Macrophage mediated cytotoxicity in man: Role of hydrocortisone, trypan blue, chloroquine and prednisolone

Dj, Cameron; Wh, Churchill

doi:10.1016/0192-0561(81)90047-3

Cited by 12 publications

(7 citation statements)

References 21 publications

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“…We think other cells which react to trauma, including macrophages and microglia, may also be important to the host neurotrophic response. Factors released by astrocytes increase survival of neurons and stimulate neurite outgrowth, while activated microglia and macrophages secrete factors which kill neurons (Giulian et al, 1993;Cameron and Churchill, 1981). Our study shows that the time course of the appearance of macrophages (peak at day 3) and activated microglia (peak at day 5 , data not shown) was different from reactive astrocytes.…”

Section: Discussionmentioning

confidence: 58%

Time course of ciliary neurotrophic factor mRNA expression is coincident with the presence of protoplasmic astrocytes in traumatized rat striatum

Asada

et al. 1995

J of Neuroscience Research

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Adrenal grafting for Parkinson's disease has led to modest functional improvement despite poor graft survival. One explanation is a neurotrophic response within the traumatized striatum. This study was undertaken to investigate the time course of the astrocytic response in vivo and in vitro, and the expression of ciliary neurotrophic factor (CNTF) mRNA following striatal injury. Unilateral stereotaxic biopsy of the rat striatum was performed and gelatin sponge (gel-foam) was immediately placed into the biopsy cavity. Rats were sacrificed on days 1, 3, 5, 7, 14, and 28 post biopsy. Immunohistochemical staining of the traumatized striatum with antibodies to glial fibrillary acidic protein (GFAP) was carried out. The reactive astrocytes which appeared within 7 days after trauma were mostly protoplasmic on the basis of morphology, and maximal on day 7, being 30 times the level in the normal striatum. After day 7, fibrous astrocytes appeared and increased up to day 28, while protoplasmic astrocytes decreased. In addition, immunocytochemical double staining of short term cultured astrocytes from the traumatized striatum with anti-A2B5 and anti-GFAP antibodies revealed that 84% and 90% of astrocytes were type 1 astrocytes on days 3 and 7, respectively; however, by day 28 47% of astrocytes were type 2. Northern blot analysis revealed that CNTF mRNA expression was up-regulated and peaked on day 7, coincident with a predominance of protoplasmic astrocytes in vivo and type 1 astrocytes in vitro, respectively. These findings suggest that the expression of CNTF mRNA is part of the early astrocytic response to trauma, particularly associated with protoplasmic astrocytes in vivo and type 1 astrocytes in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 58%

Time course of ciliary neurotrophic factor mRNA expression is coincident with the presence of protoplasmic astrocytes in traumatized rat striatum

Asada

et al. 1995

J of Neuroscience Research

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“…In the second step, endotoxins could induce tumor cell bound macrophages to strike a lethal hit to their tar get. The nature of this lethal hit is still under discussion [31][32][33][34][35][36][37], The last step, the death of the cells, would be endotoxin-independent.…”

Section: Discussionmentioning

confidence: 99%

Differences in the Tumoricidal Activation of Rat and Mouse Macrophages by Endotoxins

Jeannin¹,

Lagadec²,

Reisser³

et al. 1985

Pathobiology

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Conventional and specific pathogen-free rat resident peritoneal macrophages were lytic to tumor cells in the presence of endotoxins even when not elicited or not stimulated in vivo or in vitro. In contrast, conventional mouse resident peritoneal macrophages were not cytolytic in the presence of endotoxins. The induction by endotoxins of rat macrophage-mediated cytolysis was only obtained after the binding of tumor cells by macrophages. Rat resident peritoneal macrophages bound faster and stronger to tumor cells than mouse resident peritoneal macrophages. These differences in binding could explain the species differences in the tumoricidal response to endotoxins.

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“…, 1998; Williams & Hickey, 2002). Macrophages may also induce neuronal injury through direct cell‐to‐cell contact (Cameron & Churchill, 1981; Thery et al. , 1993).…”

Section: Introductionmentioning

confidence: 99%

“…This is largely through their capacity to secrete soluble neurotoxins in abundance, for instance, tumor necrosis factor alpha and interleukin 1 beta, which then mediate brain immune and inflammatory reactions and ultimately neuronal dysfunction and death (Cotter et al, 1998;Williams & Hickey, 2002). Macrophages may also induce neuronal injury through direct cell-to-cell contact (Cameron & Churchill, 1981;Thery et al, 1993). Whereas many studies have shown these soluble toxins induce neuronal injury via different signaling pathways, increasing evidence indicates that macrophages can induce neuronal dysfunction and apoptosis through activation of neuronal voltage-gated K + (K v ) channels (Gelman et al, 2004;Judge & Bever, 2006;Keblesh et al, 2009a).…”

Section: Introductionmentioning

confidence: 99%

Involvement of the 4‐aminopyridine‐sensitive transient A‐type K⁺ current in macrophage‐induced neuronal injury

Liu

Keblesh

et al. 2010

Eur J of Neuroscience

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Through their capacity to secrete, upon activation, a variety of bioactive molecules brain macrophages (and resident microglia) play an important role in brain immune and inflammatory responses. To test our hypothesis that activated macrophages induce neuronal injury by enhancing neuronal outward K + current, we studied the effects of lipopolysacharride (LPS)-stimulated human monocytes-derived macrophage (MDM) on neuronal transient A-type K + current (I A ) and resultant neuronal injury in primary rat hippocampal neuronal cultures. Bath application of LPSstimulated MDM-conditioned media (MCM+) enhanced neuronal I A in a concentration-dependent manner. Non-stimulated MCM (MCM-) failed to alter I A . The enhancement of neuronal I A was recapitulated in neurons co-cultured with macrophages. The link of MCM(+)-induced enhancement of I A to MCM(+)-associated neuronal injury, as detected by propidium iodide (PI) and 4″,6-diamidino-2-phenylindol (DAPI) staining and MTT assay, was demonstrated by experimental results showing that addition of I A blocker 4-aminopyridine to the cultures protected hippocampal neurons from MCM(+)-induced neuronal injury. Further investigation revealed that glutamate was involved in MCM(+)-induced enhancement of neuronal I A . These results suggest that during brain inflammation macrophages (and microglia) might mediate neuronal injury via enhancement of neuronal I A , and that neuronal K v channel might be a potential target for the development of therapeutic strategies for some neurodegenerative disorders by which immune and inflammatory responses are believed to be involved in the pathogenesis.

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Macrophage mediated cytotoxicity in man: Role of hydrocortisone, trypan blue, chloroquine and prednisolone

Cited by 12 publications

References 21 publications

Time course of ciliary neurotrophic factor mRNA expression is coincident with the presence of protoplasmic astrocytes in traumatized rat striatum

Time course of ciliary neurotrophic factor mRNA expression is coincident with the presence of protoplasmic astrocytes in traumatized rat striatum

Differences in the Tumoricidal Activation of Rat and Mouse Macrophages by Endotoxins

Involvement of the 4‐aminopyridine‐sensitive transient A‐type K⁺ current in macrophage‐induced neuronal injury

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Macrophage mediated cytotoxicity in man: Role of hydrocortisone, trypan blue, chloroquine and prednisolone

Cited by 12 publications

References 21 publications

Time course of ciliary neurotrophic factor mRNA expression is coincident with the presence of protoplasmic astrocytes in traumatized rat striatum

Time course of ciliary neurotrophic factor mRNA expression is coincident with the presence of protoplasmic astrocytes in traumatized rat striatum

Differences in the Tumoricidal Activation of Rat and Mouse Macrophages by Endotoxins

Involvement of the 4‐aminopyridine‐sensitive transient A‐type K+ current in macrophage‐induced neuronal injury

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Involvement of the 4‐aminopyridine‐sensitive transient A‐type K⁺ current in macrophage‐induced neuronal injury