Characterization of interleukin-1 production by microglia in culture
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The production of interleukin-1 (IL-1) by cultured neonatal rat microglia was studied using the D10 cell assay. The results show that IL-1 was secreted in response to lipopolysaccharide (LPS) in a dose- and time-dependent fashion. IL-1 production was specific to microglia and was not induced in astrocytes. Indomethacin, which is known to modulate the release of IL-1 from monocytes, had no effect on LPS-stimulated microglia. Aging of the microglia from two weeks to 4 weeks in culture, however, reduced the release of IL-1 in response to LPS. Our data indicate that microglia are a major source of IL-1 and that the release of IL-1 depends on the presence of inflammatory mediators such as LPS and the age of the culture.Keywords:
Neuroglia
Methylcholanthrene
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Interleukin 1β
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Interleukin (IL)-1beta may effectively decrease introcular pressure (IOP) when administered by subconjunctival injection in normal rabbit. However, IL-1beta is a large molecular agent and an inflammation factor. The aim of this study was to evaluate the penetrability of IL-1beta, and the concentrations of both tumor necrosis factor (TNF)-alpha and IL-6 in the aqueous humor of normal rabbits treated with IL-1beta.A total of 170 rabbits were used in the study and were assigned to several different treatment groups as follows: 125 of the rabbits were assigned to two groups. In one group, 33 rabbits were injected subconjunctivally with IL-1beta and 39 were injected with saline alone. In the other group, 27 rabbits were given eye drops containing IL-1beta (400 ng/ml) and 26 were given saline alone. Aqueous humor (AH) was drawn and the concentration of IL-1beta within the fluid measured. The IOP was measured in another six rabbits after administration of eye drops containing IL-1beta (400 ng/ml). A further 20 rabbits were assigned to 3 groups as follows: eight untreated normal controls; six injected subconjunctivally with IL-1beta; and six injected subconjunctivally with saline alone. AH was drawn and the concentration of TNF-alpha in the fluid was measured. Another 19 rabbits were assigned to 3 groups as follows: seven untreated normal controls; and six injected subconjunctivally with IL-1beta; and six injected subconjunctivally with saline alone. AH was drawn and the concentration of IL-6 in the fluid measured. Measurement of cytokine concentration was by radio-immunoassay in all cases.The IL-1beta concentration in the AH was higher in those animals in which it had been administered subconjunctivally (P < 0.01). The IL-1beta concentration in the AH of the animals given eye drops was almost the same as that in the controls (P > 0.05). The administration of IL-1beta in the form of eye drops had little effect upon IOP reduction. Lower TNF-alpha concentrations were seen in the AH after the subconjunctival administration of IL-1beta, but the concentration of IL-6 was the same as in the normal controls.IL-1beta shows good corneal penetrability after subconjunctival injection into normal rabbit eyes. The IOP reduction induced by IL-1beta is unlikely be associated with an inflammatory response.
Lagomorpha
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The production of interleukin-1 (IL-1) by cultured neonatal rat microglia was studied using the D10 cell assay. The results show that IL-1 was secreted in response to lipopolysaccharide (LPS) in a dose- and time-dependent fashion. IL-1 production was specific to microglia and was not induced in astrocytes. Indomethacin, which is known to modulate the release of IL-1 from monocytes, had no effect on LPS-stimulated microglia. Aging of the microglia from two weeks to 4 weeks in culture, however, reduced the release of IL-1 in response to LPS. Our data indicate that microglia are a major source of IL-1 and that the release of IL-1 depends on the presence of inflammatory mediators such as LPS and the age of the culture.
Neuroglia
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Abstract Reactive gliosis is a response noted after nearly every type of CNS injury and involves both activated microglia and astroglia. Although many investigators believe that reactive glia in some way regulate the survival of injured neurons, the influence of glial elements upon damaged neural tissues remains uncertain. To examine relationships between reactive glia and neurons, secretion products from both microglia and astroglia are tested for their effects upon the survival of cultured neurons. Microglia are found to secrete neurotoxic agents, while astroglia are a source of neuronotrophic factors. Similar patterns of soluble factor production are noted for astroglia‐rich or microglia‐rich regions of rat neocortex damaged by ischemia. These observations suggest that microglia and astroglia compete for control of neuronal survival. Importantly, microglial neurotoxins might hinder the recovery of neurologic function at sites of inflammation.
Gliosis
Neocortex
Neuroglia
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STIMULATED MICROGLIA SUPERNATANTS INDUCED OVEREXPRESSION OF NEURONAL NITRIC OXIDE GENE IN ASTROCYTES
The glia- glia, glia-neuron interactions are very complex and have not yet been clearly understood. Microglia gain reactivity in almost every type of brain insult and by affecting astrocytes and neurons, they determine the fate of damaged brain. In the present study we aimed to see the effect of stimulated microglia on nNOS and iNOS expression of astrocytes. The microglia cultures were stimulated with zymosanA and astrocytes were treated with the medium of microglia for 48 h. The results revealed that the astrocytes treated with microglia medium expressed more nNOS and iNOS than the ones treated with normal medium.
Neuroglia
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Interleukin 6 (IL6) plasma levels were measured in 63 patients with multiple myeloma and 8 individuals with benign monoclonal gammopathy. 15 of these 71 samples showed by an enzyme linked immunosorbent assay (ELISA) detectable levels that ranged from 5 to 107 pg of IL6/ml. The IL6 levels of patients with multiple myeloma did not differ significantly from those of normal individuals (N = 25, range 5-27 pg IL6/m1) (Student's t-test, p = 0.295). The samples were negative for IL4; 3 were found positive for IL1β. A correlation between IL6, IL4 and IL1β levels and disease status was not observed for this group of patients.
Monoclonal gammopathy
Plasma levels
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Objective To study the effect of Interleukin-25 on expressing Th2 inflammatory factor in mouse asthma by nuocyte cells. Methods Nuocytes were collected from mouse spleen of OVA-induced asthma model by density gradient centrifugation. Samples were divided into 3 groups according to different intervention conditions:Interleukin-25 group; control group; anti-Interleukin-25 group. The expression of Interleukin-5 and Interleukin-13 proteins in nuocyte cells supernatant was detected by ELISA. The expression of Interleukin-5 and Interleukin-13 in nuocyte cells was detected by Western blot. The expression of Interleukin-5 and Interleukin-13 mRNA was detected by RT-PCR. The number of nuocyte cells was detected by flow cytometry. Results The expression of Interleukin-5 and Interleukin-13 protein and related gene in Interleukin-25 group was higer than that in the control group or anti-Interleukin-25 group( P 0. 05). The number of nuocyte cells in Interleukin-25 groupwas more than that in control group or anti-interleukin-25( P 0. 05). Conclusions Interleukin-25 can promote the expressing Interleukin-5 and Interleukin-13 in asthma by nuocyte cells and promote the occurrence and development of asthma.
Interleukin 19
Interleukin 1β
Interleukin 3
Interleukin 8
Interleukin 9
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Objective:To analysis the role and clinical significance of interleukin-10(IL-10),interleukin-17(IL-17),interleukin-18(IL-18)and C reactive protein(CRP) in the process of coronary heart disease(CHD).Method:The levels of plasma interleukin-10(IL-10),interleukin-17(IL-17),interleukin-18(IL-18) and C reactive protein(CRP) in 160 patients(AMI 50,UA 68,SA 42) with CHD and 40 normal volunteers were determined by enzyme linked immunoadsorbent assay(ELISA).Result:The plasma levels of interleukin-10(IL-10),interleukin-17(IL-17),interleukin-18(IL-18) and C reactive protein(CRP) in patients with CHD were significantly higher than normal controls(P0.05).Conclusion:The findings suggest IL-10 is a protective factor of CHD,it can not hamper the genesis and development of CHD,meanwhile interleukin-17(IL-17),interleukin-18(IL-18) and Creactive protein(CRP) participate in the pathogenesis and progression of CHD.The plasma levels of these inflammatory factor will contribute to the diagnosis and monitoring of CHD.
Pathogenesis
Interleukin 1β
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