The Numerous Postulated Biological Manifestations of Interleukin-1

Kampschmidt, Ralph F.

doi:10.1002/jlb.36.3.341

Cited by 141 publications

(43 citation statements)

References 113 publications

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“…Interleukin-1 (IL-1) and tumor necrosis factor (TNF) are proinflammatory cytokines that activate cell proliferation and play an important role in local and systemic immune responses (Dinarello and Wolff, 1993;Dinarello, 1994Dinarello, , 1996Kampschmidt, 1984;BankersFulbright et al, 1996). Despite the importance, the molecular mechanism by which these cytokines induce cellular response is not completely understood.…”

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confidence: 99%

A role for SHPS-1/SIRPα1 in IL-1β- and TNFα-dependent signaling

et al. 2002

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We investigated the role of SHPS-1/SIRPa1 in IL-1b-and TNFa-dependent signaling that leads to the activation of Erk 1/2 and Akt. Treatment of Balb3T3 cells with IL-1b or TNFa activated tyrosine phosphorylation of SHPS-1, its association with SHP-2 and the phosphorylation of Erk 1/2 and Akt. PP1, a specific inhibitor for the Src family protein tyrosine kinases, strongly inhibited tyrosine phosphorylation of SHPS-1 and complex formation of SHPS-1 with SHP-2 by IL1b. In addition, PP1 substantially inhibited the IL-2b-and TNFa-dependent activation of Erk 1/2 and Akt. Exogenous expression of either SHPS-1 mutants that lack SHP-2 binding function or a dominant negative mutant of SHP-2 markedly inhibited the activation of Erk 1/2 and Akt by IL-1b, whereas wild type SHPS-1 did not. Moreover, IL-1b-stimulation induced association of SHPS-1 with IL-1RAcP, a second subunit of IL-1 receptor, whereas expression of SHPS-1 mutant that lack SHP-2 binding function clearly blocked the association and tyrosine phosphorylation of endogenous SHPS-1. Taken together, our results strongly suggest that activation of Erk 1/2 and Akt by proinflammatory cytokines requires tyrosine phosphorylation of SHPS-1 and subsequent association of SHPS-1 with SHP-2.

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confidence: 99%

A role for SHPS-1/SIRPα1 in IL-1β- and TNFα-dependent signaling

et al. 2002

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“…In addition, macrophages are an important source of interleukin (IL)-lar, shown to be identical with haemopoietin-1 (Bartelmez & Stanley, 1985;Mochizuki et al 1987). This molecule, which has a broad range of biological activities (Kampschmidt, 1984), is able to synergize with haematopoietic growth factors to promote the growth of developmentally very early progenitor cells (Stanley et al 1986). In vitro, IL-1 and the macrophage product, tumour necrosis factor (TNF)a, can promote myelomonocytic growth indirectly by stimulating the production of GM-CSF, G-CSF and M-CSF from fibroblasts and endothelial cells (Zucali et al 1986;Broudy et al 1987;Seelentage^ al.…”

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confidence: 99%

Novel cell surface adhesion receptors involved in interactions between stromal macrophages and haematopoietic cells

Crocker

Morris

Gordon

1988

Journal of Cell Science

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SummaryImmunocytochemical staining of tissues with the mouse macrophage-specific monoclonal antibody, F4/80, has shown that large numbers of stromal macrophages are present in adult and foetal haematopoietic tissues. Macrophage plasma membrane processes are seen to establish extensive associations with myeloid and erythroid cells in adult bone marrow and with developing erythroblasts in foetal liver, suggestive of local trophic interactions. To explore the nature of these interactions, methods were developed for isolation of resident bone marrow macrophages (RBMM) and foetal liver macrophages (FLM). Following collagenase digestion of bone marrow or foetal liver, clusters were obtained which were composed of one or more central macrophages surrounded by proliferating haematopoietic cells. After attachment of clusters to glass coverslips, adherent macrophages could be stripped free of haematopoietic cells by pipetting in the absence of divalent cations. The purified RBMM, but not FLM, expressed a novel haemagglutinin, which mediated binding, without ingestion, of large numbers of unopsonized sheep erythrocytes by a divalent cation-independent mechanism. In view of the possibility that this sheep erythrocyte receptor (SER) could interact with a homologous ligand on mouse bone marrow cells, its properties were examined. SER was found to be a lectin-like protein which recognized protease-resistant sialylated glycoconjugates on sheep erythrocytes. The expression of SER was restricted to certain stromal tissue macrophages and was low or absent on monocytes and macrophages obtained from serous cavities. High levels of SER could be induced on elicited peritoneal macrophages by cultivation in mouse serum and the induced receptor was found to mediate low-avidity binding of murine bone marrow cells with characteristics indistinguishable from those seen for binding of sheep erythrocytes. However, maximal binding of bone marrow cells to RBMM depended on a distinct, divalent cation-dependent adhesion system. Using erythroblasts as a ligand, FLM were selected to explore the properties and expression of this adhesion receptor, the erythroblast receptor (EbR). Similar to SER, EbR did not mediate ingestion, and was restricted in its expression to foetal and adult stromal tissue macrophages. Unlike SER, EbR activity was not affected by neuraminidase treatment of the ligand and the receptor was not induced on peritoneal macrophages cultured in mouse serum. EbR appears to be a novel cell adhesion receptor because it was unaffected by inhibitors of several previously described cell adhesion molecules, including the fibronectin receptor. Future studies will attempt to explore the functional significance of these two receptors in macrophage-haematopoietic cell interactions.

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“…Second, the intensity of the change in temper ature caused by the leukocytic pyrogen was less than that caused by exposure to an elevated am bient temperature. Third, the primary site of initia tion of the fever in the present study was in the preoptic-anterior hypothalamic area of the brain with the leukocytic pyrogen (Dinarello, 1984a,b;Gery and Lepe-Zuniga, 1984;Kampschmidt, 1984), whereas peripheral temperature sensors were in volved in the earlier study. Changes in central tem perature induced by a thermode or exposure to am bient changes in temperature have been reported to have selective effects on glucose metabolism (Mor imoto and Murakami, 1985).…”

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confidence: 49%

“…Neither indomethacin nor dexamethasone caused remarkable changes in rates of local glucose utili zation. Key Words: Dexamethasone-Indomethacin Leukocytic pyrogen-Local cerebral glucose utilization.cause a number of physiological changes, one of which is fever (reviews include Dinarello, 1984a,b;Gery and Lepe-Zuniga, 1984;Kampschmidt, 1984). …”

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Effects of Leukocytic Pyrogen (Interleukin-1) on Local Cerebral Glucose Utilization in Rats with and without Premedication with Indomethacin or Dexamethasone

Domer

Mori

Dinarello

et al. 1988

J Cereb Blood Flow Metab

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Summary: Changes in body temperature were recorded in freely moving rats given phosphate-buffered saline or leukocytic pyrogen (interleukin-l) while the animals were in an infant incubator maintained at 25.5 ± OSC. The leukocytic pyrogen increased body temperature by at least 1 DC within 1 h. This rise in temperature was pre vented by premedication with indomethacin (10 mg/kg) but not dexamethasone (0.5 mg/kg) given 15 min before the leukocytic pyrogen. Local rates of glucose utilization were measured in 47 regions of the central nervous system. In none of the regions previously reported to McCulloch et al. (1982b) have reported that rats exposed to ambient temperatures that resulted in either hypothermia or hyperthermia showed re gionally selective decreases or increases in local ce rebral glucose utilization. The range in rectal tem peratures examined in that study was 31.8-40.2°C.These are rather large changes from the normal control range of 37 -37 SC and provide little infor mation about the changes in local cerebral meta bolic rate associated with more common variations in body temperature, e.g., during fever.A family of proteins variously referred to as en dogenous pyrogen, leukocytic endogenous medi ator, lymphocyte-activating factor, B-cell-acti vating factor, and mononuclear cell factor, for which the name interleukin-l was proposed, all Received July 27, 1987; accepted October 6, 1987 Address correspondence and reprint requests to Dr. F. R. 173have an increased rate of glucose utilization associated with an ambient temperature of 32.5DC (McCulloch et al., 1982b) was an increase found in the present experiments. It was concluded that the intensity of the changes in local cerebral glucose utilization in response to the fever caused by the leukocytic pyrogen was insufficient to be measured. Neither indomethacin nor dexamethasone caused remarkable changes in rates of local glucose utili zation. Key Words: Dexamethasone-Indomethacin Leukocytic pyrogen-Local cerebral glucose utilization.cause a number of physiological changes, one of which is fever (reviews include Dinarello, 1984a,b;Gery and Lepe-Zuniga, 1984;Kampschmidt, 1984).

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The Numerous Postulated Biological Manifestations of Interleukin-1

Cited by 141 publications

References 113 publications

A role for SHPS-1/SIRPα1 in IL-1β- and TNFα-dependent signaling

A role for SHPS-1/SIRPα1 in IL-1β- and TNFα-dependent signaling

Novel cell surface adhesion receptors involved in interactions between stromal macrophages and haematopoietic cells

Effects of Leukocytic Pyrogen (Interleukin-1) on Local Cerebral Glucose Utilization in Rats with and without Premedication with Indomethacin or Dexamethasone

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