branched‐chain amino acids alters the balance between pro‐inflammatory and anti‐inflammatory cytokines." International Journal of Developmental Neuroscience 48, no. 1 (November 30, 2015): 24–30. http://dx.doi.org/10.1016/j.ijdevneu.2015.11.002.

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Nicola Conran and Erich V. De Paula. "Thromboinflammatory mechanisms in sickle cell disease - challenging the hemostatic balance." Haematologica 105, no. 10 (May 21, 2020): 2380–90. http://dx.doi.org/10.3324/haematol.2019.239343.

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Sickle cell disease (SCD) is an inherited hemoglobinopathy that is caused by the presence of abnormal hemoglobin S (HbS) in red blood cells, leading to alterations in red cell properties and shape, as the result of HbS dexoygenation and subsequent polymerization. SCD pathophysiology is characterized by chronic inflammatory processes, triggered by hemolytic and vaso-occlusive events, which lead to the varied complications, organ damage and elevated mortality seen in individuals with the disease. In association with activation of the endothelium and leukocytes, hemostatic alterations and thrombotic events are well-documented in SCD. Here we discuss the role for inflammatory pathways in modulating coagulation and inducing platelet activation in SCD, due to tissue factor activation, adhesion molecule expression, inflammatory mediator production and the induction of innate immune responses, amongst other mechanisms. Thromboinflammatory pathways may play a significant role in some of the major complications of SCD, such as stroke, venous thromboembolism and possibly acute chest syndrome, besides exacerbating the chronic inflammation and cellular interactions that trigger vaso-occlusion, ischemia-reperfusion processes, and eventually organ damage.

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Barry, Rachael, David Ruano-Gallego, Shiva T. Radhakrishnan, Scott Lovell, Lu Yu, Olga Kotik, Izabela Glegola-Madejska, et al. "Faecal neutrophil elastase-antiprotease balance reflects colitis severity." Mucosal Immunology 13, no. 2 (November 26, 2019): 322–33. http://dx.doi.org/10.1038/s41385-019-0235-4.

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AbstractGiven the global burden of diarrheal diseases on healthcare it is surprising how little is known about the drivers of disease severity. Colitis caused by infection and inflammatory bowel disease (IBD) is characterised by neutrophil infiltration into the intestinal mucosa and yet our understanding of neutrophil responses during colitis is incomplete. Using infectious (Citrobacter rodentium) and chemical (dextran sulphate sodium; DSS) murine colitis models, as well as human IBD samples, we find that faecal neutrophil elastase (NE) activity reflects disease severity. During C. rodentium infection intestinal epithelial cells secrete the serine protease inhibitor SerpinA3N to inhibit and mitigate tissue damage caused by extracellular NE. Mice suffering from severe infection produce insufficient SerpinA3N to control excessive NE activity. This activity contributes to colitis severity as infection of these mice with a recombinant C. rodentium strain producing and secreting SerpinA3N reduces tissue damage. Thus, uncontrolled luminal NE activity is involved in severe colitis. Taken together, our findings suggest that NE activity could be a useful faecal biomarker for assessing disease severity as well as therapeutic target for both infectious and chronic inflammatory colitis.

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Kim, Jisu, Yoogyung Hong, Suji Baek, Kang Pa Lee, and Sanghyun Ahn. "The synergistic effect of physical activity and nutrition to improve the quality of life in breast cancer patients: a systemic review." Physical Activity and Nutrition 26, no. 4 (December 31, 2022): 022–31. http://dx.doi.org/10.20463/pan.2022.0021.

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[Purpose] Medical recommendations for balanced control of exercise, physical activity, and nutritional intake after breast cancer diagnosis remain unclear. Therefore, this review aims to summarize effective exercise methods and dietary opinions by reviewing clinical trial results.[Methods] We systematically reviewed studies that evaluated 1) the relationship between exercise methods and quality of life improvement in patients with breast cancer and 2) the recommendations for physical activity, exercise, nutrition, and potential ways to improve life after breast cancer. To conduct this literature review, we searched the PubMed database for articles published until October 1, 2022, using the terms “physical activity OR exercise,” “breast cancer,” and “nutrition.” After a primary review of the retrieved articles, we included clinical trials in this systematic review.[Results] We hypothesized that physical activity improves the quality of life after the onset of breast cancer, suggesting that a balanced approach to aerobic exercise and resistance exercise increases the efficacy of anticancer treatment. From a nutritional point of view, it is recommended that both physical activity and diet management are necessary for patients with breast cancer.[Conclusion] Customized exercise and diet can help with weight loss, the reduction of cancer-induced fatigue, the regulation of hormonal changes, the reduction of inflammatory factors, and the improvement of mental health and vitality. Understanding the integrated mechanisms of physical activity and nutritional balance will improve the quality of life of patients with breast cancer. Therefore, it is necessary to continuously advance exercise programs and develop an alimentary balance control program.

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Wang, Chun, Jun Yuan, Hua-xun Wu, Yan Chang, Qing-tong Wang, Yu-jing Wu, Li-hua Liu, and Wei Wei. "Paeoniflorin inhibits inflammatory responses in mice with allergic contact dermatitis by regulating the balance between inflammatory and anti-inflammatory cytokines." Inflammation Research 62, no. 12 (October 5, 2013): 1035–44. http://dx.doi.org/10.1007/s00011-013-0662-8.

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Thiviya, Punniamoorthy, Ashoka Gamage, Dinushika Piumali, Othmane Merah, and Terrence Madhujith. "Apiaceae as an Important Source of Antioxidants and Their Applications." Cosmetics 8, no. 4 (November 22, 2021): 111. http://dx.doi.org/10.3390/cosmetics8040111.

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The excess level of reactive oxygen species (ROS) disturbs the oxidative balance leading to oxidative stress, which, in turn, causes diabetes mellites, cancer, and cardiovascular diseases. These effects of ROS and oxidative stress can be balanced by dietary antioxidants. In recent years, there has been an increasing trend in the use of herbal products for personal and beauty care. The Apiaceae (previously Umbelliferae) family is a good source of antioxidants, predominantly phenolic compounds, therefore, widely used in the pharmaceutical, cosmetic, cosmeceutical, flavor, and perfumery industries. These natural antioxidants include polyphenolic acids, flavonoids, carotenoids, tocopherols, and ascorbic acids, and exhibit a wide range of biological effects, including anti-inflammatory, anti-aging, anti-atherosclerosis, and anticancer. This review discusses the Apiaceae family plants as an important source of antioxidants their therapeutic value and the use in cosmetics.

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JEFCOAT, A. M., J. G. WAGNER, and N. E. ROBINSON. "The neutrophil: understanding ancient and powerful responses in the inflammatory balance." Equine Veterinary Journal 35, no. 1 (January 5, 2010): 5–6. http://dx.doi.org/10.2746/042516403775467559.

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Roger, Anais, Ana Reynders, Guillaume Hoeffel, and Sophie Ugolini. "Neuroimmune crosstalk in the skin: a delicate balance governing inflammatory processes." Current Opinion in Immunology 77 (August 2022): 102212. http://dx.doi.org/10.1016/j.coi.2022.102212.

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Chang, Yaoyao, Lixiang Zhai, Jiao Peng, Haiqiang Wu, Zhaoxiang Bian, and Haitao Xiao. "Phytochemicals as regulators of Th17/Treg balance in inflammatory bowel diseases." Biomedicine & Pharmacotherapy 141 (September 2021): 111931. http://dx.doi.org/10.1016/j.biopha.2021.111931.

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McBride, William T., and Samuel J. McBride. "The balance of pro- and anti-inflammatory cytokines in cardiac surgery." Current Opinion in Anaesthesiology 11, no. 1 (February 1998): 15–22. http://dx.doi.org/10.1097/00001503-199802000-00004.

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Honda, T., H. Domon, T. Okui, K. Kajita, R. Amanuma, and K. Yamazaki. "Balance of inflammatory response in stable gingivitis and progressive periodontitis lesions." Clinical and Experimental Immunology 144, no. 1 (April 2006): 35–40. http://dx.doi.org/10.1111/j.1365-2249.2006.03028.x.

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Ng, Tien MH, and Myron L. Toews. "Impaired norepinephrine regulation of monocyte inflammatory cytokine balance in heart failure." World Journal of Cardiology 8, no. 10 (2016): 584. http://dx.doi.org/10.4330/wjc.v8.i10.584.

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Noack, Mélissa, and Pierre Miossec. "Th17 and regulatory T cell balance in autoimmune and inflammatory diseases." Autoimmunity Reviews 13, no. 6 (June 2014): 668–77. http://dx.doi.org/10.1016/j.autrev.2013.12.004.

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Ostrowski, Kenneth, Thomas Rohde, Sven Asp, Peter Schjerling, and Bente Klarlund Pedersen. "Pro- and anti-inflammatory cytokine balance in strenuous exercise in humans." Journal of Physiology 515, no. 1 (February 1999): 287–91. http://dx.doi.org/10.1111/j.1469-7793.1999.287ad.x.

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Ma, Jian, Ruiqing Wang, Xianfeng Fang, and Zuoming Sun. "PKC-θ shifts balance between inflammatory and regulatory T cells (123.42)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 123.42. http://dx.doi.org/10.4049/jimmunol.188.supp.123.42.

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Abstract We demonstrate here that PKC-θ is a critical molecule to maintain immunological balance by shifting the ratio of inflammatory Th17 and inhibitory Treg cells. TGFβ-induced T regulatory cell (iTreg) differentiation was enhanced in naive PKC-θ -/- T cells or WT cells treated with a specific PKC-θ inhibitor. PKC-θ -/- T cells had reduced activity of the AKT kinase, and the expression of a constitutively active form of AKT in PKC-θ -/- T cells restored ability to inhibit iTreg differentiation. Furthermore, knockdown or overexpression of the AKT downstream targets FoxO1 and FoxO3a was found to inhibit or promote iTreg differentiation in PKC-θ -/- T cells, indicating that the AKT-FoxO1/3A pathway plays an inhibitory role in the differentiation of iTreg downstream of PKC-θ. In the other hand, we show that naive PKC-θ -/- T cells were defective in Th17 differentiation in vitro, whereas in vitro differentiation of Th1 and Th2 appeared normal. PKC-θ -/- T cells had notably lower levels of Stat3, a transcription factor required for Th17 differentiation. PKC-θ-mediated activation of the Stat3 promoter was inhibited by dominant negative AP-1 and IκB kinase β mutations, but stimulated by WT AP-1 and IκB kinase β, suggesting that PKC-θ stimulates Stat3 transcription via the AP-1 and NF-κB pathways. We conclude that PKC-θ is able to control T cell-mediated immune responses by shifting the balance between the differentiation of Th17 inflammatory and regulatory T cells.

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