Relevant bibliographies by topics / Inflammation balance

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Inflammation balance'

Author: Grafiati
Published: 21 December 2024

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Journal articles on the topic "Inflammation balance"

1

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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2

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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4

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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Dissertations / Theses on the topic "Inflammation balance"

1

Motta, Jean-Paul. "Rôle de la balance protéolytique dans l'immunité de la muqueuse intestinale." Toulouse 3, 2012. http://thesesups.ups-tlse.fr/1883/.

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Le traitement des patients atteints de Maladies Inflammatoires Chroniques de l'Intestin (MICI) représente un enjeu d'avenir. La réponse inflammatoire dans l'intestin impliquent la libération de plusieurs médiateurs, comme les protéases. Dans cette thèse, nous avons montré qu'il y avait un déséquilibre entre ces protéases et leurs inhibiteurs au cours des MICI. D'une part, les tissus coliques de ces patients libéraient davantage d'activité protéolytique en comparaison aux tissus sains. D'autre part, les patients atteints de MICI exprimaient dans la muqueuse intestinale une quantité réduite d'ARN messager de l'élafine, un inhibiteur de protéase. Nous avons donc émis l'hypothèse que l'inflammation peut être réduite en rééquilibrant cette balance grâce à l'administration d'élafine. Nous avons utilisé des souris transgéniques pour l'expression de l'élafine de façon constitutive. Puis, nous avons utilisé un virus et des bactéries lactiques pour exprimer de façon transitoire cette molécule dans le côlon. En parallèle, nous avons développé des approches in vitro pour connaître le rôle de l'élafine dans la physiologie des cellules épithéliales de l'intestin. Grâce à ces différentes approches, nous avons montré que l'élafine réduisait : les symptômes de la maladie dans différents modèles, la libération de cytokines pro-inflammatoire, l'infiltration des cellules immunitaire et restaurait l'homéostasie de l'épithélium intestinal au cours de l'inflammation. Ces résultats nous ont permis de proposer que l'utilisation d'inhibiteurs de protéases dans l'intestin au cours de l'inflammation constitue une nouvelle piste thérapeutique contre les MICI
Treatment of Inflammatory Bowel Disease (IBD) represents a major medical challenge. Inflammatory processes in the gut are induced by several cells and mediators. Among them, serine proteases are mediators involved in many pathways leading to inflammation in the gut. During this thesis, we have shown that serine proteases and their inhibitors were dysregulated during IBD. On one hand, colonic biopsies from IBD patients released higher amount of proteolytic activity than healthy controls did. On the other hand, the expression of elafin mRNA (i. E. A protease inhibitor) was downregulated in the mucosa of patients suffering from IBD. We have hypothesized that gut inflammation could be reduced by re-equilibrating that balance in the gut, using elafin inhibitor. We have developed several in vivo approaches to evaluate the therapeutic properties of elafin. We used transgenic mice expressing elafin constitutively, we have used recombinant viral vectors and recombinant lactic acid bacteria to express transiently elafin in the gut during colitis. We have also evaluated in vitro the role of elafin in the physiology of human intestinal epithelial cells. Using those different approaches, we have demonstrated that elafin reduced the clinical score of colitis in different models in mice, reduced the release of pro-inflammatory cytokines, reduced immune cell infiltration and also restored epithelium homeostasis during inflammation. Those results led us to think that protease inhibitors have a promising therapeutic potential for the treatment of IBD
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Walhin, Jean-Philippe. "The impact of exercise and energy balance on metabolic control and inflammation in humans." Thesis, University of Bath, 2013. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608332.

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The aims of the work described in this thesis are to examine the impact of physical activity/exercise and energy balance on metabolic control and inflammation and specifically whether exercise has independent benefits on various health-related outcomes above a role in energy balance. Chapter 3 examined whether a lifestyle intervention combining dietary advice with increased physical activity would further improve inflammatory markers compared to dietary advice alone and usual care in 494 patients with newly diagnosed type 2 diabetes. Motivational unsupervised diet and diet plus physical activity interventions led to reductions in inflammatory markers. Interestingly, there was no greater benefit from adding physical activity advice to dietary advice. Chapter 4 investigated whether daily vigorous-intensity exercise would counteract the metabolic changes induced by short-term overfeeding and reduced physical activity independent of any net attenuation of energy imbalance in healthy young men. The overfeeding and reduced activity model induced a state of insulin resistance, hyperinsulinaemia and altered expression of several key genes within adipose tissue. The inclusion of a daily vigorous-intensity exercise bout largely prevented these changes from taking place independent of any net effect on energy imbalance. Chapter 5 examined whether caloric restriction combined with vigorous-intensity exercise would further improve metabolic control and inflammatory markers compared to moderate-intensity exercise in middle-aged, overweight/obese men and postmenopausal women. Three weeks of caloric restriction combined with either vigorous or moderate-intensity physical exercise improved insulin sensitivity, lipid profiles and markers of inflammation. These results confirm the positive effects of combined caloric restriction and increased exercise in sedentary overweight men and women, but that exercise intensity does not seem to be so important. In conclusion, this thesis presents reasonable evidence that exercise per se has a positive impact upon metabolic control and inflammation independent of energy balance during an energy surplus but that a role in contributing to the health benefits during an energy deficit are less convincing.
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Lorvellec, Marie. "Dialogue entre le complément C1 et l'alarmine HMGB1 dans l'inflammation." Electronic Thesis or Diss., Université Grenoble Alpes, 2024. http://www.theses.fr/2024GRALV033.

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La protéase C1s est un élément central dans l’initiation de la voie classique du système du complément. Elle était auparavant considérée comme ciblant exclusivement les protéines C2 et C4 dans cette cascade protéolytique. Des découvertes récentes ont cependant mis en lumière la présence de C1s libre constitutivement active dans certaines pathologies, suggérant un rôle plus large de cette protéase au-delà de l'activation du complément. Parmi les cibles non-canoniques identifiées de C1s figure la protéine HMGB1, initialement décrite comme une protéine nucléaire impliquéedans la condensation de la chromatine et l'expression des gènes. Des études récentes ont démontré que HMGB1 peut également être localisée dans différents compartiments cellulaires et qu'elle joue un rôle crucial dans l'inflammation lorsqu'elle est libérée dans le milieu extracellulaire. Ce projet de thèse avait pour objectif principal d'élucider le rôle du clivage de HMGB1 par C1s dans la modulation de la réponse inflammatoire. Nos travaux ont démontré que les fragments de digestion de HMGB1 possèdent des effets distincts de la protéine entière sur l'activation du complément et laréponse cytokinique des macrophages. Nous avons notamment confirmé que la protéine entière active la voie classique du complément lorsqu’elle est fixée à une surface et qu’elle favorise la polarisation M1 des macrophages en réponse aux LPS. En revanche, le fragment f2 est capable d'activer la voie classique du complément même lorsqu’il est en solution, tandis que le fragment f3 inhibe la sécrétion de cytokines pro-inflammatoires dans les études cellulaires. De plus, nous avons exploré l'impact de l'état d'oxydo-réduction des cystéines sur les effets de HMGB1 et de ses fragmentsen utilisant des mutants mimétiques. La digestion de HMGB1 est restreinte lorsque la protéine est sous forme disulfure, suggérant un rôle important du pont disulfure dans l’accès aux sites de digestion par C1s. Les formes redox de la protéine entière ne semblent pas affecter sa capacité à activer le complément, tandis que le fragment f2 oxydé pourrait perdre sa capacité d'activation en solution. Ces résultats révèlent que le clivage de HMGB1 par C1s agit comme un chronomètre de l’inflammation, orchestrant la réponse inflammatoire via la transition d’une phase d’amplification pro-inflammatoireà une phase de résolution. Ces découvertes ouvrent de nouvelles perspectives pour la compréhension des mécanismes complexes de l'inflammation et le développement de thérapies pour le traitement de pathologies inflammatoires
C1s protease is a central component in the initiation of the classical pathway of the complement system. It was originally believed to exclusively target proteins C2 and C4 in this proteolytic cascade. However, recent discoveries have highlighted the presence of constitutively active free C1s in certain pathologies, suggesting a broader role for this protease beyond complement activation. Among the non-canonical targets identified for C1s is the HMGB1 protein, initially described as a nuclear protein involved in chromatin condensation and gene expression.Recent studies have shown that HMGB1 can also be localized in different cellular compartments and plays a crucial role in inflammation when released into the extracellular environment. The main objective of this thesis project was to elucidate the role of C1s cleavage of HMGB1 in modulating the inflammatory response. Our work has shown that HMGB1 digestion fragments have distinct effects from the whole protein on complement activation and macrophage cytokine responses.In particular, we confirmed that the whole protein activates the classical complement pathway when bound to a surface and promotes M1 macrophage polarization in response to LPS. In contrast, fragment f2 is capable of activating the classical complement pathway, even when in solution, while fragment f3 inhibits the secretion of pro-inflammatory cytokines in cell studies. In addition, we explored the impact of cysteine redox state on the effects of HMGB1 and its fragments using mimetic mutants. HMGB1 digestion is restricted when the protein is in disulfide form, suggesting an important role of the disulfide bridge in access to the C1s digestion site. The redox forms of the whole protein do notappear to affect its ability to activate complement, while oxidized fragment f2 may lose its ability to activate it in solution. These results reveal that C1s cleavage of HMGB1 acts as an inflammation timer, orchestrating the inflammatory response through the transition from a pro-inflammatory amplification phase to a resolution phase. These findings open new perspectives for understanding the complex mechanisms of inflammation and the development of therapies for the treatment of inflammatory diseases
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Morton, Brian Edward. "The role of microRNA-155 as a master switch determining the balance of inflammation and fibrosis in chronic disorders." Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/9118/.

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Macrophages are a dynamic cell type and represent a key component of the immune response, with a broad range of activities throughout the body. They respond to external cues, including microbes, alarmins, and growth factors, to eliminate invading pathogens through initiation of inflammation. Subsequently, they carry out several regulatory roles, including clearance of cellular debris, the resolution of inflammation, and wound healing to restore tissue homeostasis after an inflammatory response. The ability of macrophages to change their phenotype in this manner must be tightly regulated, as dysregulated macrophage activity is central to the pathogenesis of both inflammatory and fibrotic autoimmune disorders, such as Rheumatoid Arthritis (RA) and Idiopathic Pulmonary Fibrosis (IPF), respectively. One of the mechanisms by which regulation of macrophages occurs is the microRNA network. MicroRNAs (miRNAs) are a class of short, non-protein coding RNAs that post-transcriptionally regulate gene expression through translational repression, destabilisation or degradation of target mRNA. miR-155 is a multi-functional miRNA that has roles in regulating the development and function of many immune cells, including macrophages. Abnormal expression of miR-155 is associated with a number of autoimmune disorders and cancers. We reported previously that miR-155 is elevated in RA and contributes to the chronic, pro- inflammatory response of macrophages by repressing key anti-inflammatory proteins. However, the role of miR-155 in the regulation of remodelling responses by macrophages is less well characterised. Modulation of miRNA activity in cells through the use of mimics and inhibitors has emerged as a potential therapeutic strategy for the treatment of diseases. Technologies involving the use of lipid vesicles as delivery agents for introducing therapeutics into target cells have shown potential in increasing the drug efficacy.
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Lattuada, Marco. "Effect of Ventilatory Support on Abdominal Fluid Balance in a Sepsis Model." Doctoral thesis, Uppsala universitet, Klinisk fysiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-207218.

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In patients affected by acute respiratory failure or acute respiratory distress syndrome (ARDS) the leading cause of death is failure of different vital organs other than the lungs, so called multiple organ dysfunction syndrome (MODS). The abdominal organs have a crucial role in the pathogenesis of this syndrome. There is a lack of knowledge regarding the mechanisms by which mechanical ventilation can affect the abdominal compartment. One hypothesis is that mechanical ventilation can interfere with abdominal fluid balance causing edema and inflammation. We addressed the question whether different levels of ventilatory support (mechanical ventilation with different levels of positive end-expiratory pressure, PEEP, and spontaneous breathing with or without PEEP) can influence abdominal edema and inflammation in both healthy and endotoxin-exposed animals. The effect on lymphatic drainage from the abdomen exerted by different degrees of ventilatory support was evaluated (paper I). We demonstrated that endotoxin increases abdominal lymph production, that PEEP and mechanical ventilation increase lymph production but also impede lymphatic drainage; spontaneous breathing improves lymphatic drainage from the abdomen. By adapting a non-invasive nuclear medicine imaging technique and validating it (paper II), we have been able to evaluate extravascular fluid accumulation (edema formation) in the abdomen over time (paper III) demonstrating that edema increases during endotoxemia, mimicking a sepsis-like condition, and that spontaneous breathing, compared to mechanical ventilation, reduces extravascular fluid. Pro-inflammatory cytokines TNF-α and IL-6 in intestinal biopsies are reduced during spontaneous breathing compared to mechanical ventilation. Abdominal edema results in increased intra-abdominal pressure (IAP): in paper IV we analyzed the effect of increased intra-abdominal pressure on the respiratory system. Pulmonary shunt fraction increased with high IAP both in healthy and LPS animals, resulting in decreased level of oxygenation. These changes are only partially reversible by reducing IAP. In conclusion, mechanical ventilation is a life-saving tool but the possible side effect at the extra-pulmonary level should be considered, and the introduction of some degree of spontaneous breathing when clinically possible is a suggested choice.
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Le, Thuc Ophélia. "Rôle de l'inflammation hypothalamique dans les dérégulations de la balance énergétique." Electronic Thesis or Diss., Nice, 2015. http://theses.unice.fr/2015NICE4122.

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L’hypothalamus est une aire cérébrale clé pour le contrôle de la prise alimentaire et des dépenses énergétiques ; en intégrant des signaux périphériques (hormones, nutriments). Une inflammation dans l’hypothalamus pourrait perturber le fonctionnement de ce dernier, dérégulant l’homéostasie énergétique et induire une perte de poids ou l’obésité. Nous avons cherché à identifier les relais moléculaires entre l’inflammation et les systèmes neuropeptidergiques hypothalamiques régulant l’homéostasie énergétique, en nous concentrant sur les chimiokines. D’une part, nous avons montré que le récepteur CCR2 participe à la perte de poids liée à une inflammation aigue induite chez la souris par l’injection centrale de lipopolysaccharide bactérien, possiblement en induisant l’inhibition de l’activité des neurones hypothalamiques à MCH, peptide aux effets orexigènes. D’autre part, nous avons étudié les liens entre inflammation hypothalamique, gain de poids et/ou la consommation de régimes hyperlipidiques pouvant induire à terme une obésité. Nous avons trouvé, chez la souris, que 1) la chimiokine CCL5 favoriserait la prise de poids, possiblement en activant les neurones hypothalamiques à MCH ; 2) la nature des lipides d’un régime hyperlipidique impacterait la cinétique de développement de l’obésité, avec des changements du profil inflammatoire et 3) la consommation excessive de lipides induirait une gliose très précoce dans l’hypothalamus. L’ensemble de nos résultats souligne l’intérêt de cibler l’inflammation hypothalamique dans ces pathologies et identifient les chimiokines comme cibles thérapeutiques potentielles dans le traitement des dérégulations de la balance énergétique
The hypothalamus is a key brain region in the regulation of energy homeostasis, in particular by controlling food intake and energy storage and expenditure by integration of peripheral humoral and nutrient-related signals. Hypothalamic inflammation could alter hypothalamic function, thus deregulate energy homeostasis and induce weight-loss or obesity. We sought to identify mediators that could act as intermediaries between inflammation and neuropeptidergic systems of the hypothalamus that are involved in the regulation of energy homeostasis, focusing on chemokines. First, we studied the effect of a central injection of bacterial lipopolysaccharide, mimicking a acute and strong inflammation state in mice. We identified the receptor CCR2 as a central actor in the weight-loss induced by this treatment, possibly by direct inhibitory effects on hypothalamic neurons expressing MCH, a peptide known to have orexigenic and energy conservative effects. Second, we studied links between hypothalamic inflammation, weight-gain and/or high-fat diets consumption that can induce, eventually, obesity. We found in mice that: 1) the chemokine CCL5 would promote weight-gain, possibly by enhancing the activity of hypothalamic MCH neurons; 2) altering the lipid composition of a high-fat diet changes the kinetics of the development of diet-induced obesity, together with changes in the inflammatory profile and 3) an excessive dietary lipid intake can induce very early gliosis in the hypothalamus. Taken together, our results underline the interest of reducing hypothalamic inflammation to fight feeding behavior deregulations and identify chemokines as putative therapeutic targets
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MERLOT, Élodie. "Modulation de la production de cytokines par l'environnement." Phd thesis, Institut national agronomique paris-grignon - INA P-G, 2003. http://tel.archives-ouvertes.fr/tel-00007518.

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Les conséquences immunitaires d'un stress d'origine environnementale sont complexes et encore difficilement prévisibles. Le stress affecte le système immunitaire soit en agissant sur l'immunité innée, en altérant la réactivité inflammatoire, soit en agissant sur l'immunité acquise, en modulant la production de cytokines dites Th1 et Th2. L'environnement social
contribue largement au développement et à l'expression de maladies. Dans les espèces sociales, la position sociale occupée dans le groupe module la susceptibilité aux infections mais les supports endocriniens et immunitaires de ces différences de susceptibilité sont ignorés. La remise en cause de l'organisation sociale engendre un stress important dont les conséquences immunitaires sont encore sujettes à controverse.
Ce travail de thèse a pour objectifs (1) de décrire l'influence du statut social sur le fonctionnement des systèmes endocrinien et immunitaire, (2) de préciser les effets du stress
social sur la production de cytokines et la susceptibilité aux infections et (3) de rechercher des facteurs à l'origine de la variabilité des conséquences immunitaires du stress social.
Chez le porcelet, un regroupement après le sevrage élève transitoirement le cortisol salivaire et altère le comportement mais n'affecte pas la réactivité des lymphocytes sanguins.
La suite des travaux a utilisé une procédure de défaite sociale chronique chez la souris. Les résultats obtenus mettent en évidence une influence du statut social. En absence de stress, les
dominants présentent des niveaux de base de corticostérone et une réponse spécifique à la tuberculine supérieurs aux dominés. Suite à une défaite sociale, les dominants sont plus affectés que les dominés. La défaite sociale augmente la réactivité inflammatoire mais ne modifie pas de façon nette l'équilibre de la production de cytokines de type Th1 et Th2 et n'affecte pas l'immunité spécifique développée contre une infection mycobactérienne. Les conséquences immunitaires de la défaite sociale ne sont observées que lorsque le stress est associé à des combats et à des blessures. Ces travaux montrent que la réponse au stress dépend de l'histoire sociale de l'individu, en particulier de son statut social. De plus, les
répercussions immunitaires du stress dépendent aussi de l'histoire immunitaire récente. En effet, une réaction inflammatoire systémique inhibe la libération plasmatique de cytokines
inflammatoires en réponse à un stress psychologique ultérieur.
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Jonsson, Yvonne. "Cytokines and immune balance in preeclampsia : a survey of some immunological variables and methods in the study of preeclampsia." Doctoral thesis, Linköping : Linköpings universitet, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med924s.pdf.

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9

Le, Thuc Ophélia. "Rôle de l'inflammation hypothalamique dans les dérégulations de la balance énergétique." Thesis, Nice, 2015. http://www.theses.fr/2015NICE4122/document.

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L’hypothalamus est une aire cérébrale clé pour le contrôle de la prise alimentaire et des dépenses énergétiques ; en intégrant des signaux périphériques (hormones, nutriments). Une inflammation dans l’hypothalamus pourrait perturber le fonctionnement de ce dernier, dérégulant l’homéostasie énergétique et induire une perte de poids ou l’obésité. Nous avons cherché à identifier les relais moléculaires entre l’inflammation et les systèmes neuropeptidergiques hypothalamiques régulant l’homéostasie énergétique, en nous concentrant sur les chimiokines. D’une part, nous avons montré que le récepteur CCR2 participe à la perte de poids liée à une inflammation aigue induite chez la souris par l’injection centrale de lipopolysaccharide bactérien, possiblement en induisant l’inhibition de l’activité des neurones hypothalamiques à MCH, peptide aux effets orexigènes. D’autre part, nous avons étudié les liens entre inflammation hypothalamique, gain de poids et/ou la consommation de régimes hyperlipidiques pouvant induire à terme une obésité. Nous avons trouvé, chez la souris, que 1) la chimiokine CCL5 favoriserait la prise de poids, possiblement en activant les neurones hypothalamiques à MCH ; 2) la nature des lipides d’un régime hyperlipidique impacterait la cinétique de développement de l’obésité, avec des changements du profil inflammatoire et 3) la consommation excessive de lipides induirait une gliose très précoce dans l’hypothalamus. L’ensemble de nos résultats souligne l’intérêt de cibler l’inflammation hypothalamique dans ces pathologies et identifient les chimiokines comme cibles thérapeutiques potentielles dans le traitement des dérégulations de la balance énergétique
The hypothalamus is a key brain region in the regulation of energy homeostasis, in particular by controlling food intake and energy storage and expenditure by integration of peripheral humoral and nutrient-related signals. Hypothalamic inflammation could alter hypothalamic function, thus deregulate energy homeostasis and induce weight-loss or obesity. We sought to identify mediators that could act as intermediaries between inflammation and neuropeptidergic systems of the hypothalamus that are involved in the regulation of energy homeostasis, focusing on chemokines. First, we studied the effect of a central injection of bacterial lipopolysaccharide, mimicking a acute and strong inflammation state in mice. We identified the receptor CCR2 as a central actor in the weight-loss induced by this treatment, possibly by direct inhibitory effects on hypothalamic neurons expressing MCH, a peptide known to have orexigenic and energy conservative effects. Second, we studied links between hypothalamic inflammation, weight-gain and/or high-fat diets consumption that can induce, eventually, obesity. We found in mice that: 1) the chemokine CCL5 would promote weight-gain, possibly by enhancing the activity of hypothalamic MCH neurons; 2) altering the lipid composition of a high-fat diet changes the kinetics of the development of diet-induced obesity, together with changes in the inflammatory profile and 3) an excessive dietary lipid intake can induce very early gliosis in the hypothalamus. Taken together, our results underline the interest of reducing hypothalamic inflammation to fight feeding behavior deregulations and identify chemokines as putative therapeutic targets
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10

Coquerelle, Caroline. "Contrôle des réponses immunitaires de type Th1 par les lymphocytes T régulateurs naturels et induits." Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210397.

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Depuis leur découverte en 1973 par Steinman et Cohn, le rôle des cellules dendritiques dans l’initiation des réponses immunitaires a largement été documenté. En effet, les cellules dendritiques constituent les cellules présentatrices d’antigènes professionnelles capables de détecter des molécules microbiennes et inflammatoires afin d’activer le système immunitaire. Outre leur implication dans l’induction des réponses immunes, de plus en plus d’études suggèrent que les cellules dendritiques interviennent dans le contrôle des réponses immunitaires via la sécrétion de cytokines anti-inflammatoires et/ou l’activation ou l’induction de lymphocytes T régulateurs. Ceux-ci incluent les cellules T régulatrices issues naturellement du thymus et les cellules T régulatrices induites en périphérie.

Des résultats obtenus au sein de notre laboratoire ont mis en évidence l’importance des cellules T régulatrices dans le contrôle des réponses de type Th1 induites à l’aide de cellules dendritiques matures chargées avec des antigènes étrangers. Nous avons, dès lors, étudié le rôle du récepteur CTLA-4 exprimé constitutivement à la surface des cellules T régulatrices dans le contrôle des réponses immunitaires induites à l’aide de cellules dendritiques matures et dans un modèle d’inflammation intestinale. L’injection d’anticorps anti-CTLA-4 induit in vitro et in vivo une inhibition de la production d’IFNγ et protège les souris de la colite pro-Th1 induite par l’instillation de TNBS. Cette protection corrèle étroitement avec l’induction de lymphocytes T régulateurs exprimant fortement la molécule ICOS et sécrétant de l’interleukine 10. De plus, nos résultats suggèrent que l’interleukine 10 et l’indoléamine 2, 3 dioxygénase seraient impliquées dans la fonction régulatrice des lymphocytes T ICOShigh.

Nous avons également analysé les mécanismes impliqués dans le contrôle des réponses de type Th1 par les lymphocytes T régulateurs naturels. Nos résultats suggèrent une régulation différente des réponses Th1 en présence et en absence de cette population régulatrice. En effet, les réponses Th1 sont dépendantes de l’interleukine 12 en présence de lymphocytes T régulateurs naturels, alors qu’en leur absence, la molécule CD70 est requise.

En conclusion, nos résultats suggèrent que les lymphocytes T régulateurs naturels et induits contrôlent les réponses immunes de type Th1. Au cours de ce travail, nous avons mis en évidence des stratégies distinctes par lesquelles ces deux populations régulatrices contrôlent la réponse immune. Ces résultats complètent la compréhension des mécanismes de régulation du système immunitaire et ouvrent de nouvelles perspectives d’approche immunothérapeutique.


Doctorat en Sciences
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Books on the topic "Inflammation balance"

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Scharpf, Shavon. Nutritional Guide for Beginners and Seniors : Repair Vital Organs, Curb Inflammation: Balance Hormones. Independently Published, 2021.

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Clark, Ruth. Cool the Fire : Curb Inflammation and Balance Hormones: 28 Days to Renewed Vitality. Smart Nutrition LLC, 2019.

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Durst-Pulkys, Jane. Metabolic Balance Kitchen: Deliciously Satisfying Recipes to Reset Your Metabolism, Fight Inflammation, and Lose Weight. BenBella Books, 2024.

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Lundin, Mia, and Ulrika Davidsson. Hormone Balance Cookbook: 60 Anti-Inflammatory Recipes to Regulate Hormonal Balance, Lose Weight, and Improve Brain Function. Skyhorse Publishing Company, Incorporated, 2018.

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Stone, Jennifer. Alkaline Diet for Beginners: 4 Weeks to Lose Weight, Fight Inflammation and Balance Your Health and Energy. Independently Published, 2018.

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Nelson-Dooley, Cass. Heal Your Oral Microbiome: Balance and Repair Your Mouth Microbes to Improve Gut Health, Reduce Inflammation and Fight Disease. Ulysses Press, 2019.

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Tucker, Rhys. Vagus Nerve: How to Relieve Anxiety, Reduce Chronic Inflammation, and Prevent Illness by Stimulating Vagal Tone to Restore Balance. Independently Published, 2022.

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Nelson-Dooley, Cass. Heal Your Oral Microbiome: Balance and Repair Your Mouth Microbes to Improve Gut Health, Reduce Inflammation and Fight Disease. Ulysses Press, 2019.

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Ott, Christine. Survive and Thrive Through Hormone Balance: An Anti-Aging Approach to Improve Gut Health, Control Inflammation and Reduce Stress. Independently Published, 2020.

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Barr, Emily. Everything Guide to the Blood Sugar Diet: Balance Your Blood Sugar Levels to Reduce Inflammation, Lose Weight, and Prevent Disease. Adams Media Corporation, 2015.

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Book chapters on the topic "Inflammation balance"

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Pinsky, Michael R. "Immune Balance in Critically Ill Patients." In Inflammation, 1–7. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9702-9_1.

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Bachmann, F., and R. Medcalf. "Disturbance of the Hemostasis and Fibrinolysis Balance by Tumor Necrosis Factor." In Molecular Aspects of Inflammation, 167–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76412-7_13.

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Bertagnolli, Monica M. "Cyclooxygenase-2 and Chronic Inflammation: Drivers of Colorectal Tumorigenesis." In Energy Balance and Gastrointestinal Cancer, 157–82. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2367-6_10.

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Bowen, Deborah J., and Stacey Zawacki. "The Role of Policy in Reducing Inflammation." In Impact of Energy Balance on Cancer Disparities, 259–82. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-06103-0_11.

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Cakir, Isin, and Eduardo A. Nillni. "Brain Inflammation and Endoplasmic Reticulum Stress." In Textbook of Energy Balance, Neuropeptide Hormones, and Neuroendocrine Function, 75–108. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89506-2_4.

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Kwon, Hyokjoon, and Jeffrey E. Pessin. "Adipokines, Inflammation, and Insulin Resistance in Obesity." In Textbook of Energy Balance, Neuropeptide Hormones, and Neuroendocrine Function, 225–52. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89506-2_9.

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Klampfer, Lidija, Barbara G. Heerdt, Anna Velcich, Erin Gaffney-Stomberg, Donghai Wang, Elaine Lin, and Leonard H. Augenlicht. "Dietary Modulation of Colon Cancer: Effects on Intermediary Metabolism, Mucosal Cell Differentiation, and Inflammation." In Energy Balance and Gastrointestinal Cancer, 47–64. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2367-6_3.

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Schmidt, Ingrid. "The Role of Juvenile Thermoregulatory Thermogenesis in the Development of Normal Energy Balance or Obesity." In Thermotherapy for Neoplasia, Inflammation, and Pain, 215–25. Tokyo: Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-67035-3_25.

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Cardona, Sandra M., Jenny A. Garcia, and Astrid E. Cardona. "The Fine Balance of Chemokines During Disease: Trafficking, Inflammation, and Homeostasis." In Methods in Molecular Biology, 1–16. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-426-5_1.

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Yilmaz, Umitcan. "Labyrinthitis." In Infections in Otolaryngology, 23–36. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359401.3.

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Labyrinthitis is an inflammation of the part of the inner ear called the labyrinth and is usually caused by viral or bacterial infections. This condition affects balance and hearing functions, causing symptoms such as dizziness, imbalance, hearing loss and tinnitus. The infection can develop following upper respiratory tract infections such as colds, flu or middle ear infections. In the treatment of labyrinthitis, medications are used to relieve symptoms and antiviral or antibiotic therapy may be administered depending on the cause of the infection. Most patients recover within a few weeks with appropriate treatment, but some cases may have permanent balance problems or hearing loss.
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Conference papers on the topic "Inflammation balance"

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Watanabe, Masato, Keitaro Nakamoto, Toshiya Inui, Mitsuru Sada, Miku Oda, Kojiro Honda, Masaki Tamura, Haruyuki Ishii, and Hajime Takizawa. "IL-33/sST2 balance regulates neutrophilic inflammation in the human airways." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3338.

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Kesic, Matthew J., Megan Meyer, Rebecca N. Bauer, and Ilona Jaspers. "Inflammation Modulates The Human Airway Protease/Antiprotease Balance Contributing To Increased Influenza A Infection." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2632.

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Lei, Xiaoxiao, Michael B. Lawrence, and Cheng Dong. "Mechanics of Cell Rolling Adhesion in Shear Flow." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0284.

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Abstract Leukocyte rolling along endothelial cells is a critical step of leukocyte-endothelium interaction, which plays important roles in tissue inflammation and wound healing [1]. The occurrence of rolling results from the dynamic balance of hemodynamic shearing force acting on the cell and adhesive bond force between cell and endothelium, while the balance strongly depends on the leukocyte deformability [2]. The objective of this study is to elucidate the effects of (1) hydrodynamic shear stress, (2) cell deformation, and (3) surface adhesion strength on the rolling adhesion event through in vitro experiment and theoretical simulation.
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Xu, Mo, Yi Yang, Maria Pokrovskii, Carolina Galan, and Dan R. Littman. "Abstract A080: Balance of commensal bacteria specific Th17 and RORγt+Treg cells in intestinal homeostasis and inflammation." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a080.

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Tanaka, Martin L., Benjamin L. Long, Allston J. Stubbs, and David C. Holst. "Evaluating Pelvis Dynamics in Patients With Acetabular Labral Tears." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80103.

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Common forms of hip disease include labral tears, synovitis, chondromalacia, or femoroacetabular impingement [1, 2]. Most patients with one of these medical conditions seek treatment to alleviate the pain. However, in addition to the pain, dynamic control of hip joint movement may also be impaired. This impairment may result from damage to proprioceptive organs or alterations in sensory capability caused by inflammation. Reduced biofeedback can lead to a loss of joint control that may result in additional injuries due to excessive tissue strain or falling due to a loss of balance. Our hypothesis is that acetabular labral tears alter normal pelvic movement and reduce subject balance control placing the patient at increased risk for additional injuries.
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Whalen, Kristine, Marji McCullough, W. Dana Flanders, Terryl J. Hartman, Suzanne Judd, and Roberd M. Bostick. "Abstract 1889: Paleolithic and Mediterranean diet pattern scores and their associations with biomarkers of inflammation and oxidative balance." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1889.

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Ai, Xiangyan, Guochao Shi, huangying Wan, and Xiaoxia Hou. "The Effect Of 4-1BBL/4-1BB Co-Stimulation On Th17/Treg Balance And Airway Inflammation In Allergic Asthma." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2785.

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Murphy, M. P., M. Casey, C. Gabillard, O. F. Mcelvaney, O. Mcelvaney, T. P. Carroll, C. Gunaratnam, and N. G. Mcelvaney. "ETI Triple Therapy Shows Sustained, Progressive Normalisation of Airway Cytokine and Antiprotease Balance and Systemic Inflammation Over One Year of Treatment." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1381.

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Bobeck, Elizabeth. "Bioactive lipids and related nutrients in companion animal and poultry diets for reducing inflammation and improving immunity." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/vqxl3869.

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Beyond meeting nutritional requirements for growth and maintenance, select dietary ingredients can have additional effects, intended or not, on animal physiology and immune function. Diets can be enriched to benefit the animal, and a dual benefit can be achieved in the case of enriching animal products for the downstream human consumer. Many immune-altering nutrients are fat-soluble, including Vitamin E and D. Importantly, dietary lipids themselves can impact immune function; therefore, a focused and intentional selection of specific dietary fats, specifically omega-3 polyunsaturated fatty acids (PUFA), is one method to alter inflammatory cascades in animals consuming the diet. Examples of other related ingredients to which the immune system is responsive include zinc and probiotics. While work in human, livestock, and companion animal models is working to identify therapeutic inclusion rates for these nutrients and ingredients, it should be noted that physiological alterations are seen in both over and under-inclusion and are nutrient-specific. For example, inclusion above currently recommended levels may optimize immune function and reduce inflammation in the case of vitamin D or omega-3 PUFA, while for zinc, additional pharmacological supplementation above requirements may inhibit immune function. Importantly, when a diet is formulated to reduce overall systemic inflammation, it must be considered that important “background” functions of the immune system, including monitoring for and clearing pathogenic microbial populations, may be down-regulated due to a general reduction in immune reactivity. Continued work to understand how diet and nutrition impact immunity, and how to balance inflammation through nutrition, is an area of active research and will inform downstream users how to best use data to impact consumers of that feed in desirable ways.
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Kim, J. W., S. M. Kim, J. Lee, S. K. Kwok, J. H. Ju, and S. H. Park. "FRI0277 Metformin reduces salivary gland inflammation by controlling b cell differentiation and regulating balance of th17 and treg cell in non-obese diabetic mice." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.2815.

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Reports on the topic "Inflammation balance"

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Liu, Yangjun, Wei Xie, Zbigniew Ossowski, Juan Li, Juan Yang, Yiming Luo, Xia Wu, and Liying Liu. Physical activity, abdominal obesity and inflammatory response in the elderly: a systematic review and meta-analysis of randomized-controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2023. http://dx.doi.org/10.37766/inplasy2023.3.0051.

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Review question / Objective: The purpose of this study was to explore the effects of physical activity (i.e., type of exercise, FITT criteria, control group, other interventions) on abdominal obesity and inflammatory response in elderly? The study method was a randomized controlled trial. Condition being studied: An increasing number of studies have demonstrated that chronic inflammation is closely associated with the initiation and progression of a broad range of age-related diseases, such as cardiovascular disease, cancer, diabetes, Alzheimer’s disease, and other neurodegenerative diseases and is an independent risk factor for mortality in healthy adults. Moreover, there is strong evidence that the development of age-related diseases is linked to low-grade elevation of circulating inflammatory mediators. Therefore, future interventional researches should focus on preserving overall homeostatic balance and controlling inflammatory status in the aging patient.
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