Identification of a specific interleukin 1 inhibitor in the urine of febrile patients.

Liao, Zenghua; Grimshaw, Robert S.; Rosenstreich, David L.

doi:10.1084/jem.159.1.126

Cited by 171 publications

(66 citation statements)

References 22 publications

(10 reference statements)

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“…4 Its activation induces the release of the soluble IL-1 receptor antagonist that can neutralize the biologic effects of IL-1a and IL-1b. 9,34 IL-1R2 has the same inhibitory effect. 4,35 IL-1R1 ligation signals via the adaptor protein MyD88 to the kinases IRAK-2 and -4 and uses TRAF6 to involve NF-ĸB, p38, Janus kinase, and ERK for initiating the transcription of inflammatory cytokines including pro-IL-1a and pro-IL-1b.…”

Section: Il-1 Receptormentioning

confidence: 49%

Of Inflammasomes and Alarmins: IL-1β and IL-1α in Kidney Disease

Anders

2016

JASN

195

148

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Kidney injury implies danger signaling and a response by the immune system. The inflammasome is a central danger recognition platform that triggers local and systemic inflammation. In immune cells, inflammasome activation causes the release of mature IL-1b and of the alarmin IL-1a. Dying cells release IL-1a also, independently of the inflammasome. Both IL-1a and IL-1b ligate the same IL-1 receptor (IL-1R) that is present on nearly all cells inside and outside the kidney, further amplifying cytokine and chemokine release. Thus, the inflammasome-IL-1a/IL-b-IL-1R system is a central element of kidney inflammation and the systemic consequences. Seminal discoveries of recent years have expanded this central paradigm of inflammation. This review gives an overview of arising concepts of inflammasome and IL-1a/b regulation in renal cells and in experimental kidney disease models. There is a pipeline of compounds that can interfere with the inflammasome-IL-1a/IL-b-IL-1R system, ranging from recently described small molecule inhibitors of NLRP3, a component of the inflammasome complex, to regulatory agency-approved IL-1-neutralizing biologic drugs. Based on strong theoretic and experimental rationale, the potential therapeutic benefits of using such compounds to block the inflammasome-IL-1a/IL-b-IL-1R system in kidney disease should be further explored.

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Section: Il-1 Receptormentioning

confidence: 49%

Of Inflammasomes and Alarmins: IL-1β and IL-1α in Kidney Disease

Anders

2016

JASN

195

148

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“…and purified material (13,(14)(15)(16)(17)(18)(19)(20)(21)(22). However, these inhibitors found in vivo did not seem to affect MCF/IL-1 as defined by PGE2 production-stimulating activity (23).…”

Section: Methodsmentioning

confidence: 99%

“…Abbreviations used in this paper: Con A, concanavalin A; DME, Dulbecco's modified Eagles medium; hrIL-l ,B, human recombinant IL-I f,; IL-1, interleukin 1; LAF, lymphocyte-activating factor; MCF, mononuclear cell factor; PGE2, prostaglandin E2-glandin E2 (PGE2) and collagenase, both of which reflect mechanisms of tissue destruction (4)(5)(6)(7)(8). IL-1 has been found in synovial fluid (9,10), serum (11,12), and urine (13,14). However, the control of IL-I activities and its regulation in vivo is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

“…However, the control of IL-I activities and its regulation in vivo is poorly understood. Inhibitors of LAF/IL-1 have been revealed in urine (13,14), serum (15), and cell culture supernatant (16)(17)(18)(19), but no in vivo inhibitory activity against MCF/IL-l has been described as yet. We now report MCF/IL-l activities ('-67, -35, and 17 kD) and MCF/IL-l inhibitor(s) (-25 kD) in urine from patients with monocytic leukemia.…”

Section: Introductionmentioning

confidence: 99%

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Prostaglandin E2 and collagenase production by fibroblasts and synovial cells is regulated by urine-derived human interleukin 1 and inhibitor(s).

Balavoine¹,

Rochemonteix²,

Williamson³

et al. 1986

J. Clin. Invest.

200

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Interleukin 1 (IL-1) possesses multiple biological activities that may be blocked selectively by different inhibitors. Some known inhibitors block the lymphocyte activating factor (LAF/IL-1) but not the mononuclear cell factor (MCF/IL-1) measured by its capacity to stimulate prostaglandin E2 (PGE2) and colingenase production. The presence of IL-1 in vivo may be difficult to detect due to the presence of inhibitor(s) and the level of the inhibitor(s) may vary depending upon pathological conditions. We have found that urine from three patients with monocytic leukemia (M5) contained high levels of inhibitor(s) of MCF/II-1, whereas urine of normal subjects did not contain significant amounts. Urine from two patients with other blood neoplasic diseases also contained little inhibitory activity. The MCF/IL-1 inhibitor(s), which also acts on human recombinant IL-1 ft, is -25-35 kD, is not retained on concanavalin A-Sepharose column and can be partially destroyed with urea and boiling. At this stage of the purification the fraction containing the MCF/IL-1 inhibitor(s) also inhibits the LAF/IL-1 assay. However, this inhibitor(s) is probably distinct from other inhibitors already described.

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“…In vitro, HGP.43 induced cytotoxic activity in macrophages against Lewis carcinoma cells. In vivo, growth of the primary Lewis tumor was not delayed in HGP.43-treated mice, but the size and number of lung metastases were significantly reduced (5 Thymocytes were harvested from C3H/HeJ mice as described by Liao et al (9).…”

mentioning

confidence: 99%

A 92-kDa human immunostimulatory protein.

Fontan

Briend²,

Saklani-Jusforgues³

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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We purified to apparent homogeneity a human urinary glycoprotein of 92 kDa (HGP.92) that, administered intravenously at 250 pg/kg, fully protected mice against a lethal inoculum of Listeria monocytogenes. Since HGP.92 protected scid mice, which lack B and T lymphocytes, this increased resistance toListeria did not appear to be lymphocyte mediated. Furthermore, inflammatory macrophages incubated with 6 nM HGP.92 inhibited the growth of Lewis carcinoma cells in vitro. These two activities appeared to depend on an oligosaccharlde moiety, as they were lost after N-Glycanase treatment of HGP.92. Thus, the biological activity of HGP.92 was in some way related to a glycan moiety. Thymocytes were harvested from C3H/HeJ mice as described by Liao et al. (9).Urinary Fractions. Twenty-four-hour urine specimens were collected from healthy male and female human beings and stored at -200C as described by Fontan et al. (4). THP was isolated from pooled urine after two salt precipitations as described by Tamm and Horsfall (10 tTo whom reprint requests should be addressed. 8353The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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Identification of a specific interleukin 1 inhibitor in the urine of febrile patients.

Cited by 171 publications

References 22 publications

Of Inflammasomes and Alarmins: IL-1β and IL-1α in Kidney Disease

Of Inflammasomes and Alarmins: IL-1β and IL-1α in Kidney Disease

Prostaglandin E2 and collagenase production by fibroblasts and synovial cells is regulated by urine-derived human interleukin 1 and inhibitor(s).

A 92-kDa human immunostimulatory protein.

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