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Relevant bibliographies by topics / Centrally administered interleukin-4

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Academic literature on the topic 'Centrally administered interleukin-4'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Centrally administered interleukin-4"

1

Pepe, Giovanna, Giorgia Calderazzi, Maglie Marcella De, Alessandro Maria Villa, and Elisabetta Vegeto. "Heterogeneous induction of microglia M2a phenotype by central administration of interleukin-4." J Neuroinflammation. 11, no. 1 (2014): 1031. https://doi.org/10.1186/s12974-014-0211-6.

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BackgroundAcquisition of the M1 or M2 phenotypes by microglia has been shown to occur during the development of pathological conditions, with M1 activation being widely involved in neurotoxicity in relation with the anatomical localization and the reactivity of subtypes of microglia cells. On the contrary, little is known on the ability of microglia to undergo M2 polarization by interleukin-4 (IL4), the typical M2a polarization signal for peripheral macrophages.MethodsRecombinant mouse IL4 was injected in the third cerebral ventricle of mice to induce brain alternative polarization. The mRNA l

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2

Sonti, G., S. E. Ilyin, and C. R. Plata-Salaman. "Anorexia induced by cytokine interactions at pathophysiological concentrations." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 6 (1996): R1394—R1402. http://dx.doi.org/10.1152/ajpregu.1996.270.6.r1394.

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Interleukin (IL)-1 beta, IL-8, and tumor necrosis factor-alpha (TNF-alpha) induce anorexia when administered intracerebroventricularly at doses that yield estimated pathophysiological concentrations reported in the cerebrospinal fluid (CSF). Our hypothesis is that pivotal cytokines released during pathological processes interact to induce anorexia during disease. In the present study, we investigated the effects of the intracerebroventricular microinfusion of individual or multiple combinations (8 dyads and 5 triads) of IL-1 beta, IL-8, and TNF-alpha on feeding and the microstructure of eating

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3

Wernstedt, Ingrid, Amanda Edgley, Anna Berndtsson, et al. "Reduced stress- and cold-induced increase in energy expenditure in interleukin-6-deficient mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 3 (2006): R551—R557. http://dx.doi.org/10.1152/ajpregu.00514.2005.

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Interleukin-6 (IL-6) deficient (-/-) mice develop mature onset obesity. Pharmacological studies have shown that IL-6 has direct lipolytic effects and when administered centrally increases sympathetic outflow. However, the metabolic functions of endogenous IL-6 are not fully elucidated. We aimed to investigate the effect of IL-6 deficiency with respect to cold exposure and cage-switch stress, that is, situations that normally increase sympathetic outflow. Energy metabolism, core temperature, heart rate, and activity were investigated in young preobese IL-6−/− mice by indirect calorimetry togeth

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4

Gurish, Michael F., Hong Tao, J. Pablo Abonia та ін. "Intestinal Mast Cell Progenitors Require CD49dβ7 (α4β7 Integrin) for Tissue-specific Homing". Journal of Experimental Medicine 194, № 9 (2001): 1243–52. http://dx.doi.org/10.1084/jem.194.9.1243.

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Mast cells (MCs) are centrally important in allergic inflammation of the airways, as well as in the intestinal immune response to helminth infection. A single lineage of bone marrow (BM)-derived progenitors emigrates from the circulation and matures into phenotypically distinct MCs in different tissues. Because the mechanisms of MC progenitor (MCp) homing to peripheral tissues have not been evaluated, we used limiting dilution analysis to measure the concentration of MCp in various tissues of mice deficient for candidate homing molecules. MCp were almost completely absent in the small intestin

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5

Cheon, Y. H., H. N. Lee, and M. Kim. "THU0072 THE RELATIONSHIP BETWEEN INFLAMMATION AND COGNITIVE IMPAIRMENT IN RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 248.1–249. http://dx.doi.org/10.1136/annrheumdis-2020-eular.3985.

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Background:The pathophysiology of cognitive impairment remains unclear, however, several studies have demonstrated that pro-inflammatory cytokines such as Interleukin-6 (IL-6), Tumor necrosis factor-α (TNF-α) and lipocalin-2 (LCN2) are related with cognitive impairment by activation of microglia and astrocyte in brain. Rheumatoid arthritis (RA) is a representative inflammatory disease; however, the association of pro-inflammatory cytokines and LCN2 with cognitive impairment has seldomly been investigated in RA.Objectives:Here, we determined the effect of pro-inflammatory cytokines and LCN2 on

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6

Sonti, Gayatri, Mark C. Flynn та Carlos R. Plata-Salamán. "Interleukin-1 (IL-1) Receptor Type I Mediates Anorexia but not Adipsia Induced by Centrally Administered IL-1β". Physiology & Behavior 62, № 5 (1997): 1179–83. http://dx.doi.org/10.1016/s0031-9384(97)80019-4.

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