Evidence map›Paper›PMID 22442442›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Activation of the classical complement pathway by Bacillus anthracis is the primary mechanism for spore phagocytosis and involves the spore surface protein BclA.

Chunfang Gu, Sarah A Jenkins, Qiong Xue, Yi Xu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  5. Coalescence modeling of intrainfectionProceedings of the National Academy of Sciences of the United States of America · 2020
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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.

Chunfang GuInstitute of Biosciences and Technology, Texas A&M Health Science Center, Houston, TX 77030, USA.
Sarah A Jenkins
Qiong Xue
Yi Xu
Texas A&M Health Science Center · USTexas A&M Health Science Center · US

Funding

Bacillus Anthracis and ComplementR01AI095293 · NIAID · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI XU, YI · 2012 to 2015
$1.4M
The Role of Lung Epithelium in B. anthracis PathogenesisR21AI082306 · NIAID · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI XU, YI · 2009 to 2010
$403k
NIAID NIH HHS AI082306NIAID NIH HHS R01 AI095293NIAID NIH HHS R21 AI082306
6 · The paper itself

Abstract

Interactions between spores of Bacillus anthracis and macrophages are critical for the development of anthrax infections, as spores are thought to use macrophages as vehicles to disseminate in the host. In this study, we report a novel mechanism for phagocytosis of B. anthracis spores. Murine macrophage-like cell line RAW264.7, bone marrow-derived macrophages, and primary peritoneal macrophages from mice were used. The results indicated that activation of the classical complement pathway (CCP) was a primary mechanism for spore phagocytosis. Phagocytosis was significantly reduced in the absence of C1q or C3. C3 fragments were found deposited on the spore surface, and the deposition was dependent on C1q and Ca(2+). C1q recruitment to the spore surface was mediated by the spore surface protein BclA, as recombinant BclA bound directly and specifically to C1q and inhibited C1q binding to spores in a dose-dependent manner. C1q binding to spores lacking BclA (ΔbclA) was also significantly reduced compared with wild-type spores. In addition, deposition of both C3 and C4 as well as phagocytosis of spores were significantly reduced when BclA was absent, but were not reduced in the absence of IgG, suggesting that BclA, but not IgG, is important in these processes. Taken together, these results support a model in which spores actively engage CCP primarily through BclA interaction with C1q, leading to CCP activation and opsonophagocytosis of spores in an IgG-independent manner. These findings are likely to have significant implications on B. anthracis pathogenesis and microbial manipulation of complement.

Indexed as

AnimalsAnthraxAntibodies, BacterialBacillus anthracisCell LineComplement C1qComplement C3Complement Pathway, ClassicalImmunoglobulin GMacrophagesMembrane GlycoproteinsMiceMice, KnockoutPhagocytosisSpores, BacterialAntibodies, BacterialBclA protein, Bacillus anthracisComplement C1qComplement C3Immunoglobulin GMembrane Glycoproteins

Identifiers

PMID22442442
PMCPMC3331890
OpenAlexW1930649809

What OpenQuestion holds

Textmetadata
LicenceTDM
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.