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Production of hemolymphopoietic cytokines (IL-6, IL-8, colony-stimulating factors) by normal human astrocytes in response to IL-1 beta and tumor necrosis factor-alpha.
J Immunol. 1992 Oct 01; 149(7):2358-66.JI

Abstract

Astrocyte-enriched populations were established from human embryonic brain analyzed for their ability to synthesize cytokines potentially relevant for mechanisms of inflammation and immunity in the brain. Unstimulated astrocytes did not secrete significant IL-6, IL-8, macrophage CSF (M-CSF), granulocyte-macrophage CSF (GM-CSF), or granulocyte-CSF (G-CSF), as determined by specific ELISA and/or bioassay. With the exception of M-CSF mRNA, transcripts for the above factors were not detected in unstimulated astrocytes. On exposure of human astrocytes to IL-1 beta, high levels of IL-6, IL-8, M-CSF, G-CSF, and GM-CSF mRNAs were detected; moreover, active secretion of all the above cytokines was demonstrated. TNF-alpha was also able to stimulate IL-6, IL-8, M-CSF, GM-CSF, and G-CSF synthesis and secretion, but was generally less potent than IL-1 beta. No IL-3 mRNA or protein was detected in unstimulated or cytokine-treated astrocytes. IL-1 alpha and IL-1 beta mRNAs and proteins were not detected in unstimulated astrocytes, but were present in very small amounts after stimulation with TNF-alpha/IL-1 beta. No IL-6, M-CSF, GM-CSF, G-CSF, or IL-8 were induced by IL-1 beta or TNF-alpha in early primary cultures, which mainly contain undifferentiated neuronal/glial progenitor cells. These studies demonstrate for the first time the production of multiple cytokines by normal human astrocytes stimulated in culture by IL-1 beta and TNF-alpha. The capacity of human astrocytes to synthesize and release cytokines active on hemolymphopoietic cells supports the concept that these cells play an important role in the regulation of inflammatory and immune responses in a variety of brain pathologies.

Authors+Show Affiliations

Laboratory of Organ and System Pathophysiology, Istituto Superiore di Sanità, Rome, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

1382099

Citation

Aloisi, F, et al. "Production of Hemolymphopoietic Cytokines (IL-6, IL-8, Colony-stimulating Factors) By Normal Human Astrocytes in Response to IL-1 Beta and Tumor Necrosis Factor-alpha." Journal of Immunology (Baltimore, Md. : 1950), vol. 149, no. 7, 1992, pp. 2358-66.
Aloisi F, Carè A, Borsellino G, et al. Production of hemolymphopoietic cytokines (IL-6, IL-8, colony-stimulating factors) by normal human astrocytes in response to IL-1 beta and tumor necrosis factor-alpha. J Immunol. 1992;149(7):2358-66.
Aloisi, F., Carè, A., Borsellino, G., Gallo, P., Rosa, S., Bassani, A., Cabibbo, A., Testa, U., Levi, G., & Peschle, C. (1992). Production of hemolymphopoietic cytokines (IL-6, IL-8, colony-stimulating factors) by normal human astrocytes in response to IL-1 beta and tumor necrosis factor-alpha. Journal of Immunology (Baltimore, Md. : 1950), 149(7), 2358-66.
Aloisi F, et al. Production of Hemolymphopoietic Cytokines (IL-6, IL-8, Colony-stimulating Factors) By Normal Human Astrocytes in Response to IL-1 Beta and Tumor Necrosis Factor-alpha. J Immunol. 1992 Oct 1;149(7):2358-66. PubMed PMID: 1382099.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Production of hemolymphopoietic cytokines (IL-6, IL-8, colony-stimulating factors) by normal human astrocytes in response to IL-1 beta and tumor necrosis factor-alpha. AU - Aloisi,F, AU - Carè,A, AU - Borsellino,G, AU - Gallo,P, AU - Rosa,S, AU - Bassani,A, AU - Cabibbo,A, AU - Testa,U, AU - Levi,G, AU - Peschle,C, PY - 1992/10/1/pubmed PY - 1992/10/1/medline PY - 1992/10/1/entrez SP - 2358 EP - 66 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 149 IS - 7 N2 - Astrocyte-enriched populations were established from human embryonic brain analyzed for their ability to synthesize cytokines potentially relevant for mechanisms of inflammation and immunity in the brain. Unstimulated astrocytes did not secrete significant IL-6, IL-8, macrophage CSF (M-CSF), granulocyte-macrophage CSF (GM-CSF), or granulocyte-CSF (G-CSF), as determined by specific ELISA and/or bioassay. With the exception of M-CSF mRNA, transcripts for the above factors were not detected in unstimulated astrocytes. On exposure of human astrocytes to IL-1 beta, high levels of IL-6, IL-8, M-CSF, G-CSF, and GM-CSF mRNAs were detected; moreover, active secretion of all the above cytokines was demonstrated. TNF-alpha was also able to stimulate IL-6, IL-8, M-CSF, GM-CSF, and G-CSF synthesis and secretion, but was generally less potent than IL-1 beta. No IL-3 mRNA or protein was detected in unstimulated or cytokine-treated astrocytes. IL-1 alpha and IL-1 beta mRNAs and proteins were not detected in unstimulated astrocytes, but were present in very small amounts after stimulation with TNF-alpha/IL-1 beta. No IL-6, M-CSF, GM-CSF, G-CSF, or IL-8 were induced by IL-1 beta or TNF-alpha in early primary cultures, which mainly contain undifferentiated neuronal/glial progenitor cells. These studies demonstrate for the first time the production of multiple cytokines by normal human astrocytes stimulated in culture by IL-1 beta and TNF-alpha. The capacity of human astrocytes to synthesize and release cytokines active on hemolymphopoietic cells supports the concept that these cells play an important role in the regulation of inflammatory and immune responses in a variety of brain pathologies. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/1382099/Production_of_hemolymphopoietic_cytokines__IL_6_IL_8_colony_stimulating_factors__by_normal_human_astrocytes_in_response_to_IL_1_beta_and_tumor_necrosis_factor_alpha_ L2 - https://www.jimmunol.org/lookup/pmidlookup?view=long&pmid=1382099 DB - PRIME DP - Unbound Medicine ER -