Journal articles: 'Inflammation balance'

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Pravinkumar, Egbert. "Balance of Inflammation in Sepsis." American Journal of Respiratory and Critical Care Medicine 169, no. 5 (March 2004): 655–56. http://dx.doi.org/10.1164/ajrccm.169.5.954.

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Wiesner, Darin L., and Bruce S. Klein. "The balance between immunity and inflammation." Science 357, no. 6355 (September 7, 2017): 973–74. http://dx.doi.org/10.1126/science.aao3086.

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Leza, Juan C., Borja García-Bueno, Miquel Bioque, Celso Arango, Mara Parellada, Kim Do, Patricio O’Donnell, and Miguel Bernardo. "Inflammation in schizophrenia: A question of balance." Neuroscience & Biobehavioral Reviews 55 (August 2015): 612–26. http://dx.doi.org/10.1016/j.neubiorev.2015.05.014.

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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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Chan, Chi Hang, Valeria On Yue Leung, Mary Sau Man Ip, and Daisy Kwok Yan Shum. "HS/syndecan modulate proteolytic balance in airway inflammation." Matrix Biology 27 (December 2008): 56. http://dx.doi.org/10.1016/j.matbio.2008.09.406.

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Covarrubias, Anthony J., and Tiffany Horng. "IL-6 Strikes a Balance in Metabolic Inflammation." Cell Metabolism 19, no. 6 (June 2014): 898–99. http://dx.doi.org/10.1016/j.cmet.2014.05.009.

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Tadokoro, Carlos E. "The Delicate Balance Between Inflammation, Conception and Pregnancy." American Journal of Reproductive Immunology 68, no. 5 (June 5, 2012): 363–65. http://dx.doi.org/10.1111/j.1600-0897.2012.01162.x.

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Faenza, Irene, and William L. Blalock. "Innate Immunity: A Balance between Disease and Adaption to Stress." Biomolecules 12, no. 5 (May 23, 2022): 737. http://dx.doi.org/10.3390/biom12050737.

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Since first being documented in ancient times, the relation of inflammation with injury and disease has evolved in complexity and causality. Early observations supported a cause (injury) and effect (inflammation) relationship, but the number of pathologies linked to chronic inflammation suggests that inflammation itself acts as a potent promoter of injury and disease. Additionally, results from studies over the last 25 years point to chronic inflammation and innate immune signaling as a critical link between stress (exogenous and endogenous) and adaptation. This brief review looks to highlight the role of the innate immune response in disease pathology, and recent findings indicating the innate immune response to chronic stresses as an influence in driving adaptation.

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Lark, Daniel S., and David H. Wasserman. "Meta-fibrosis links positive energy balance and mitochondrial metabolism to insulin resistance." F1000Research 6 (September 27, 2017): 1758. http://dx.doi.org/10.12688/f1000research.11653.1.

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Obesity and insulin resistance often emerge from positive energy balance and generally are linked to low-grade inflammation. This low-grade inflammation has been called “meta-inflammation” because it is a consequence of the metabolic dysregulation that can accompany overnutrition. One means by which meta-inflammation is linked to insulin resistance is extracellular matrix expansion secondary to meta-inflammation, which we define here as “meta-fibrosis”. The significance of meta-fibrosis is that it reflects a situation in which the extracellular matrix functions as a multi-level integrator of local (for example, mitochondrial reactive oxygen species production) and systemic (for example, inflammation) inputs that couple to cellular processes creating insulin resistance. While adipose tissue extracellular matrix remodeling has received considerable attention, it is becoming increasingly apparent that liver and skeletal muscle extracellular matrix remodeling also contributes to insulin resistance. In this review, we address recent advances in our understanding of energy balance, mitochondrial energetics, meta-inflammation, and meta-fibrosis in the development of insulin resistance.

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Cavanagh, Mary M., Cornelia M. Weyand, and Jörg J. Goronzy. "Chronic inflammation and aging: DNA damage tips the balance." Current Opinion in Immunology 24, no. 4 (August 2012): 488–93. http://dx.doi.org/10.1016/j.coi.2012.04.003.

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Zimmermann, Nives, and Marc E. Rothenberg. "The arginine–arginase balance in asthma and lung inflammation." European Journal of Pharmacology 533, no. 1-3 (March 2006): 253–62. http://dx.doi.org/10.1016/j.ejphar.2005.12.047.

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Nurieva, Roza I., Yang-Zhi Zhao, Andrei Alekseev, Elena Galkina, and Sang T. Kim. "Role of Grail in intestinal inflammation." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 111.27. http://dx.doi.org/10.4049/jimmunol.208.supp.111.27.

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Abstract Intestinal homeostasis depends on interaction between the microbiota and host immune system, and disruption of this balance results in predominance of inflammatory responses leading to inflammatory bowel disease. However, to date, precise cell-intrinsic regulatory mechanisms that controls intestinal inflammation are poorly understood. Here we show that expression of the E3 ubiquitin ligase Grail is diminished in colon tissues of mice with colitis and Grail deficiency leads to increased susceptibility to colitis. Importantly, Grail deficiency disrupted pro-/anti-inflammatory balance towards inflammatory immune responses at the steady state and during colitis. Mechanistically, loss of Grail intrinsically diminished the expression of IL-10 and IL-10 receptor (IL-10R) by adaptive and innate immune cells in colonic mucosa. Besides the intestinal immunity, Grail deficiency leads to a decrease in microbial diversity and an enrichment of pro-inflammatory microbiota. Thus, Grail plays a protective role during intestinal inflammation by supporting regulatory immune responses and shaping the microbiota.

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Hou, Jingyi, Rui Yang, Ivan Vuong, Fangqi Li, Jiayuan Kong, and Hai-Quan Mao. "Biomaterials strategies to balance inflammation and tenogenesis for tendon repair." Acta Biomaterialia 130 (August 2021): 1–16. http://dx.doi.org/10.1016/j.actbio.2021.05.043.

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Steiner, Alexandre A., and Andrej A. Romanovsky. "Leptin: At the crossroads of energy balance and systemic inflammation." Progress in Lipid Research 46, no. 2 (March 2007): 89–107. http://dx.doi.org/10.1016/j.plipres.2006.11.001.

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Badjatia, N., A. Monahan, A. Carpenter, J. Zimmerman, J. M. Schmidt, J. Claassen, E. S. Connolly, S. A. Mayer, W. Karmally, and D. Seres. "Inflammation, negative nitrogen balance, and outcome after aneurysmal subarachnoid hemorrhage." Neurology 84, no. 7 (January 16, 2015): 680–87. http://dx.doi.org/10.1212/wnl.0000000000001259.

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Rygiel, Tomasz P., and Linde Meyaard. "CD200R signaling in tumor tolerance and inflammation: A tricky balance." Current Opinion in Immunology 24, no. 2 (April 2012): 233–38. http://dx.doi.org/10.1016/j.coi.2012.01.002.

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Lauridsen, Charlotte. "From oxidative stress to inflammation: redox balance and immune system." Poultry Science 98, no. 10 (October 2019): 4240–46. http://dx.doi.org/10.3382/ps/pey407.

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Kagnoff, M. F. "A question of balance: ups and downs of mucosal inflammation." Journal of Clinical Investigation 94, no. 1 (July 1, 1994): 1. http://dx.doi.org/10.1172/jci117294.

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Giraud, Thomas, Charlotte Jeanneau, Charlotte Rombouts, Hengameh Bakhtiar, Patrick Laurent, and Imad About. "Pulp capping materials modulate the balance between inflammation and regeneration." Dental Materials 35, no. 1 (January 2019): 24–35. http://dx.doi.org/10.1016/j.dental.2018.09.008.

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Kadatane, Saurav Prashant, Matthew Satariano, Michael Massey, Kai Mongan, and Rupesh Raina. "The Role of Inflammation in CKD." Cells 12, no. 12 (June 7, 2023): 1581. http://dx.doi.org/10.3390/cells12121581.

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Chronic kidney disease (CKD) affects many adults worldwide. Persistent low-grade inflammation is a substantial factor in its development and progression and has correlated with increased mortality and cardiovascular problems. This low-grade inflammation is a product of dysregulation of the normal balance between pro- and anti-inflammatory markers. Various factors such as increased innate immune system activation, reactive oxygen species production, periodontal disease, dysregulation of anti-inflammatory systems and intestinal dysbiosis result in the dysregulation of this balance. Furthermore, this low-grade inflammation has down-effects such as hypertension, renal fibrosis and acceleration of renal function decline. Moreover, low-grade inflammation over time has been linked to malignancy in CKD. As CKD progresses, many patients require dialysis, which has a negative bidirectional relationship with persistent inflammation. Treatment options for inflammation in CKD are vast, including cytokine inhibitors, statins and diets. However, more research is needed to create a standardized management plan. In this review, we will examine the normal physiology of the kidney and its relationship with the immune system. We will then delve into the pathology behind persistent inflammation, the various causes of inflammation, the downstream effects of inflammation, dialysis and potential treatments for inflammation in CKD.

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Sokolovskaya, Irina, Valentina Nechiporenko, Natalia Gordiyenko, Olena Pozdnyakova, Svitlana Volkova, Victor Cymbal, and Galina Makurina. "Lipid peroxidation during chronic inflammation." French-Ukrainian Journal of Chemistry 6, no. 2 (2018): 38–53. http://dx.doi.org/10.17721/fujcv6i2p38-53.

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To keep needed level of peroxide lipid oxidation is necessary for the normal functioning of physiological systems. It is supported by the balance of anti-and prooxidant systems. The positive influence of lipid peroxidation processes in the organism is manifested by the restoration of the composition and maintenance of the properties of biological membranes, participation in energy processes, cell division, synthesis of biologically active substances. It has been established that the inflammatory process is accompanied by changes in lipid metabolism and the intensity of peroxide oxidation.

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Martin, Kylie, Sven-Jean Tan, and Nigel D. Toussaint. "Total Body Sodium Balance in Chronic Kidney Disease." International Journal of Nephrology 2021 (September 22, 2021): 1–10. http://dx.doi.org/10.1155/2021/7562357.

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Excess sodium intake is a leading but modifiable risk factor for mortality, with implications on hypertension, inflammation, cardiovascular disease, and chronic kidney disease (CKD). This review will focus mainly on the limitations of current measurement methods of sodium balance particularly in patients with CKD who have complex sodium physiology. The suboptimal accuracy of sodium intake and excretion measurement is seemingly more marked with the evolving understanding of tissue (skin and muscle) sodium. Tissue sodium represents an extrarenal influence on sodium homeostasis with demonstrated clinical associations of hypertension and inflammation. Measurement of tissue sodium has been largely unexplored in patients with CKD. Development and adoption of more comprehensive and dynamic assessment of body sodium balance is needed to better understand sodium physiology in the human body and explore therapeutic strategies to improve the clinical outcomes in the CKD population.

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Zhang, Zhiyou, Wenyi Zhang, Dae Young Jung, Hwi Jin Ko, Yongjin Lee, Randall H. Friedline, Eunjung Lee, et al. "TRPM2 Ca2+ channel regulates energy balance and glucose metabolism." American Journal of Physiology-Endocrinology and Metabolism 302, no. 7 (April 1, 2012): E807—E816. http://dx.doi.org/10.1152/ajpendo.00239.2011.

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TRPM2 Ca2+-permeable cation channel is widely expressed and activated by markers of cellular stress. Since inflammation and stress play a major role in insulin resistance, we examined the role of TRPM2 Ca2+ channel in glucose metabolism. A 2-h hyperinsulinemic euglycemic clamp was performed in TRPM2-deficient (KO) and wild-type mice to assess insulin sensitivity. To examine the effects of diet-induced obesity, mice were fed a high-fat diet for 4–10 mo, and metabolic cage and clamp studies were conducted in conscious mice. TRPM2-KO mice were more insulin sensitive partly because of increased glucose metabolism in peripheral organs. After 4 mo of high-fat feeding, TRPM2-KO mice were resistant to diet-induced obesity, and this was associated with increased energy expenditure and elevated expressions of PGC-1α, PGC-1β, PPARα, ERRα, TFAM, and MCAD in white adipose tissue. Hyperinsulinemic euglycemic clamps showed that TRPM2-KO mice were more insulin sensitive, with increased Akt and GSK-3β phosphorylation in heart. Obesity-mediated inflammation in adipose tissue and liver was attenuated in TRPM2-KO mice. Overall, TRPM2 deletion protected mice from developing diet-induced obesity and insulin resistance. Our findings identify a novel role of TRPM2 Ca2+ channel in the regulation of energy expenditure, inflammation, and insulin resistance.

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Kohlhapp, Frederick, Andrew Zloza, James McCracken, Jeremy O'Sullivan, Michael Jagoda, Andrew Lacek, and José Guevara-Patiño. "CD8+ T cells adversely effect their own memory potential via the regulation of the IL-12/IL-15Rα axis (52.32)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 52.32. http://dx.doi.org/10.4049/jimmunol.186.supp.52.32.

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Abstract Current paradigms establish that CD8+ T cell memory potential is adversely affected by the degree of inflammation during an effector response. However, the regulation of this balance between inflammation and memory potential remains poorly understood. Here we demonstrate that CD8+ T cells, themselves, limit their own memory potential through direct regulation of inflammatory cytokine production by antigen presenting cells (APCs) during vaccination. By depleting CD8+ T cells during vaccination, we show augmented formation of memory precursor effector cells (MPECs), which results in the enhanced quantity (antigen-specific CD8+ T cell number) and quality (cytolytic function) of the resulting memory responses. Furthermore, we show that CD8+ T cells promote inflammation and shift the balance towards terminal effector CD8+ T cell responses by increasing IL-12 production and decreasing IL-15Rα expression by APCs in an IFN-γ-dependent manner. These results identify an unrecognized role for CD8+ T cells in the regulation of their own effector differentiation fate and a previously uncharacterized relationship between the balance of inflammation (IFN-γ, IL-12) and memory formation (IL-15Rα).

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Kwon, So Yeon, Karen Massey, Mark A. Watson, Tayab Hussain, Giacomo Volpe, Christopher D. Buckley, Anna Nicolaou, and Paul Badenhorst. "Oxidised metabolites of the omega-6 fatty acid linoleic acid activate dFOXO." Life Science Alliance 3, no. 2 (January 28, 2020): e201900356. http://dx.doi.org/10.26508/lsa.201900356.

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Obesity-induced inflammation, or meta-inflammation, plays key roles in metabolic syndrome and is a significant risk factor in diabetes and cardiovascular disease. To investigate causal links between obesity, meta-inflammation, and insulin signaling we established a Drosophila model to determine how elevated dietary fat and changes in the levels and balance of saturated fatty acids (SFAs) and polyunsaturated fatty acids (PUFAs) influence inflammation. We observe negligible effect of saturated fatty acid on inflammation but marked enhancement or suppression by omega-6 and omega-3 PUFAs, respectively. Using combined lipidomic and genetic analysis, we show omega-6 PUFA enhances meta-inflammation by producing linoleic acid–derived lipid mediator 9-hydroxy-octadecadienoic acid (9-HODE). Transcriptome analysis reveals 9-HODE functions by regulating FOXO family transcription factors. We show 9-HODE activates JNK, triggering FOXO nuclear localisation and chromatin binding. FOXO TFs are important transducers of the insulin signaling pathway that are normally down-regulated by insulin. By activating FOXO, 9-HODE could antagonise insulin signaling providing a molecular conduit linking changes in dietary fatty acid balance, meta-inflammation, and insulin resistance.

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DeFuria, Jason, Madhu Jagannathan-Bogdan, Ramya Kuchibhatla, Marie McDonnell, Caroline Apovian, Barbara Nikolajczyk, and Gerald Denis. "B lymphocytes regulate a pro-inflammatory T cell balance in human Type 2 diabetes (P3101)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 43.12. http://dx.doi.org/10.4049/jimmunol.190.supp.43.12.

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Abstract Lymphocytes play key roles in the chronic inflammation critical for T2D pathogenesis. We have shown T2D patients have an elevated ratio of pro- to anti-inflammatory T cells, and B cells that produce a pro-inflammatory cytokine profile. Thus lymphocytes promote T2D-associated inflammation. Numerous studies implicate the pro-inflammatory CD4+ T cell balance in T2D pathogenesis, but mechanisms that underlie elevated CD4+ T cell inflammation are poorly understood. We explored the possibility that the T2D-associated changes we identified in B cell function regulate T cell inflammation. We show that B cells control the T2D-associated increase in Th17-mediated inflammation in T2D patients and in obese/insulin resistant mice. Surprisingly, the disease-associated ability of B cells to regulate T cell function is contact-dependent, despite evidence that B cell cytokines hyper-secreted in T2D patients activate T cells. In contrast, elevated activation of Th1 cytokines is B cell-independent. We conclude that both T cell-intrinsic and T cell-extrinsic (B cell-dependent) changes regulate T cell inflammation in T2D. These data indicate that B cell depletion may partially curb T2D-associated T cell inflammation, and thus disease pathogenesis; however, combinatorial treatments aimed at multiple inflammatory axes may be required for favorable clinical outcomes.

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Grigoryev, E. V., V. G. Matveeva, D. L. Shukevich, A. S. Radivilko, E. A. Velikanova, and M. Yu Khanova. "Induced immunosuppression in critical care: diagnostic opportunities in clinical practice." Bulletin of Siberian Medicine 18, no. 1 (May 16, 2019): 18–29. http://dx.doi.org/10.20538/1682-0363-2019-1-18-29.

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The immune system in critical illnesses initiates local inflammation in the damaged area. In the absence of a balance between local and systemic inflammations, an infectious or non-infectious systemic inflammatory response follows, which has a stage of "hyper inflammation - compensatory anti-inflammatory response", that may result in multi-organ failure. The final stage of critical ill-nesses, therefore, will be characterized by induced immunosuppression with the impaired function of neutrophils, monocytes, macrophages and dendritic cells and release of myeloid-derived suppres-sor cells. The aim of the review is to evaluate the contribution of various components of the im-mune response to the formation of induced immune suppression from the perspective of candidate diagnostic markers.

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Yuan, Qing, Z. L. Zeng, Shiqi Yang, Anqi Li, Xuyu Zu, and Jianghua Liu. "Mitochondrial Stress in Metabolic Inflammation: Modest Benefits and Full Losses." Oxidative Medicine and Cellular Longevity 2022 (November 22, 2022): 1–17. http://dx.doi.org/10.1155/2022/8803404.

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Energy intake and metabolic balance are the pillars of health preservation. Overnutrition causes nonspecific, persistently low inflammatory state known as metabolic inflammation. This condition contributes to the pathophysiology of various metabolic disorders, such as atherosclerosis, obesity, diabetes mellitus, and metabolic syndrome. The mitochondria maintain the balance of energy metabolism. Excessive energy stress can lead to mitochondrial dysfunction, which promotes metabolic inflammation. The inflammatory environment further impairs mitochondrial function. Accordingly, excellent organism design keeps the body metabolically healthy in the context of mitochondrial dysfunction, and moderate mitochondrial stress can have a beneficial effect. This review summarises the research progress on the multifaceted characterisation of mitochondrial dysfunction and its role in metabolic inflammation.

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Zhang, Jingxiao, Jiakun Tian, Hongzhi Sun, Kumar Digvijay, Mauro Neri, Vinant Bhargava, Yongjie Yin, and Claudio Ronco. "How Does Continuous Renal Replacement Therapy Affect Septic Acute Kidney Injury?" Blood Purification 46, no. 4 (2018): 326–31. http://dx.doi.org/10.1159/000492026.

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Sepsis is the leading cause of acute kidney injury (AKI) in the intensive care unit. As the most common treatment of septic AKI, it is believed that continuous renal replacement therapy (CRRT) can not only maintain the water balance and excrete the metabolic products but also regulate the inflammation and promote kidney recovery. CRRT can remove the inflammatory cytokines to regulate the metabolic adaption in kidney and restore the kidney recovery to protect the kidney in septic AKI. Second, CRRT can provide extra energy supply in septic AKI to improve the kidney energy balance in septic AKI. Third, the anticoagulant used in CRRT also regulates the inflammation in septic AKI. CRRT is not only a treatment to deal with the water balance and metabolic products, but also a method to regulate the inflammation in septic AKI. Video Journal Club ‘Cappuccino with Claudio Ronco’ at https://www.karger.com/Journal/ArticleNews/223997?sponsor=52.

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Biolik, Grzegorz, Dariusz Gajniak, Maciej Kubicz, Damian Ziaja, Krzysztof Ziaja, and Wacław Kuczmik. "The Influence of Inflammation on Fibrinogen Turnover and Redistribution of the Hemostatic Balance to a Prothrombotic State in High On-Treatment Platelet Reactivity-Dual Poor Responder (HTPR-DPR) Patients." Mediators of Inflammation 2019 (July 17, 2019): 1–6. http://dx.doi.org/10.1155/2019/3767128.

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Knowledge about the influence of inflammation on platelet function and relocation of hemostatic balance to hypercoagulable state is still unclear. We compared two groups of patients who suffer from acute vs. chronic inflammatory process and additionally present high on-treatment platelet reactivity-dual platelet resistance. We did not found any differences in platelet aggregation between both investigated groups, but patients who suffer from chronic inflammation presented stronger relocation of the hemostatic balance to the hypercoagulability. A high concentration of prothrombin fragment F1+2 together with higher activity of von Willebrand factor in critical limb ischemia shows more exaggerated fibrinogen turnover although the blood concentration of this factor was in normal range. We concluded that high on-treatment platelet reactivity-dual platelet resistance and intensified inflammation are linked with elevated platelet and fibrinogen turnover to counteract proper hemostatic balance in favor of a prothrombotic state.

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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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Bellanti, Francesco, Aurelio Lo Buglio, Michał Dobrakowski, Aleksandra Kasperczyk, Sławomir Kasperczyk, Gaetano Serviddio, and Gianluigi Vendemiale. "Adherence to Mediterranean Diet and Biomarkers of Redox Balance and Inflammation in Old Patients Hospitalized in Internal Medicine." Nutrients 16, no. 19 (October 2, 2024): 3359. http://dx.doi.org/10.3390/nu16193359.

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Background/Objectives: We have previously described that low adherence to the Mediterranean diet (MD) in elderly patients admitted in internal medicine wards is linked to poorer clinical outcomes. This investigation was designed to explore whether adherence to the MD is related to circulating markers of redox balance and inflammation in this clinical scenario. Methods: A cross-sectional study was performed on 306 acute old patients hospitalized in internal medicine wards. Adherence to the MD was estimated by the Italian Mediterranean Index (IMI). The circulating markers of redox balance were assessed in serum and erythrocytes and correlated with inflammatory markers across different MD adherence groups. Results: Compared to the patients with high adherence, those with low adherence to the MD exhibited severely impaired redox balance, as evidenced by a higher GSSG/GSH ratio and increased serum hydroxynonenal/malondialdehyde–protein adducts. No modifications were described in the expression of antioxidant enzymes in peripheral blood mononuclear cells. Patients with low adherence to the MD exhibited a higher neutrophil-to-lymphocyte ratio and markers of systemic inflammation, as well as raised levels of interleukin-6 and tumor necrosis factor, compared to those with high MD adherence. A strong association was observed between the circulating markers of redox balance and inflammation/immune response, with the highest regression coefficients found in the low adherence group. Conclusions: Old patients admitted to internal medicine wards with low adherence to the MD display unfavorable profiles of the circulating markers of redox balance and inflammation. It is conceivable that such effects on redox balance can be linked to the high polyphenol content of MD. This study supports the rationale for intervention trials that attest to the effectiveness of MD as a nutritional strategy for disease prevention.

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Soliman, Amro M., and Daniel R. Barreda. "Acute Inflammation in Tissue Healing." International Journal of Molecular Sciences 24, no. 1 (December 30, 2022): 641. http://dx.doi.org/10.3390/ijms24010641.

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There are well-established links between acute inflammation and successful tissue repair across evolution. Innate immune reactions contribute significantly to pathogen clearance and activation of subsequent reparative events. A network of molecular and cellular regulators supports antimicrobial and tissue repair functions throughout the healing process. A delicate balance must be achieved between protection and the potential for collateral tissue damage associated with overt inflammation. In this review, we summarize the contributions of key cellular and molecular components to the acute inflammatory process and the effective and timely transition toward activation of tissue repair mechanisms. We further discuss how the disruption of inflammatory responses ultimately results in chronic non-healing injuries.

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Hashemi, Seyed Mahmoud. "Immune Regulation by Regulatory Cells." Immunoregulation 5, no. 1 (July 1, 2022): 1–2. http://dx.doi.org/10.32598/immunoregulation.5.1.8.

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Inflammation is a protective response that occurs in response to tissue injury and microbial infections. A significant advancement has been made in our understanding of inflammation, which is one of the most fundamental concepts in medicine. Immunoregulation of immune-mediated inflammatory diseases depends on Th17/Treg balance. Costimulatory receptors, cytokines, metabolic pathways, and the intestinal microbiome all affect this balance in inflammatory conditions. Maintaining a functional equilibrium between these two subsets is very important to design an appropriate and effective treatment strategy.

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McNally, Leah, Zubin Bhagwagar, and Jonas Hannestad. "Inflammation, Glutamate, and Glia in Depression: A Literature Review." CNS Spectrums 13, no. 6 (June 2008): 501–10. http://dx.doi.org/10.1017/s1092852900016734.

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ABSTRACTMultiple lines of evidence suggest that inflammation and glutamate dysfunction contribute to the pathophysiology of depression. In this review we provide an overview of how these two systems may interact. Excess levels of inflammatory mediators occur in a subgroup of depressed patients. Studies of acute experimental activation of the immune system with endotoxin and of chronic activation during interferon-α treatment show that inflammation can cause depression. Peripheral inflammation leads to microglial activation which could interfere with excitatory amino acid metabolism leading to inappropriate glutamate receptor activation. Loss of astroglia, a feature of depression, upsets the balance of anti- and pro-inflammatory mediators and further impairs the removal of excitatory amino acids. Microglia activated by excess inflammation, astroglial loss, and inappropriate glutamate receptor activation ultimately disrupt the delicate balance of neuroprotective versus neurotoxic effects in the brain, potentially leading to depression.

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Wang, Zengfang, Ruizhen Yang, Jiaojiao Zhang, Pingping Wang, Zengyan Wang, Jian Gao, and Xue Liu. "Role of Extracellular Vesicles in Placental Inflammation and Local Immune Balance." Mediators of Inflammation 2021 (June 18, 2021): 1–10. http://dx.doi.org/10.1155/2021/5558048.

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Background. Pregnancy maintenance depends on the formation of normal placentas accompanied by trophoblast invasion and vascular remodeling. Various types of cells, such as trophoblasts, endothelial cells, immune cells, mesenchymal stem cells (MSCs), and adipocytes, mediate cell-to-cell interactions through soluble factors to maintain normal placental development. Extracellular vesicles (EVs) are diverse nanosized to microsized membrane-bound particles released from various cells. EVs contain tens to thousands of different RNA, proteins, small molecules, DNA fragments, and bioactive lipids. EV-derived microRNAs (miRNAs) and proteins regulate inflammation and trophoblast invasion in the placental microenvironment. Maternal-fetal communication through EV can regulate the key signaling pathways involved in pregnancy maintenance, from implantation to immune regulation. Therefore, EVs and the encapsulating factors play important roles in pregnancy, some of which might be potential biomarkers. Conclusion. In this review, we have summarized published studies about the EVs in the placentation and pregnancy-related diseases. By summarizing the role of EVs and their delivering active molecules in pregnancy-related diseases, it provides novel insight into the diagnosis and treatment of diseases.

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Russa, Daniele La, Daniela Pellegrino, Alberto Montesanto, Paolo Gigliotti, Anna Perri, Antonella La Russa, and Renzo Bonofiglio. "Oxidative Balance and Inflammation in Hemodialysis Patients: Biomarkers of Cardiovascular Risk?" Oxidative Medicine and Cellular Longevity 2019 (February 11, 2019): 1–7. http://dx.doi.org/10.1155/2019/8567275.

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During chronic kidney disease, the progressive deterioration of renal function induces several biological/clinical dysfunctions, including enhancement of synthesis of inflammation/oxidative stress mediators. Impaired renal function is an independent cardiovascular risk factor; indeed, cardiovascular complications dominate the landscape of both chronic kidney disease and end-stage renal disease. The aim of this study is to explore the correlation between the global oxidative balance in hemodialysis patients and both inflammatory markers and cardiovascular events. Using photometric tests, this study explored plasmatic oxidative balance in 97 hemodialysis patients compared to a healthy population. In the hemodialysis patients, we showed that oxidative stress values were significantly lower than in controls while effectiveness in the antioxidant barrier was significantly increased in the hemodialysis group. Furthermore, we highlighted a strong correlation between oxidative index and blood levels of C-reactive protein. When patients were divided into two groups based on previous cardiovascular events, we found that subjects with previous cardiovascular events had higher values of both oxidative stress and antioxidant barrier than patients without cardiovascular events. Our results indicated that in hemodialysis patients, the clinical and prognostic significance of oxidative status is very different from general population. As cardiovascular complications represent a strong negative factor for survival of hemodialysis patients, the research of new cardiovascular risk biomarkers in these patients takes on particular importance in order to translate them into clinical practice/primary care.

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Penn, Marc S., and Chinedu Igwe. "Role of Inflammation in Modulating Thrombotic–Fibrinolytic Balance in Venous Thrombosis." Circulation Research 119, no. 12 (December 9, 2016): 1256–57. http://dx.doi.org/10.1161/circresaha.116.310105.

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Matyszak, M. "Inflammation in the CNS: balance between immunological privilege and immune responses." Progress in Neurobiology 56, no. 1 (September 1, 1998): 19–35. http://dx.doi.org/10.1016/s0301-0082(98)00014-8.

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Hube, B., R. Hay, J. Brasch, S. Veraldi, and M. Schaller. "Dermatomycoses and inflammation: The adaptive balance between growth, damage, and survival." Journal de Mycologie Médicale 25, no. 1 (March 2015): e44-e58. http://dx.doi.org/10.1016/j.mycmed.2014.11.002.

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Dyson, Alex, Nathan S. Bryan, Bernadette O. Fernandez, Maria-Francisca Garcia-Saura, Fumito Saijo, Nicolas Mongardon, Juan Rodriguez, Mervyn Singer, and Martin Feelisch. "An integrated approach to assessing nitroso-redox balance in systemic inflammation." Free Radical Biology and Medicine 51, no. 6 (September 2011): 1137–45. http://dx.doi.org/10.1016/j.freeradbiomed.2011.06.012.

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Liu, Yuting, Shuai Zong, and Jinglei Li. "Carboxymethyl chitosan perturbs inflammation profile and colonic microbiota balance in mice." Journal of Food and Drug Analysis 28, no. 1 (January 2020): 175–82. http://dx.doi.org/10.1016/j.jfda.2019.07.002.

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Najar, Mehdi, Hussein Fayyad-Kazan, Wissam H. Faour, Adil El Taghdouini, Gordana Raicevic, Mustapha Najimi, Michel Toungouz, Leo A. van Grunsven, Etienne Sokal, and Laurence Lagneaux. "Human hepatic stellate cells and inflammation: A regulated cytokine network balance." Cytokine 90 (February 2017): 130–34. http://dx.doi.org/10.1016/j.cyto.2016.11.008.

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Kelbich, Petr, Vilém Malý, Inka Matuchová, Martin Čegan, Ivan Staněk, Jiří Král, Ondřej Karpjuk, et al. "Cytological-energy analysis of pleural effusions." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 56, no. 6 (May 16, 2019): 630–37. http://dx.doi.org/10.1177/0004563219845415.

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Background Simultaneous cytological and metabolic investigation of the pleural effusion provides clinically relevant information about the type and intensity of immune response in the pleural cavity. Methods We investigated 1329 pleural effusions from patients with different pathological changes in the pleural cavity. Evaluated parameters were differential cell count of neutrophils, eosinophils, lymphocytes and monocytes, and values of the coefficient of energy balance. Results We found the lowest numbers of cells and the highest coefficient of energy balance values in patients with heart failure and sepsis; relatively high frequency of eosinophils and slightly decreased coefficient of energy balance values in patients with pneumothorax and haemothorax; the predominance of lymphocytes and low coefficient of energy balance values in patients with tuberculous pleuritis; the predominance of neutrophils and variable coefficient of energy balance values in patients after chest surgery; the highest presence of neutrophils and very low coefficient of energy balance values in patients with chest empyema and the predominance of lymphocytes and normal to low coefficient of energy balance values in patients with pleural malignancy. Conclusions Our findings in patients with heart failure and sepsis suggest the absence of inflammation in the pleural cavity. We observed the manifestation of tissue repair in patients with pneumothorax and haemothorax. Patients with tuberculous pleuritis were predominantly characterized by T cell-driven immune response and oxidative burst of macrophages. We found different intensities of immune responses to the chest surgery. The typical finding in patients with empyema was oxidative burst of neutrophils. In patients with pleural malignancy, weak cytotoxic inflammation predominates together with the intensive inflammation characterized by oxidative burst of macrophages.

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Ryba-Stanisławowska, Monika, Maria Skrzypkowska, Jolanta Myśliwska, and Małgorzata Myśliwiec. "The Serum IL-6 Profile and Treg/Th17 Peripheral Cell Populations in Patients with Type 1 Diabetes." Mediators of Inflammation 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/205284.

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IL-6 is a pleiotropic cytokine involved in the regulation of the immune response, inflammation, and hematopoeisis. Its elevated levels are found in a range of autoimmune and chronic inflammatory diseases. IL-6 is also involved in regulation of the balance between two T cell subsets: Tregs and Th17, which have contradictory functions in the control of inflammation. The present study provides a quantitative analysis regarding the Th17/Treg cell balance in peripheral blood of children with type 1 diabetes and its association with serum IL-6 level.

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Meiliana, Anna, and Andi Wijaya. "Update on Obesity: Induced Inflammation to Cause Cardiometabolic Diseases." Indonesian Biomedical Journal 14, no. 2 (June 28, 2022): 116–38. http://dx.doi.org/10.18585/inabj.v14i2.1937.

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BACKGROUND: Obesity incidence has risen dramatically during the last 50 years, reaching epidemic proportions. Obesity's growing prevalence, as well as its numerous metabolic and cardiovascular problems, poses a danger to human health and lifespan across the world.CONTENT: Numerous studies have shown that obesity causes inflammation, and suggest that inflammation may have a causal role in the development of insulin resistance, defective insulin secretion, and energy homeostasis disturbance. Obesity-induced inflammation is different from other inflammatory models because it includes tonic activation of the innate immune system, which has a long-term influence on metabolic balance. Inflammation can cause tissue damage by causing maladaptive responses such as fibrosis and necrosis. Obesity-induced inflammation is unique since it affects a variety of organs, including the adipose tissue, pancreas, liver, skeletal muscle, heart, and brain. These characteristics of obesity-induced inflammation make it difficult to decipher the underlying processes and how they affect metabolic systems.SUMMARY: The disruption of energy homeostasis caused by a positive energy balance is most likely the first trigger of metabolic inflammation, and the initial adaptive response aim to relieve the anabolic pressure caused by obesity. However, over time, this adaptive reaction becomes maladaptive, and the persistence of inflammation shows that the initial response has failed. The inflammation affects so many organ systems during obesity, and to develop novel treatment methods, a greater knowledge of the process was needed.KEYWORDS: obesity, inflammation, diabetes mellitus, non-alcoholic fatty liver disease, cardiovascular diseases, heart failure

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Jäger, Simon, Eduard F. Stange, and Jan Wehkamp. "Antimicrobial Peptides in Gastrointestinal Inflammation." International Journal of Inflammation 2010 (2010): 1–11. http://dx.doi.org/10.4061/2010/910283.

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Acute and chronic inflammations of mucosal surfaces are complex events in which the effector mechanisms of innate and adaptive immune systems interact with pathogenic and commensal bacteria. The role of constitutive and inducible antimicrobial peptides in intestinal inflammation has been investigated thoroughly over the recent years, and their involvement in various disease states is expanded ever more. Especially in the intestines, a critical balance between luminal bacteria and the antimicrobial peptides is essential, and a breakdown in barrier function by impaired production of defensins is already implicated in Crohn's disease. In this paper, we focus on the role of antimicrobial peptides in inflammatory processes along the gastrointestinal tract, while considering the resident and pathogenic flora encountered at the specific sites. The role of antimicrobial peptides in the primary events of inflammatory bowel diseases receives special attention.

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Cheng, Naixuan, Chang Liu, Yulin Li, Shijuan Gao, Ying-Chun Han, Xiaonan Wang, Jie Du, and Congcong Zhang. "MicroRNA-223-3p promotes skeletal muscle regeneration by regulating inflammation in mice." Journal of Biological Chemistry 295, no. 30 (June 3, 2020): 10212–23. http://dx.doi.org/10.1074/jbc.ra119.012263.

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After injury, the coordinated balance of pro- and anti-inflammatory factors in the microenvironment contribute to skeletal muscle regeneration. However, the underlying molecular mechanisms regulating this balance remain incompletely understood. In this study, we examined the roles of microRNAs (miRNAs) in inflammation and muscle regeneration. miRNA-Seq transcriptome analysis of mouse skeletal muscle revealed that miR-223-3p is upregulated in the early stage of muscle regeneration after injury. miR-223-3p knockout resulted in increased inflammation, impaired muscle regeneration, and increased interstitial fibrosis. Mechanistically, we found that myeloid-derived miR-223-3p suppresses the target gene interleukin-6 (Il6), associated with the maintenance of the proinflammatory macrophage phenotype during injury. Administration of IL-6-neutralizing antibody in miR-223-3p-knockout muscle could rescue the impaired regeneration ability and reduce the fibrosis. Together, our results reveal that miR-223-3p improves muscle regeneration by regulating inflammation, indicating that miRNAs can participate in skeletal muscle regeneration by controlling the balance of pro- and anti-inflammatory factors in the skeletal muscle microenvironment.

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Fairweather, DeLisa. "Regulating Inflammation in the Heart." International Journal of Biomedical Science 3, no. 1 (March 15, 2007): 9–13. http://dx.doi.org/10.59566/ijbs.2007.3009.

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Cardiovascular disease is the leading cause of death in the United States and estimated to be the leading cause of death worldwide by the year 2020. Many pathogens including bacteria, protozoa, and viruses are associated with inflammatory heart disease in patients, and can induce similar disease in animal models. Recognition of pathogens by the innate immune system leads to the release of proinflammatory cytokines that both reduce infection and increase inflammation in the heart. Signaling pathways that will eventually down-regulate cardiac inflammation, such as anti-inflammatory cytokines and regulatory T cells, are also initiated during the innate immune response. A careful balance between activation and regulation of the immune response to infection reduces the severity of inflammation in the heart, the leading cause of cardiovascular diseases such as atherosclerosis, myocarditis and dilated cardiomyopathy.

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Liu, Qingmei, Yu Zhou, Yuanyuan Gao, Zhendan Shu, Jun Zhang, Hong Liu, Minjie Cao, Guangming Liu, and Jinlyu Sun. "Degraded Porphyra haitanensis sulfated polysaccharide relieves ovalbumin-induced food allergic response by restoring the balance of T helper cell differentiation." Food & Function 12, no. 10 (2021): 4707–19. http://dx.doi.org/10.1039/d1fo00335f.

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Journal articles on the topic 'Inflammation balance'

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