Evidence map›Paper›PMID 31993058›Full record

ArticleFrontiers in immunology2019

Complement Receptor-Mediated Phagocytosis Induces Proinflammatory Cytokine Production in Murine Macrophages.

Durga Acharya, Xiao Rui Lisa Li, Rebecca Emily-Sue Heineman, Rene E Harrison

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.4field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
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  4. Piezo1-specific deletion in macrophage attenuates radiation-induced lung injury progression in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  12. The Arp2/3 complex is required forbioRxiv : the preprint server for biology · 2025
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  19. iScience · 2023
    Article
  20. Perspectives on complement and phagocytic cell responses to nanoparticles: From fundamentals to adverse reactions.Journal of controlled release : official journal of the Controlled Release Society · 2023
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Durga AcharyaUniversity of Toronto Scarborough, Toronto, ON, Canada.
Xiao Rui Lisa LiUniversity of Toronto Scarborough, Toronto, ON, Canada.
Rebecca Emily-Sue HeinemanDepartment of Biological Sciences, University of Toronto Scarborough, Toronto, ON, Canada.
Rene E HarrisonUniversity of Toronto Scarborough, Toronto, ON, Canada.
The Scarborough Hospital · CAUniversity of Toronto · CA

Funding

CIHR PJT-166084
6 · The paper itself

Abstract

Macrophages are professional phagocytes that are uniquely situated between the innate and adaptive arms of immunity with a high capacity for phagocytosis and proinflammatory cytokine production as well as antigen presentation. Phagocytosis is a critical process to eliminate microbes, apoptotic cells and other foreign particles and is accelerated by host-generated opsonins, such as antibodies and complement. Early phagocytosis studies established the paradigm that FcγR-mediated phagocytosis was more proinflammatory than Complement Receptor (CR)-mediated uptake in macrophages. Using qPCR, cytokine antibody arrays and ELISA, we revisited this research question in primary macrophages. Using qPCR we determined that CR-mediated phagocytosis increases levels of TNF-α, IL-1β, IL-6, and MMP-9, compared to FcγR-mediated phagocytosis and control unstimulated cells. We confirmed these findings at the protein level using cytokine antibody arrays and ELISAs. We next investigated the mechanism behind upregulated cytokine production during CR-mediated phagocytosis. IκBα protein levels were reduced after phagocytosis of both IgG- and C3bi-sRBCs indicating proteolytic degradation and implicating NF-κB activation. Inhibition of NF-κB activation impacted IL-6 production during phagocytosis in macrophages. Due to the roles of calpain in IκBα and integrin degradation, we hypothesized that CR-mediated phagocytosis may utilize calpain for proinflammatory mediator enhancement. Using qPCR and cytokine antibody array analysis, we saw significant reduction of cytokine expression during CR-mediated phagocytosis following the addition of the calpain inhibitor, PD150606, compared to untreated cells. These results suggest that the upregulation of proinflammatory mediators during CR-mediated phagocytosis is potentially dependent upon calpain-mediated activation of NF-κB.

Indexed as

AnimalsCalpainCytokinesInflammationMacrophagesMiceNF-kappa BPhagocytosisReceptors, ComplementCalpainCytokinesNF-kappa BReceptors, ComplementcomplementcytokineFc receptorinflammationmacrophagephagocytosis

Identifiers

PMID31993058
PMCPMC6970972
OpenAlexW2999447321

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.