Cytokine Biology

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Patrick T Walsh - One of the best experts on this subject based on the ideXlab platform.

  • current perspectives on the interleukin 1 family as targets for inflammatory disease
    European Journal of Immunology, 2019
    Co-Authors: Yasmina E Hernandezsantana, Eirini Giannoudaki, Gemma Leon, Margaret B Lucitt, Patrick T Walsh
    Abstract:

    Since the first description of interleukin-1 (IL-1) and the genesis of the field of Cytokine Biology, the understanding of how IL-1 and related Cytokines play central orchestrating roles in the inflammatory response has been an area of intense investigation. As a consequence of these endeavours, specific strategies have been developed to target the function of the IL-1 family in human disease realizing significant impacts for patients. While the most significant advances to date have been associated with inhibition of the prototypical family members IL-1α/β, approaches to target more recently identified family members such as IL-18, IL-33 and the IL-36 subfamily are now beginning to come to fruition. This review summarizes current knowledge surrounding the roles of the IL-1 family in human disease and describes the rationale and strategies which have been developed to target these Cytokines to inhibit the pathogenesis of a wide range of diseases in which inflammation plays a centrally important role.

Bernhard T Baune - One of the best experts on this subject based on the ideXlab platform.

  • evidence for a Cytokine model of cognitive function
    Neuroscience & Biobehavioral Reviews, 2009
    Co-Authors: Jordan Mcafoose, Bernhard T Baune
    Abstract:

    Aiming at a formulation of a Cytokine model of cognitive function under immunologically unchallenged physiological conditions, this article reviews the Cytokine Biology in the central nervous system (CNS) and recent developments in normal Cytokine functions within the CNS that subserve cognitive processes. Currently available evidence shows that the Cytokines IL-1β, IL-6 and TNF-α play a role in complex cognitive processes at the molecular level, such as synaptic plasticity, neurogenesis, as well as neuromodulation. Such findings provide evidence for a Cytokine model of cognitive function, which shows that Cytokines play an intimate role in the molecular and cellular mechanisms subserving learning, memory and cognition under physiological conditions. These Cytokine-mediated cognitive processes have implications in the long-term development and pathogenesis of specific neuropsychiatric disorders such as major depression and dementia. The identification of this central role of Cytokines in various brain activities during health provides greater insight into normal brain functions, especially synaptic plasticity, memory and cognition, and facilitates the understanding of specific biological mechanisms involved in neuropsychiatric diseases, such as dementia and depression. In order to extend the suggested Cytokine model of cognitive function onto other members of the Cytokine family, future research is required to investigate the physiological effects of other Cytokines such as interferon-gamma (IFNγ), alpha(1)-antichymotrypsin and IL-2 on cognitive function at the molecular level under immunologically unchallenged conditions.

Fabio Cominelli - One of the best experts on this subject based on the ideXlab platform.

  • Cytokine Biology cloning il 1 and the birth of a new era in
    2013
    Co-Authors: Theresa T Pizarro, Fabio Cominelli
    Abstract:

    Theresa T. Pizarro and Fabio Cominellihttp://www.jimmunol.org/content/178/9/5411J Immunol€2007; 178:5411-5412; ;Referenceshttp://www.jimmunol.org/content/178/9/5411.full#ref-list-1This article cites 26 articles, 10 of which you can access for free at: Subscriptionshttp://jimmunol.org/subscriptionsInformation about subscribing to The Journal of Immunology is online at: Permissionshttp://www.aai.org/ji/copyright.htmlSubmit copyright permission requests at: Email Alertshttp://jimmunol.org/cgi/alerts/etocReceive free email-alerts when new articles cite this article. Sign up at:

  • cloning il 1 and the birth of a new era in Cytokine Biology
    Journal of Immunology, 2007
    Co-Authors: Theresa T Pizarro, Fabio Cominelli
    Abstract:

    In December of 1984, the sequence of the cDNA encoding for the human precursor of IL-1 was reported in a seminal paper by Charles Dinarello’s group ([1][1]). This work is the subject of this month’s selected paper for Pillars of Immunology based on its significant impact on the field of Cytokine

Robert H Silverman - One of the best experts on this subject based on the ideXlab platform.

  • progress in interferon and Cytokine Biology
    Cytokine & Growth Factor Reviews, 1998
    Co-Authors: Bryan R G Williams, Robert H Silverman
    Abstract:

    The 15th Annual Meeting of the International Society for Interferon and Cytokine Research was held on October 19-24, 1997, at the Sheraton San Diego Hotel and Marina. In this meeting Bryan Williams and Robert Silverman review the scientific highlights of the proceedings. Interferon regulatory factors (IRFs) were among the major topics discussed at this meeting. Fortunately, the scientific program of the meeting, organized by Tom Cesario (U.C., Irvine), was sufficiently interesting to hold Cytokine biologists in darkened halls away from the splendid marina and sunny San Diego skies.

Robert F. Grimble - One of the best experts on this subject based on the ideXlab platform.

  • nutritional modulation of Cytokine Biology
    Nutrition, 1998
    Co-Authors: Robert F. Grimble
    Abstract:

    Abstract The pro-inflammatory Cytokines and oxidant molecules produced during the inflammatory response, which follows infection and injury, may be beneficial, or detrimental to the patient, depending on the amounts and contexts in which they are produced. Aberrant or excessive production has been implicated in inflammatory disease, and sepsis. The upregulation of Cytokine production by NFκB and NFIL-6 activation by oxidants increases the likelihood of Cytokine-induced mortality and morbidity. Complex systems exist for the control of Cytokine production and oxidant actions. The former include the hormones of the hypothalamo-pituitary-adrenal axis, acute phase proteins, and endogenous inhibitors of interleukin (IL)-1 and tumor necrosis factor (TNF). The latter include endogenously synthesized antioxidants, such as glutathione and dietary antioxidants, such as tocopherols, ascorbates and cachectins. Nutrients change Cytokine production and potency by influencing tissue concentrations of many of the molecules involved in Cytokine Biology. Monounsaturated fatty acids and ω-3 polyunsaturated fatty acids (PUFAs) suppress TNF and IL-1 production and actions, while n-6 PUFAs exert the opposite effect. Changes in eicosanoid production are more likely to underlie this effect than alterations in membrane fluidity. Low antioxidant intake results in enhanced Cytokine production and effects. The anorexia that follows infection and injury, may be purposeful to permit release of substrate from endogenous sources to support and control the inflammatory process. Therefore, prior as well as concurrent nutrient intake are of importance in determining the outcome of the inflammatory response.

  • Modulation of pro-inflammatory Cytokine Biology by unsaturated fatty acids.
    European Journal of Nutrition, 1998
    Co-Authors: Robert F. Grimble, Paramjit S. Tappia
    Abstract:

    The production of pro-inflammatory Cytokines, such as interleukins 1 and 6 and tumour necrosis factors, occurs rapidly following trauma or invasion of the body by pathogenic organisms. The Cytokines mediate the wide range of symptoms associated with trauma and infection, such as fever, anorexia, tissue wasting, acute phase protein production and immunomodulation. In part, the symptoms result from a co-ordinated response, in which the immune system is activated and nutrients released, from endogenous sources, to provide substrate for the immune system. Although the Cytokine mediated response is an essential part of the response to trauma and infection, excessive production of pro-inflammatory Cytokines, or production of Cytokines in the wrong biological context, are associated with mortality and pathology in a wide range of diseases, such as malaria, sepsis, rheumatoid arthritis, inflammatory bowel disease, cancer and AIDS. Cytokine Biology can be modulated by antiinflammatory drugs, recombinant Cytokine receptor antagonists and nutrients. Among the nutrients, fats have a large potential for modulating Cytokine Biology. A number of trials have demonstrated the anti-inflammatory effects of fish oils, which are rich in n-3 polyunsaturated fatty acids, in rheumatoid arthritis, inflammatory bowel disease, psoriasis and asthma. Animal studies, conducted by ourselves and others, indicate that a range of fats can modulate pro-inflammatory Cytokine production and actions. In summary fats rich in n-6 polyunsaturated fatty acids enhance IL1 production and tissue responsiveness to Cytokines, fats rich in n-3 polyunsaturated fatty acids have the opposite effect, monounsaturated fatty acids decrease tissue responsiveness to Cytokines and IL6 production is enhanced by total unsaturated fatty acid intake. There are a large number of potential cellular mechanisms which may mediate the effects observed. The majority relate to the ability of fats to alter the composition of membrane phospholipids. As a consequence of alterations in phospholipid composition, membrane fluidity may change, altering binding of Cytokines to receptors and G protein activity. The nature of substrate for various signalling pathways associated with Cytokine production and actions may also be changed. Consequently, alterations in eicosanoid production and activation of protein kinase C may occur. We have examined a number of these potential mechanisms in peritoneal macrophages of rats fed fats with a wide range of fatty acid composition. We have found that the total C18:2 and 20:4 diacyl species of phosphatidylethanolamine in peritoneal macrophages relates in a positive curvilinear fashion with dietary linoleic acid intake; that TNF induced IL1 and IL6 production relate in a positive curvilinear fashion to linoleic acid intake; that leukotriene B4 production relates positively with dietary linoleic acid intake over a range of moderate intakes and is suppressed at high intakes, while PGE2 production is enhanced. There was no clear relationship between linoleic acid intake and membrane fluidity, however fluidity was influenced in a complex manner by the type of fat in the diet, the period over which the fat was fed and the presence of absence of TNF stimulation. None of the proposed mechanisms, acting alone, can explain the positive effect of dietary linoleic acid intake on pro-inflammatory Cytokine production. However each may be involved, in part, in the modulatory effects observed.

  • 2 impact of nutrients on Cytokine Biology in infection
    Transactions of The Royal Society of Tropical Medicine and Hygiene, 1994
    Co-Authors: Robert F. Grimble
    Abstract:

    Interleukins 1 and 6 and tumour necrosis factor orchestrate a co-ordinated series of metabolic changes following invasions by pathogens. The changes are designed to destroy the pathogen. The response is characterized by fever, proteolysis in peripheral tissues, acute phase protein and antioxidant synthesis, and enhancement of the activity of the immune system. Cytokine production is enhanced by free radicals. Damage to the host may occur as a consequence. The deterious actions of these molecules are held in check by sophisticated antioxidant defences and systems which exert feedback control on Cytokine Biology. Nutrients have a profound effect upon the production and actions of Cytokines. Protein energy malnutrition, dietary n-3 polyunsaturated fatty acids and vitamin E suppress Cytokine production and actions. An opposite influence is exerted by n-6 polyunsaturated fatty acids, poor antioxidant defence, and supplementation of the diet with protein and branched chain amino acids. The synthesis of acute phase proteins and glutathione is dependent upon the adequacy of dietary sulphur amino acid intake. The consequences of the modulatory effects of previous and concurrent nutrient intake on Cytokine Biology are depletion of resources and damage to the host, which ranges from mild and temporary to severe, chronic or lethal.

  • influence of butter and of corn coconut and fish oils on the effects of recombinant human tumour necrosis factor alpha in rats
    Clinical Science, 1993
    Co-Authors: Hilda M Mulrooney, Robert F. Grimble
    Abstract:

    1. Tumour necrosis factor-α is produced in response to inflammatory stimuli. Fish oil can suppress the production and actions of Cytokines. Little information is available on the effects of other fats on Cytokine Biology. We compared the effects of fats, with a wide range of fatty acid characteristics, on the effects of tumour necrosis factor-α on protein and zinc metabolism in rats. 2. Weanling rats were fed for 8 weeks on diets containing 10% fat in the form of corn, fish or coconut oils or butter before an intraperitoneal injection of recombinant human tumour necrosis factor-α was given. Measurements were made 24 h after the injection. 3. In rats fed corn oil, food intake was reduced by 62% and rates of protein synthesis were increased by 86, 32 and 39% in the liver, lung and kidney, respectively. Zinc concentrations increased by 23% in the liver but decreased by 10% in the kidney. Plasma caeruloplasmin and complement C3 levels increased by 25% and 28%, respectively, and plasma albumin level decreased by 24%. 4. Fish oil prevented the increase in hepatic protein synthesis and changed the response of protein synthesis in lung and kidney to a decrease. Changes in hepatic and renal zinc concentrations were prevented. The response of the plasma caeruloplasmin level was unaltered but those of the plasma complement C3 and albumin concentrations were prevented. 5. Coconut oil and butter, although similarly low in linoleic acid, differed in their modulatory effects. With the exception of the rise in the plasma complement C3 concentration, all responses were prevented or greatly inhibited in rats fed butter. In rats fed coconut oil the increase in liver protein synthesis was reduced but that in the lung and kidney was unaffected. Changes in hepatic zinc concentration were unaffected but those in renal zinc concentration were prevented. 6. Fish and coconut oils and butter reduced the intensity of anorexia caused by tumour necrosis factor-α. The extent to which fats rich in (n-3) polyunsaturates or poor in linoleic acid modulate the metabolic response to tumour necrosis factor-α depends upon additional fatty acid characteristics.