What question did this study set out to answer?

Investigate the modulation, release, and cleavage mechanisms of soluble TNF receptors (TNF-sR55 and TNF-sR75) by human alveolar macrophages and peripheral monocytes in response to inflammatory stimuli.

March 1, 1996American Journal of Respiratory Cell and Molecular Biology

Tumor Necrosis Factor Soluble Receptor 75: The Principal Receptor Form Released by Human Alveolar Macrophages and Monocytes in the Presence of Interferon γ

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Population

Human alveolar macrophages (AM) and peripheral blood monocytes (Mo)

Comparison

Stimulation with lipopolysaccharide, phorbol… vs Unstimulated cells (basal release)

Design

Preclinical

Follow-up

24 h

Authors

BRBéatrice Galve-de RochemonteixFondation Hans Wilsdorf LNLaurent NicodUniversity Hospital of Lausanne JDJean‐Michel DayerUniversity of Geneva

Discussion

Member takes

Implication

May modulate TNF bioavailability in alveolar macrophages; hypothesis-generating for differential signaling and requires validation before clinical consideration.

Key Points

Investigate the modulation, release, and cleavage mechanisms of soluble TNF receptors (TNF-sR55 and TNF-sR75) by human alveolar macrophages and peripheral monocytes in response to inflammatory stimuli.
Cultured human alveolar macrophages and peripheral blood monocytes with stimuli including LPS, PMA, and cytokines (IL-2, IL-4, IL-6, GM-CSF, and IFN-gamma).
Evaluated receptor internalization and cellular recycling pathways using pharmacological inhibitors including monensin, chloroquine, and colchicine.
Unstimulated alveolar macrophages released 0.3 ± 0.1 ng/ml of TNF-sR55 and 0.5 ± 0.1 ng/ml of TNF-sR75, whereas monocytes released 1.2 ± 1.2 ng/ml and 5.1 ± 0.1 ng/ml, respectively.
IFN-gamma increased the release of TNF-sR75 by 3-fold compared to a 1.5- to 2-fold increase for TNF-sR55 in alveolar macrophages, while PMA enhanced TNF-sR75 release approximately 4-fold.
Receptor shedding persisted despite the presence of chloroquine, monensin, and colchicine, indicating that cleavage takes place at the cell surface rather than intracellularly.

Structured PICO

Population

Human alveolar macrophages (AM) and peripheral blood monocytes (Mo)

Intervention

Stimulation with lipopolysaccharide (LPS), phorbol myristate acetate (PMA), cytokines (IL-2, IL-4, IL-6, GM-CSF, IFN-gamma), and inhibitors (monensin, chloroquine, colchicine)

Comparator

Unstimulated cells (basal release)

Outcome

Release of TNF-sR55 and TNF-sR75 into the cell culture supernatantsurrogate

Human alveolar macrophages and monocytes differ in their ability to release TNF soluble receptors, with IFN-gamma being a potent inducer of TNF-sR75 shedding.

Cite This Study

Rochemonteix et al. (1996) studied this question.

synapsesocial.com/papers/6a7fcb8d82118c5eabe51db0 https://doi.org/10.1165/ajrcmb.14.3.8845179

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Implication

May modulate TNF bioavailability in alveolar macrophages; hypothesis-generating for differential signaling and requires validation before clinical consideration.

Tumor Necrosis Factor Soluble Receptor 75: The Principal Receptor Form Released by Human Alveolar Macrophages and Monocytes in the Presence of Interferon γ

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Tumor Necrosis Factor Soluble Receptor 75: The Principal Receptor Form Released by Human Alveolar Macrophages and Monocytes in the Presence of Interferon γ

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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