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Journal articles on the topic 'Inflammation Mediators'

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Published: 4 June 2021
Last updated: 20 February 2023

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1

GREAVES, M. W. "Inflammation and mediators." British Journal of Dermatology 119, no. 4 (October 1988): 419–26. http://dx.doi.org/10.1111/j.1365-2133.1988.tb03245.x.

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2

Sacca, R. "Mediators of inflammation." Current Opinion in Immunology 9, no. 6 (December 1997): 851–57. http://dx.doi.org/10.1016/s0952-7915(97)80189-6.

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3

Moore, Terry L., and Terry D. Weiss. "Mediators of inflammation." Seminars in Arthritis and Rheumatism 14, no. 4 (May 1985): 247–62. http://dx.doi.org/10.1016/0049-0172(85)90044-7.

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4

Lazarus, Stephen C. "Inflammation, Inflammatory Mediators, and Mediator Antagonists in Asthma." Journal of Clinical Pharmacology 38, no. 7 (July 1998): 577–82. http://dx.doi.org/10.1002/j.1552-4604.1998.tb04463.x.

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5

Finsnes, Finn, Torstein Lyberg, Geir Christensen, and Ole H. Skjønsberg. "Effect of endothelin antagonism on the production of cytokines in eosinophilic airway inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (April 1, 2001): L659—L665. http://dx.doi.org/10.1152/ajplung.2001.280.4.l659.

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Endothelin (ET)-1 has been launched as an important mediator in bronchial asthma, which is an eosinophilic airway inflammation. However, the interplay between ET-1 and other proinflammatory mediators during the development of airway inflammation has not been elucidated. We wanted to study 1) whether the production of ET-1 precedes the production of other proinflammatory mediators and 2) whether ET-1 stimulates the production of these mediators within the airways. These hypotheses were studied during the development of an eosinophilic airway inflammation in rats. The increase in ET-1 mRNA level in lung tissue preceded the increase in mRNA levels of tumor necrosis factor-α, interleukin (IL)-1β, and IL-8. Treatment of the animals with the ET receptor antagonist bosentan resulted in a substantial decrease in the concentrations of tumor necrosis factor-α, IL-4, IL-1β, interferon-γ, and ET-1 in bronchoalveolar lavage fluid. In conclusion, the synthesis of ET-1 as measured by increased mRNA level precedes the synthesis of other proinflammatory cytokines of importance for the development of an eosinophilic airway inflammation, and ET antagonism inhibits the production of these mediators within the airways. Whether treatment with ET antagonists will prove beneficial for patients with eosinophilic airway inflammations like bronchial asthma is not yet known.
6

Alderton, Gemma. "Lipid mediators of inflammation." Science 371, no. 6526 (January 14, 2021): 248.9–250. http://dx.doi.org/10.1126/science.371.6526.248-i.

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7

Robinson, Dwight R. "Lipid Mediators of Inflammation." Rheumatic Disease Clinics of North America 13, no. 2 (August 1987): 385–405. http://dx.doi.org/10.1016/s0889-857x(21)00854-1.

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8

Laurent, G. J. "Mediators of Pulmonary Inflammation." Thorax 47, no. 9 (September 1, 1992): 764. http://dx.doi.org/10.1136/thx.47.9.764-a.

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9

Lasky, Laurence A. "Combinatorial mediators of inflammation?" Current Biology 3, no. 6 (June 1993): 366–68. http://dx.doi.org/10.1016/0960-9822(93)90203-z.

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10

du Bois, R. M. "Mediators of pulmonary inflammation." Immunology Today 13, no. 10 (January 1992): 424. http://dx.doi.org/10.1016/0167-5699(92)90100-l.

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11

Harold Adrian, Liemena, Budi Satrijo, Djanggan Sargowo, and Indra Prasetya. "The Role of Colchicine in Acute Coronary Syndrome." Heart Science Journal 1, no. 4 (December 23, 2020): 4–8. http://dx.doi.org/10.21776/ub.hsj.2020.001.04.02.

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Background: Despite the advances of current optimal treatment of atherosclerotic disease, the incidence of events after acute coronary syndrome (ACS) remains high. Colchicine, with its well-established pleiotropic anti-inflam- matory effects, may inhibit NLRP3 inflammasome, a key mediator in atherosclerosis-associated inflammation (AAI) thus reducing systemic inflammation. NRLP3 inflammasome activation inside leukocytes (mainly monocytes and neutrophils) is precipitated by cholesterol crystals that are present in all atherosclerosis stages. 􏰟􏰋􏰡􏰈􏰇􏱎􏰋􏰇􏰆􏰂 􏰍􏰀􏰂􏰅􏰩􏰍􏰂􏰅􏰃􏰆 􏰃􏰜 􏰢􏰎􏰃􏰐􏰅􏰆􏰜􏰏􏰍􏰝􏰝􏰍􏰂􏰃􏰎􏰁 􏰀􏰁􏰂􏰃􏰄􏰅􏰆􏰇􏰈 􏰈􏰋􏰀􏰌 􏰍􏰈 􏰅􏰆􏰂􏰇􏰎􏰏􏰇􏰋􏰄􏰅􏰆􏰐􏰑􏰒 􏰍􏰆􏰗 􏰅􏰆􏰂􏰇􏰎􏰏􏰇􏰋􏰄􏰅􏰆􏰐􏰑􏰣 􏰳􏰅􏰏􏰏 􏰜􏰃􏰏􏰏􏰃􏰳􏰨 􏰘􏰌􏰇􏰈􏰇 cytokines are the crucial inflammatory pathway mediators that promote the formation of plaque and instability in the inflammatory cascade. Objective: This review will elaborate on the function of immune cells in atherosclerosis, explain the mechanisms of NLRP3 inflammasome activation in the context of AAI, and address the possible role of colchicine specifically targeting NLRP3 inflammasome and its concomitant downstream mediators in ACS, and provide an overview of current or ongoing studies produced in this area. Discussion : NRLP3 inflammasome activation inside leukocytes (mainly monocytes and neutrophils) is precipitat- ed by cholesterol crystals that are present in all atherosclerosis stages. Subsequent activation of pro-inflammatory pathway mediators that promote the formation of plaque and instability in the inflammatory cascade. A potential advantage of a medication acting through an inflammatory milieu found in atherosclerotic lesions has recently become the need for novel therapeutic options. Colchicine, with its well-established pleiotropic anti-inflammato- ry effects, may inhibit NLRP3 inflammasome, a key mediator in atherosclerosis-associated inflammation (AAI) thus reducing systemic inflammation. Conclusion: Colchicine is a safe and reliable medication for ACS patients, alongside reveal various benefit in reducing inflammation through inhibition of NLRP3 Inflammasome`
12

Eerden, Menno M. Van Der. "Mediators Of Inflammation In COPD." Pulmonary Medicine and Respiratory Research 5, no. 2 (August 5, 2019): 1–10. http://dx.doi.org/10.24966/pmrr-0177/100026.

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13

Cooper, P. R., J. L. McLachlan, S. Simon, L. W. Graham, and A. J. Smith. "Mediators of Inflammation and Regeneration." Advances in Dental Research 23, no. 3 (June 15, 2011): 290–95. http://dx.doi.org/10.1177/0022034511405389.

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Characterization of the molecular response under caries lesions requires a robust and reliable transcript isolation system, and analysis of data indicated that collection of extracted teeth in either liquid nitrogen/RNA-stabilizing solution facilitated this. Subsequent transcriptional analysis indicated higher general activity in carious pulps, while characterization of inflammatory mediators, including cytokines and S100 proteins, highlighted increasing expression levels associated with both microbial front progression and elevated cellular immune response. Analysis of the pleiotropic hormone adrenomedullin (ADM) indicated that transcript and protein levels are increased in pulpal tissue during caries, and that protein levels sequestered in dentin due to primary dentinogenesis are comparable with those of TGF-β1. Expression analysis of a leucine-rich-repeat-containing protein (LRRC15/Lib) indicated that this highly conserved molecule was up-regulated during caries, is transcriptionally regulated by pro-inflammatory stimuli, and is relatively abundant in mineralized tissues.
14

Rankin, James A. "Biological Mediators of Acute Inflammation." AACN Clinical Issues: Advanced Practice in Acute and Critical Care 15, no. 1 (January 2004): 3–17. http://dx.doi.org/10.1097/00044067-200401000-00002.

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15

LUGER, T. "Mediators of immunity and inflammation." Journal of the European Academy of Dermatology and Venereology 11 (September 1998): S25—S26. http://dx.doi.org/10.1016/s0926-9959(98)94625-6.

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16

Rand, Royden. "Mediators of immunity and inflammation." Clinical Biochemistry 22, no. 3 (June 1989): 241–43. http://dx.doi.org/10.1016/s0009-9120(89)80083-9.

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17

Schlag, G., and H. Redl. "Mediators of Injury and Inflammation." World Journal of Surgery 20, no. 4 (May 1, 1996): 406–10. http://dx.doi.org/10.1007/s002689900064.

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18

Agrawal, Anshu. "Vision for Mediators of Inflammation." Mediators of Inflammation 2020 (March 4, 2020): 1. http://dx.doi.org/10.1155/2020/9202849.

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19

Lai, Kar Neng, Sydney C. W. Tang, and Joseph C. K. Leung. "Mediators of Inflammation and Fibrosis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 27, no. 2_suppl (June 2007): 65–71. http://dx.doi.org/10.1177/089686080702702s12.

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During peritoneal dialysis, peritoneal cells are repeatedly exposed to a non-physiologic hypertonic environment with high glucose content and low pH. Current sterile dialysis solutions cause inflammation in the submesothelial compact zone, leading to fibrosis, angiogenesis, and, eventually, ultrafiltration failure. Although the normal interstitium separates the peritoneal microvasculature from the dialysis fluid and makes transperitoneal transport less efficient, changes in the submesothelial compact zone can result in progressive increases in solute transfer and ultrafiltration diminution. This peritoneal dysfunction will further be amplified with the development of an epithelial-to-mesenchymal transition of mesothelial cells and dissipation of the osmotic driving force through the increased area and solute transport that accompany neoangiogenesis of the submesothelial microvasculature. The alteration of the peritoneal membrane can be further aggravated by peritonitis, advanced glycation end-products, and glucose degradation products. Furthermore, new data are emerging to support a proinflammatory role for peritoneal adipocytes.
20

Abboud, Hanna E. "Cytokine mediators of renal inflammation." Current Opinion in Nephrology and Hypertension 3, no. 3 (May 1994): 329–33. http://dx.doi.org/10.1097/00041552-199405000-00015.

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21

Schirripa, Maria Laura, Maria Pia Scarpelli, and Cristian Palmiere. "Mediators of Inflammation in Asthma." American Journal of Forensic Medicine and Pathology 38, no. 2 (June 2017): 153–58. http://dx.doi.org/10.1097/paf.0000000000000306.

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22

Steinhubl, Steven R. "Platelets as Mediators of Inflammation." Hematology/Oncology Clinics of North America 21, no. 1 (February 2007): 115–21. http://dx.doi.org/10.1016/j.hoc.2006.11.015.

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23

Reilly, Christopher, Nicole Regna, and Abigail Peairs. "EGCG Inhibits Inflammation Independently of AMPK (87.10)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 87.10. http://dx.doi.org/10.4049/jimmunol.184.supp.87.10.

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Abstract Epigallocatechin-3-gallate (EGCG), a bioactive component of green tea, has been reported to exert anti-inflammatory effects in immune cells. EGCG has been shown to activate the metabolic regulator, AMP-activated protein kinase (AMPK). Mesangial cells from MRL/lpr lupus-like mice are hyper-responsive to immune stimulation and overproduce nitric oxide (NO) and other inflammatory mediators when stimulated. In our current studies, we sought to determine if EGCG would inhibit inflammation in AMPK deficient mesangial cells. Cultured mesangial cells from MRL/lpr mice were treated with siRNA for mouse Prkaa2-Design A, specific for AMP-activated protein kinase-alpha (AMPK-α) or siRNA negative control for mouse. After 48 hours, the cells were serum-starved for 2 hours, treated with 50 μM epigallocatechin-gallate (EGCG) for one hour, and stimulated with lipopolysaccharide (LPS)/interferon (IFN)-γ for 30 minutes. The addition of siRNA inhibited AMPK expression in mesangial cells. LPS/IFN-γ induced inflammatory mediator production (iNOS expression, supernatant NO, and interleukin-6) as expected. Interestingly, EGCG blocked inflammatory mediator production in the AMPK deficient cells suggesting EGCG inhibits inflammatory pathways independently of AMPK to decrease inflammatory mediatory production. Taken together, these studies show that EGCG attenuated inflammation in MRL/lpr mouse mesangial cells independent of AMPK.
24

Lu, Yan, Song Hong, Katherine Gotlinger, and Charles Serhan. "Lipid Mediator Informatics and Proteomics in Inflammation-Resolution." Scientific World JOURNAL 6 (2006): 589–614. http://dx.doi.org/10.1100/tsw.2006.118.

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Lipid mediator informatics is an emerging area denoted to the identification of bioactive lipid mediators (LMs) and their biosynthetic profiles and pathways. LM informatics and proteomics applied to inflammation, systems tissues research provides a powerful means of uncovering key biomarkers for novel processes in health and disease. By incorporating them with system biology analysis, we review here our initial steps toward elucidating relationships among a range of bimolecular classes and provide an appreciation of their roles and activities in the pathophysiology of disease. LM informatics employing liquid chromatography-ultraviolet-tandem mass spectrometry (LC-UV-MS/MS), gas chromatography-mass spectrometry (GC-MS), computer-based automated systems equipped with databases and novel searching algorithms, and enzyme-linked immunosorbent assay (ELISA) to evaluate and profile temporal and spatial production of mediators combined with proteomics at defined points during experimental inflammation and its resolution enable us to identify novel mediators in resolution. The automated system including databases and searching algorithms is crucial for prompt and accurate analysis of these lipid mediators biosynthesized from precursor polyunsaturated fatty acids such as eicosanoids, resolvins, and neuroprotectins, which play key roles in human physiology and many prevalent diseases, especially those related to inflammation. This review presents detailed protocols used in our lab for LM informatics and proteomics using LC-UV-MS/MS, GC-MS, ELISA, novel databases and searching algorithms, and 2-dimensional gel electrophoresis and LC-nanospray-MS/MS peptide mapping.
25

Ramon, Sesquile, Charles Serhan, and Richard Phipps. "Actions of novel inflammation-resolving lipid mediators on human B cells (84.9)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 84.9. http://dx.doi.org/10.4049/jimmunol.184.supp.84.9.

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Abstract The resolution of inflammation is an active and dynamic process. Newly identified lipid mediators have been recognized as key players during the process of inflammation resolution. These lipid-derived molecules constitute three classes of compounds (lipoxins, resolvins and protectins), all derived from essential fatty acids. New data demonstrates that these lipid mediators regulate aspects of the immune response, including inhibition of neutrophil infiltration, reduction of T cell cytokine production and stimulation of macrophage phagocytic activity. However, their effects on B lymphocytes are unknown. We show for the first time that the novel lipid mediator lipoxin B4 and 17-HDHA increase the ability of normal human B cells to produce IgM and IgG when activated with CpG plus anti-IgM. The two lipid derived molecules along with lipoxin A4 also enhance B cell differentiation, measured by an increased frequency of CD38+ cells. In addition, resolvin D1 and AT-resolvin also increase antibody production in CpG-stimulated B cells. None of the inflammation resolution lipid mediators affect proliferation and are non-toxic to the cells. Increase of plasma cell differentiation and antibody production coincides with the known involvement of pro-resolving mediators during the late stages of inflammation and pathogen clearance.
26

Ishihara, Tomoaki, Mio Yoshida, and Makoto Arita. "Omega-3 fatty acid-derived mediators that control inflammation and tissue homeostasis." International Immunology 31, no. 9 (February 17, 2019): 559–67. http://dx.doi.org/10.1093/intimm/dxz001.

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AbstractOmega-3 polyunsaturated fatty acids (PUFAs), including eicosapentaenoic acid, docosapentaenoic acid and docosahexaenoic acid, display a wide range of beneficial effects in humans and animals. Many of the biological functions of PUFAs are mediated via bioactive metabolites produced by fatty acid oxygenases such as cyclooxygenases, lipoxygenases and cytochrome P450 monooxygenases. Liquid chromatography–tandem mass spectrometry-based mediator lipidomics revealed a series of novel bioactive lipid mediators derived from omega-3 PUFAs. Here, we describe recent advances on omega-3 PUFA-derived mediators, mainly focusing on their enzymatic oxygenation pathway, and their biological functions in controlling inflammation and tissue homeostasis.
27

Bannenberg, Gerhard, Makoto Arita, and Charles N. Serhan. "Endogenous Receptor Agonists: Resolving Inflammation." Scientific World JOURNAL 7 (2007): 1440–62. http://dx.doi.org/10.1100/tsw.2007.188.

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Controlled resolution or the physiologic resolution of a well-orchestrated inflammatory response at the tissue level is essential to return to homeostasis. A comprehensive understanding of the cellular and molecular events that control the termination of acute inflammation is needed in molecular terms given the widely held view that aberrant inflammation underlies many common diseases. This review focuses on recent advances in the understanding of the role of arachidonic acid and ω-3 polyunsaturated fatty acids (PUFA)–derived lipid mediators in regulating the resolution of inflammation. Using a functional lipidomic approach employing LC-MS-MS–based informatics, recent studies, reviewed herein, uncovered new families of local-acting chemical mediators actively biosynthesized during the resolution phase from the essential fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These new families of local chemical mediators are generated endogenously in exudates collected during the resolution phase, and were coined resolvins and protectins because specific members of these novel chemical families control both the duration and magnitude of inflammation in animal models of complex diseases. Recent advances on the biosynthesis, receptors, and actions of these novel anti-inflammatory and proresolving lipid mediators are reviewed with the aim to bring to attention the important role of specific lipid mediators as endogenous agonists in inflammation resolution.
28

Kharbanda, Rajat, and Tarun Bansal. "Adipokines: mediators of immunity and inflammation." International Journal of Research in Medical Sciences 8, no. 7 (June 26, 2020): 2746. http://dx.doi.org/10.18203/2320-6012.ijrms20202929.

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White adipose tissue has emerged as a highly dynamic organ that releases a plethora of immune and inflammatory mediators that are involved in obesity, metabolic syndrome and immune mediated diseases. Adipokines have complex role in various physiological and pathological processes by exerting potent modulatory actions on target tissues In this Review, In this review, we explore the effects of different adipokines, focusing primarily on leptin, adiponectin, visfatin and resistin in causing immune-mediated and/or inflammatory diseases.
29

Herkel, Johannes, and Dirk Schmidt-Arras. "Mediators of liver inflammation and carcinogenesis." Seminars in Immunopathology 43, no. 4 (August 2021): 477–79. http://dx.doi.org/10.1007/s00281-021-00880-x.

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30

Flower, R. J. "Inflammation: The mediators of steroid action." Nature 320, no. 6057 (March 1986): 20. http://dx.doi.org/10.1038/320020a0.

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31

Jose, P. J. "Complement-derived peptide mediators of inflammation." British Medical Bulletin 43, no. 2 (April 1987): 336–49. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072186.

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32

Lerner, Ulf H., and Goran Sundquist. "Mediators of inflammation-induced bone resorption." Dental Traumatology 7, no. 4 (August 1991): 186. http://dx.doi.org/10.1111/j.1600-9657.1991.tb00206.x.

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33

Wallace, John L., Angela Ianaro, Kyle L. Flannigan, and Giuseppe Cirino. "Gaseous mediators in resolution of inflammation." Seminars in Immunology 27, no. 3 (May 2015): 227–33. http://dx.doi.org/10.1016/j.smim.2015.05.004.

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34

LUGER, T. "C057 Mediators of immunity and inflammation." Journal of the European Academy of Dermatology and Venereology 9 (September 1997): S70—S71. http://dx.doi.org/10.1016/s0926-9959(97)89132-5.

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35

Leid, R. Wes, and Kathleen A. Potter. "Inflammation and Mediators of Lung Injury." Veterinary Clinics of North America: Food Animal Practice 1, no. 2 (July 1985): 377–400. http://dx.doi.org/10.1016/s0749-0720(15)31332-3.

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36

FORD-HUTCHINSON, A. W., and ANITA RACKMAN. "Leukotrienes as mediators of skin inflammation." British Journal of Dermatology 109 (July 29, 2006): 26–29. http://dx.doi.org/10.1111/j.1365-2133.1983.tb06814.x.

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37

BATSFORD, STEPHEN R. "Cationic antigens as mediators of inflammation." APMIS 99, no. 1-6 (January 1991): 1–9. http://dx.doi.org/10.1111/j.1699-0463.1991.tb05110.x.

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38

Spiropoulos, Kostas, Nikolaos Siafakas, Marc Miravitlles, Francesco Blasi, and Kiriakos Karkoulias. "Mediators of Inflammation in Pulmonary Diseases." Mediators of Inflammation 2015 (2015): 1–2. http://dx.doi.org/10.1155/2015/739219.

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39

Bacon, Kevin B., and Thomas J. Schall. "Chemokines as Mediators of Allergic Inflammation." International Archives of Allergy and Immunology 109, no. 2 (1996): 97–109. http://dx.doi.org/10.1159/000237207.

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40

Scott, Dugald T., Francis Y. Lam, and William R. Ferrell. "Acute joint inflammation—Mechanisms and mediators." General Pharmacology: The Vascular System 25, no. 7 (November 1994): 1285–96. http://dx.doi.org/10.1016/0306-3623(94)90151-1.

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41

Lowry, Stephen F. "Cytokine Mediators of Immunity and Inflammation." Archives of Surgery 128, no. 11 (November 1, 1993): 1235. http://dx.doi.org/10.1001/archsurg.1993.01420230063010.

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42

Lam, Derek, Devon Harris, and Zhenyu Qin. "Inflammatory Mediator Profiling Reveals Immune Properties of Chemotactic Gradients and Macrophage Mediator Production Inhibition during Thioglycollate Elicited Peritoneal Inflammation." Mediators of Inflammation 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/931562.

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Understanding of spatiotemporal profiling of inflammatory mediators and their associations with MΦ accumulation is crucial to elucidate the complex immune properties. Here, we used murine thioglycollate elicited peritonitis to determine concentrations of 23 inflammatory mediators in peritoneal exudates and plasma before (day 0) and after (days 1 and 3) thioglycollate administration to peritoneal cavities; these mediators included TNF-α, FGF-9, IFN-γ, IP-10, RANTES, IL-1α, IL-6, IL-7, IL-10, IL-11, IL-12p70, IL-17A, lymphotactin, OSM, KC/GRO, SCF, MIP-1β, MIP-2, TIMP-1, VEGF-A, MCP-1, MCP-3, and MCP-5. Our results showed that concentrations of most mediators in exudates and plasma reached peak levels on day 1 and were significantly reduced on day 3. Conversely, MΦnumbers started to increase on day 1 and reached peak levels on day 3. Moreover, LPS treatmentin vitrosignificantly induced mediator productions in cell culture media and lysates from MΦisolated on day 3. Our results also showed that on day 0, concentrations of many mediators in plasma were higher than those in exudates, whereas on day 1, the trend was reversed. Overall, the findings from thioglycollate elicited peritonitis reveal that reversible chemotactic gradients between peritoneal exudates and blood exist in basal and inflamed conditions and the inflammatory mediator productionin vivois disassociated with macrophage accumulation during inflammation resolution.
43

Sethu, Swaminathan, and Alirio J. Melendez. "New developments on the TNFα-mediated signalling pathways." Bioscience Reports 31, no. 1 (October 21, 2010): 63–76. http://dx.doi.org/10.1042/bsr20100040.

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TNFα (tumour necrosis factor α) is an extensively studied pleiotropic cytokine associated with the pathogenesis of a variety of inflammatory diseases. It elicits a wide spectrum of cellular responses which mediates and regulates inflammation, immune response, cell survival, proliferation and apoptosis. TNFα initiates its responses by binding to its receptors. TNFα-induced effector responses are mediated by the actions and interactions among the various intracellular signalling mediators in the cell. TNFα induces both survival and apoptotic signal in a TRADD (TNF receptor-associated DD)-dependent and -independent way. The signals are further transduced via a variety of signalling mediators, including caspases, MAPKs (mitogen-activated protein kinases), phospholipid mediators and miRNA/miR (microRNA), whose roles in specific functional responses is not fully understood. Elucidating the complexity and cross talks among signalling mediators involved in the TNFα-mediated responses will certainly aid in the identification of molecular targets, which can potentially lead to the development of novel therapeutics to treat TNFα-associated disorders and in dampening inflammation.
44

Avenatti, R. C. "The intersection of inflammation, insulin resistance and ageing: implications for the study of molecular signalling pathways in horses." Comparative Exercise Physiology 8, no. 3-4 (January 1, 2012): 153–71. http://dx.doi.org/10.3920/cep12018.

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Inflammation-associated insulin resistance contributes to chronic disease in humans and other long-lived species, such as horses. Insulin resistance arises due to an imbalance among molecular signalling mediators in response to pro-inflammatory cytokines in the aged and obese. The mammalian heat shock protein response has received much attention as an avenue for attenuating inflammatory mediator signalling and for contributing to preservation and restoration of insulin signalling in metabolically important tissues. Data on heat shock proteins and inflammatory signalling mediators in untrained and aged horses are lacking, and horses represent an untapped resource for studying the mediator imbalance contributing to insulin resistance in a comparative model.
45

Wallace, J. L. "Lipid mediators of inflammation in gastric ulcer." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 1 (January 1, 1990): G1—G11. http://dx.doi.org/10.1152/ajpgi.1990.258.1.g1.

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The interest in lipid mediators of inflammation as potential contributors to the pathogenesis of gastric ulcer has increased markedly over the past 20 yr. Although a great deal is known about the actions of mediators such as leukotrienes, thromboxane, and platelet-activating factor in experimental models of ulceration, evidence supporting a role for these mediators in human gastric ulcer is sorely lacking. This review attempts to answer a number of questions regarding the contribution of these mediators to the pathogenesis of gastric ulceration and the possible use of specific inhibitors, antagonists, and dietary manipulation in the treatment of gastric ulcer. Potential directions for future research in this field are suggested as are some of the pitfalls to be avoided in such studies.
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Shi, Xuan-Zheng, John H. Winston, and Sushil K. Sarna. "Differential immune and genetic responses in rat models of Crohn's colitis and ulcerative colitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 1 (January 2011): G41—G51. http://dx.doi.org/10.1152/ajpgi.00358.2010.

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Crohn's disease and ulcerative colitis are clinically, immunologically, and morphologically distinct forms of inflammatory bowel disease (IBD). However, smooth muscle function is impaired similarly in both diseases, resulting in diarrhea. We tested the hypothesis that differential cellular, genetic, and immunological mechanisms mediate smooth muscle dysfunction in two animal models believed to represent the two diseases. We used the rat models of trinitrobenzene sulfonic acid (TNBS)- and dextran sodium sulfate (DSS)-induced colonic inflammations, which closely mimic the clinical and morphological features of Crohn's disease and ulcerative colitis, respectively. DSS inflammation induced oxidative stress initially in mucosa/submucosa, which then propagated to the muscularis externa to impair smooth muscle function. The muscularis externa showed no increase of cytokines/chemokines. On the other hand, TNBS inflammation almost simultaneously induced oxidative stress, recruited or activated immune cells, and generated cytokines/chemokines in both mucosa/submucosa and muscularis externa. The generation of cytokines/chemokines did not correlate with the recruitment and activation of immune cells. Consequently, the impairment of smooth muscle function in DSS inflammation was primarily due to oxidative stress, whereas that in TNBS inflammation was due to both oxidative stress and proinflammatory cytokines. The impairment of smooth muscle function in DSS inflammation was due to suppression of Gαq protein of the excitation-contraction coupling. In TNBS inflammation, it was due to suppression of the α1C1b subunit of Cav1.2b channels, CPI-17 and Gαq. TNBS inflammation increased IGF-1 and TGF-β time dependently in the muscularis externa. IGF-1 induced smooth muscle hyperplasia; both IGF-1 and TGF-β induced hypertrophy. In conclusion, both TNBS and DSS induce transmural inflammation, albeit with different types of inflammatory mediators. The recruitment or activation of immune cells does not correlate directly with the intensity of generation of inflammatory mediators. The inflammatory mediators in TNBS and DSS inflammations target different genes to impair smooth muscle function.
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Gushchin, Igor S. "Interactions of mast cells and eosinophils in allergic response." Russian Journal of Allergy 17, no. 2 (July 23, 2020): 5–17. http://dx.doi.org/10.36691/rja1363.

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Mast cells (MCs) and eosinophils (EOs) appeared hundreds of millions of years ago during the evolutionary process and continue to be retained by all vertebrate species. There is no convincing evidence of the absence of these cells in vertebrates under normal conditions. These cells are involved in the reactions of innate and adaptive immunity, in the control of tissue growth and tissue remodeling, activation of adipose tissue, affect reproductive functions and have a wide range of mediators involved in homeostasis. It is known that the interaction of these cells is involved in the initiation and maintenance of allergic inflammation. FcRI-mediated MC activation leads to mediators secretion, among which there are many chemotactic agents for EOs. These agents attract the EOs to the site of allergic inflammation. The EOs come into physical contact with the MCs, accompanied by the EO activation. As a result of the action of mediators released from MCs and EO, the active state of the cells is enhanced and maintained, and, accordingly, the process of inflammation is prolonged with the corresponding consequences in the form of triggering tissue remodeling. Eosinophil-derived active substances released during the reaction, having at least anti-mediator properties, contribute to the suppression and resolution of allergic inflammation. Such a look at the nature of the interactions between EOs and MCs justifies the comparative determination of the kinetics of the release of pro-allergic mediators from those cells and the formation of EO-derived compounds with antiallergic activity. It is expected that such studies will be carried out in the nearest future.
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González-Périz, Ana, and Joan Clària. "Resolution of Adipose Tissue Inflammation." Scientific World JOURNAL 10 (2010): 832–56. http://dx.doi.org/10.1100/tsw.2010.77.

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The presence of the so-called “low-grade” inflammatory state is recognized as a critical event in adipose tissue dysfunction in obesity. This chronic “low-grade” inflammation in white adipose tissue is powerfully augmented through the infiltration of macrophages, which, together with adipocytes, perpetuate a vicious cycle of macrophage recruitment and secretion of free fatty acids and deleterious adipokines that predispose the development of obesity-related comorbidities, such as insulin resistance and nonalcoholic fatty liver disease. In the last decade, many factors have been identified that contribute to mounting uncontrolled inflammation in obese adipose tissue. Among them, bioactive lipid mediators derived from the cyclooxygenase and 5-lipoxygenase pathways, which convert the ω-6-polyunsaturated fatty acid (PUFA) arachidonic acid into potent proinflammatory eicosanoids (i.e., prostaglandins [PGs] and leukotrienes), have emerged. Interestingly, the same lipid mediators that initially trigger the inflammatory response also signal the termination of inflammation by stimulating the biosynthesis of anti-inflammatory and proresolving lipid autacoids. This review discusses the current status, characteristics, and progress in this class of “stop signals”, including the lipoxins, which were the first identified ω-6 PUFA–derived lipid mediators with potent anti-inflammatory properties; the recently described ω-3 PUFA–derived lipid mediators resolvins and protectins; and the cyclopentenone PGs of the D series. Special emphasis is given to the participation of these bioactive lipid autacoids in the resolution of adipose tissue inflammation and in preventing the development of obesity-related complications.
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Glurich, Ingrid, Sara Grossi, Boris Albini, Alex Ho, Rashesh Shah, Mohamed Zeid, Heinz Baumann, Robert J. Genco, and Ernesto De Nardin. "Systemic Inflammation in Cardiovascular and Periodontal Disease: Comparative Study." Clinical and Vaccine Immunology 9, no. 2 (March 2002): 425–32. http://dx.doi.org/10.1128/cdli.9.2.425-432.2002.

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ABSTRACT Epidemiological studies have implicated periodontal disease (PD) as a risk factor for the development of cardiovascular disease (CVD). These studies addressed the premise that local infection may perturb the levels of systemic inflammatory mediators, thereby promoting mechanisms of atherosclerosis. Levels of inflammatory mediators in the sera of subjects with only PD, only CVD, both diseases, or neither condition were compared. Subjects were assessed for levels of C-reactive protein (CRP), serum amyloid A (SAA), ceruloplasmin, α1-acid-glycoprotein (AAG), α1-antichymotrypsin (ACT), and the soluble cellular adhesion molecules sICAM-1 and sVCAM by enzyme-linked immunoabsorbent and/or radial immunodiffusion assays. CRP levels in subjects with either condition alone were elevated twofold above subjects with neither disease, whereas a threefold increase was noted in subjects with both diseases (P = 0.0389). Statistically significant increases in SAA and ACT were noted in subjects with both conditions compared to those with one or neither condition (P = 0.0162 and 0.0408, respectively). Ceruloplasmin levels were increased in subjects with only CVD (P = 0.0001). Increases in sVCAM levels were noted in all subjects with CVD (P = 0.0054). No differences in sICAM levels were noted among subject groups. A trend toward higher levels of AAG was noted in subjects with both conditions and for ACT in subjects with only PD. Immunohistochemical examination of endarterectomy specimens of carotid arteries from subjects with atherosclerosis documented SAA and CRP deposition in association with atheromatous lesions. The data support the hypothesis that localized persistent infection may influence systemic levels of inflammatory mediators. Changes in inflammatory mediator levels potentially impact inflammation-associated atherosclerotic processes.
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Knuplez, Eva, Eva Maria Sturm, and Gunther Marsche. "Emerging Role of Phospholipase-Derived Cleavage Products in Regulating Eosinophil Activity: Focus on Lysophospholipids, Polyunsaturated Fatty Acids and Eicosanoids." International Journal of Molecular Sciences 22, no. 9 (April 21, 2021): 4356. http://dx.doi.org/10.3390/ijms22094356.

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Eosinophils are important effector cells involved in allergic inflammation. When stimulated, eosinophils release a variety of mediators initiating, propagating, and maintaining local inflammation. Both, the activity and concentration of secreted and cytosolic phospholipases (PLAs) are increased in allergic inflammation, promoting the cleavage of phospholipids and thus the production of reactive lipid mediators. Eosinophils express high levels of secreted phospholipase A2 compared to other leukocytes, indicating their direct involvement in the production of lipid mediators during allergic inflammation. On the other side, eosinophils have also been recognized as crucial mediators with regulatory and homeostatic roles in local immunity and repair. Thus, targeting the complex network of lipid mediators offer a unique opportunity to target the over-activation and ‘pro-inflammatory’ phenotype of eosinophils without compromising the survival and functions of tissue-resident and homeostatic eosinophils. Here we provide a comprehensive overview of the critical role of phospholipase-derived lipid mediators in modulating eosinophil activity in health and disease. We focus on lysophospholipids, polyunsaturated fatty acids, and eicosanoids with exciting new perspectives for future drug development.
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