Pulmonary BCG induces lung-resident macrophage activation and confers long-term protection against tuberculosis

The state in which macrophages (Mphi) from regressing Moloney sarcomas could kill tumor target cells was a highly labile one which decayed rapidly in vitro. Thereafter, regressor Mphi were noncytolytic. Mphi from several different progressing sarcomas failed to kill, even when challenged with target cells immediately after explantation. Similarly, thioglycollate-induced peritoneal Mphi (TG-Mphi) did not kill. Noncytolygic Mphi derived either from progressing sarcomas or from long-term (up to 96 h) cultures of regressor Mphi were exquisitely sensitive to stimulation by bacterial lipopolysaccharide (LPS); picogram/milliliter amounts induced killing. Similar concentrations of LPS had no demonstrable effect on TG-Mphi. Thus, tumor Mphi generally appeared to have been primed in vivo, with those in regressing sarcomas having additionally acquired cytolytic activity. Inability of progressor Mphi to kill apparently stemmed from lack of, or failure to respond to, the signal needed in vivo to trigger cytolytic activity, rather than the total absence of activation.

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Macrophage activation is associated with poorer long-term outcomes in renal transplant patients

Clinical Transplantation ◽

10.1111/j.1399-0012.2010.01345.x ◽

2010 ◽

Vol 25 (5) ◽

pp. 744-754 ◽

Cited By ~ 9

Author(s):

Scott O. Grebe ◽

Uwe Kuhlmann ◽

Dominik Fogl ◽

Valerie A. Luyckx ◽

Thomas F. Mueller

Keyword(s):

Renal Transplant ◽

Macrophage Activation ◽

Long Term Outcomes ◽

Transplant Patients ◽

Renal Transplant Patients

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Killing of schistosomula of Schistosoma mansoni by macrophages: induction by T-cell clone-derived lymphokines and interferon-gamma

Parasitology ◽

10.1017/s003118200006409x ◽

1986 ◽

Vol 92 (2) ◽

pp. 325-336 ◽

Cited By ~ 7

Author(s):

C. F. Kubelka ◽

A. Ruppel ◽

P. H. Krammer ◽

D. Gemsa

Keyword(s):

T Cell ◽

Interferon Gamma ◽

Macrophage Activation ◽

Cell Clone ◽

T Cell Clones ◽

Cell Clones ◽

T Cell Clone ◽

Ifn Γ

SUMMARYThe induction of schistosomulicidal activity of peritoneal macrophages by concanavalin A-stimulated supernatants from long-term T-cell clones and by interferon-gamma (IFN-γ) was investigated in detail. Optimal conditions of in vitro macrophage activation by T-cell clone supernatants were established. Macrophages from 13-week S. mansoni-infected mice responded to lymphokine activation as well as resident mnacrophages from uninfecteci mice. IFN-γ was shown to play an essential role in induction of schistosomulicidal macrophage activity: recombinant IFN-γ at high concentration could induce schistosomula killing, and an anti-IFN-γ antiserum inhibited the induction ofschistosomulicidal activity by T-cell clone supernatants. Our data also indicate that macrophage activation could be obtained by IFN-γ in synergy with other lymphokines in the supernatant of long-term T-cell clones. Macrophages from mice injected with T-cell clone supernatants were primed in vivo and triggered to kill schistosomula in vitro in the presence of lipopolysaccharide (LPS). The data demonstrate that lymphokines produced by T-cell clones and, in particular, IFN-γ can participate in the activation of schistosomulicidal macrophages.

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A perfusion system for the long term study of macrophage activation

British Journal of Pharmacology ◽

10.1111/j.1476-5381.1992.tb12744.x ◽

1992 ◽

Vol 107 (2) ◽

pp. 317-321 ◽

Cited By ~ 16

Author(s):

Jamil Assreuy ◽

Salvador Moncada

Keyword(s):

Macrophage Activation ◽

Perfusion System ◽

Term Study ◽

Long Term Study

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Post-stroke treatment with argon preserved neurons and attenuated microglia/macrophage activation long-termly in a rat model of transient middle cerebral artery occlusion (tMCAO)

Scientific Reports ◽

10.1038/s41598-021-04666-x ◽

2022 ◽

Vol 12 (1) ◽

Author(s):

Jingjin Liu ◽

Michael Veldeman ◽

Anke Höllig ◽

Kay Nolte ◽

Lisa Liebenstund ◽

...

Keyword(s):

Ischemic Stroke ◽

Macrophage Activation ◽

Neuroprotective Effect ◽

Macrophage Polarization ◽

Artery Occlusion ◽

Brain Inflammation ◽

Long Term Effects ◽

Neuroprotective Effects ◽

Stroke Treatment

AbstractIn a previous study from our group, argon has shown to significantly attenuate brain injury, reduce brain inflammation and enhance M2 microglia/macrophage polarization until 7 days after ischemic stroke. However, the long-term effects of argon have not been reported thus far. In the present study, we analyzed the underlying neuroprotective effects and potential mechanisms of argon, up to 30 days after ischemic stroke. Argon administration with a 3 h delay after stroke onset and 1 h after reperfusion demonstrated long-term neuroprotective effect by preserving the neurons at the ischemic boundary zone 30 days after stroke. Furthermore, the excessive microglia/macrophage activation in rat brain was reduced by argon treatment 30 days after ischemic insult. However, long-lasting neurological improvement was not detectable. More sensorimotor functional measures, age- and disease-related models, as well as further histological and molecular biological analyses will be needed to extend the understanding of argon’s neuroprotective effects and mechanism of action after ischemic stroke.

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Autopsy findings after long-term treatment of COVID-19 patients with microbiological correlation

Virchows Archiv ◽

10.1007/s00428-020-03014-0 ◽

2021 ◽

Author(s):

Katja Evert ◽

Thomas Dienemann ◽

Christoph Brochhausen ◽

Dirk Lunz ◽

Matthias Lubnow ◽

...

Keyword(s):

Macrophage Activation Syndrome ◽

Macrophage Activation ◽

Fungal Infections ◽

Diffuse Alveolar Damage ◽

Fungal Species ◽

Term Treatment ◽

University Hospital ◽

Long Term Treatment ◽

The University

AbstractBetween April and June 2020, i.e., during the first wave of pandemic coronavirus disease 2019 (COVID-19), 55 patients underwent long-term treatment in the intensive care unit at the University Hospital of Regensburg. Most of them were transferred from smaller hospitals, often due to the need for an extracorporeal membrane oxygenation system. Autopsy was performed in 8/17 COVID-19-proven patients after long-term treatment (mean: 33.6 days). Autopsy revealed that the typical pathological changes occurring during the early stages of the disease (e.g., thrombosis, endothelitis, capillaritis) are less prevalent at this stage, while severe diffuse alveolar damage and especially coinfection with different fungal species were the most conspicuous finding. In addition, signs of macrophage activation syndrome was detected in 7 of 8 patients. Thus, fungal infections were a leading cause of death in our cohort of severely ill patients and may alter clinical management of patients, particularly in long-term periods of treatment.

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Collagen-derived peptide, DGEA, inhibits pro-inflammatory macrophages in biofunctional hydrogels

Journal of Materials Research ◽

10.1557/s43578-021-00423-y ◽

2021 ◽

Author(s):

Aakanksha Jha ◽

Erika Moore

Keyword(s):

Macrophage Activation ◽

Innate Immune ◽

M1 Macrophages ◽

Inflammatory Conditions ◽

M1 Macrophage ◽

Inflammatory Stimuli ◽

Poly Ethylene ◽

Inflammatory Macrophages ◽

Inflammatory Macrophage

AbstractMacrophages are innate immune cells that play important roles in wound healing. Particularly, M1 macrophages are considered pro‐inflammatory and promote initial phases of inflammation. Long-term exposure to inflammatory stimuli causes an increase in M1 macrophages, which contributes to chronic inflammation. Activated M1 macrophages have been shown to upregulate integrin α2β1 expression. To interfere with α2β1 binding, we designed a biofunctional hydrogel utilizing a collagen I-derived peptide, DGEA (Asp-Gly-Glu-Ala). We hypothesize that M1 macrophage activation can be reduced in the presence of DGEA. Effects of DGEA on M1 macrophages were studied via soluble delivery and immobilization within poly(ethylene glycol) (PEG) hydrogels. We demonstrate that M1 macrophage activation is reduced both via soluble delivery of DGEA in 2D and via immobilized DGEA in a 3D PEG-DGEA hydrogel. This novel biomaterial can manipulate inflammatory macrophage activation and can be applied to prevent chronic inflammatory conditions via macrophage manipulation. Graphical abstract

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