About: Hemozoin‐induced activation of human monocytes toward M2‐like phenotype is partially reversed by antimalarial drugs

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About: Hemozoin‐induced activation of human monocytes toward M2‐like phenotype is partially reversed by antimalarial drugs—chloroquine and artemisinin Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Hemozoin‐induced activation of human monocytes toward M2‐like phenotype is partially reversed by antimalarial drugs—chloroquine and artemisinin
Creator	Bobade, Deepali Deval, Mangesh Shastry, Padma Ashwin, \| Khandare, V
topic	covid:232e85eda8060808405e79f0dbe13309eccddf58#this
Source	Medline; PMC
abstract	Plasmodium falciparum malaria is the most severe form of malaria with several complications. The malaria pigment‐hemozoin (Hz) is associated with severe anemia, cytokine dysfunction, and immunosuppression, thus making it an interesting target for developing new strategies for antimalarial therapy. Monocytes (MO) in circulation actively ingest Hz released by Plasmodium parasites and secrete pro‐ and anti‐inflammatory cytokines. M1 and M2 types represent the two major forms of MO/macrophages (MQ) with distinct phenotypes and opposing functions. Imbalance in the polarization of these types is reported in many infectious diseases. Though the association of Hz with immunosuppression is well documented, its role in activation of MO in context of M1/M2 phenotypes remains to be addressed. We report here that natural Hz drives human MO toward M2‐like phenotype as evidenced by the expression of M2 signature markers. Hz‐fed MO showed elevated transcript and secreted level of IL‐10, CCL17, CCL1, expression of mannose‐binding lectin receptor (CD206), and arginase activity. Hz attenuated HLA‐DR expression, nitric oxide, and reactive oxygen species production, which are the features of M1 phenotype. Our data also implicate the involvement of p38 MAPK, PI3K/AKT, and NF‐κB signaling pathways in skewing of Hz‐fed MO toward M2‐like type and suppression of mitogen‐stimulated lymphocyte proliferation. Importantly, antimalarial drugs—chloroquine and artemisinin—partially reversed activation of Hz‐induced MO toward M2‐like phenotype. Considering the limitations in the current therapeutic options for malaria, we propose that these drugs may be re‐examined for their potential as immunomodulators and candidates for adjunctive treatment in malaria.
has issue date	2018-06-07(xsd:dateTime)
bibo:doi	10.1002/mbo3.651
bibo:pmid	29877619
has license	cc-by
sha1sum (hex)	232e85eda8060808405e79f0dbe13309eccddf58
schema:url	https://doi.org/10.1002/mbo3.651
resource representing a document's title	Hemozoin‐induced activation of human monocytes toward M2‐like phenotype is partially reversed by antimalarial drugs—chloroquine and artemisinin
has PubMed Central identifier	PMC6436431
has PubMed identifier	29877619
schema:publication	Microbiologyopen
resource representing a document's body	covid:232e85eda8060808405e79f0dbe13309eccddf58#body_text
is http://vocab.deri.ie/void#inDataset of	https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/232e85eda8060808405e79f0dbe13309eccddf58
is schema:about of	named entity 'HUMAN MONOCYTES' named entity 'activation' named entity 'drives' named entity 'Information' named entity 'complications' named entity 'activation' named entity 'human' named entity 'released' named entity 'expression' named entity 'anemia' named entity 'arginase' named entity 'monocytes' named entity 'ARTEMISININ' named entity 'REPRESENT' named entity 'INDUCED' named entity 'PLASMODIUM FALCIPARUM MALARIA' named entity 'CCL1' named entity 'PARASITES' named entity 'SEVERE' named entity 'ADJUNCTIVE TREATMENT' named entity 'CYTOKINES' named entity 'ADDITIONAL' named entity 'HUMAN MONOCYTES' named entity 'ASSOCIATED WITH' named entity 'HEMOZOIN' named entity 'ANTIMALARIAL DRUGS' named entity 'ROLE' named entity 'CONTEXT' named entity 'FEATURES' named entity '2019' named entity 'LYMPHOCYTE PROLIFERATION' named entity 'ATTENUATED' named entity 'ATI' named entity 'MANNOSE-BINDING LECTIN' named entity 'SECRETE' named entity 'INTERESTING' named entity 'MONOCYTES' named entity 'NEW' named entity 'ACTIVATION' named entity 'INVOLVEMENT' named entity 'IMBALANCE' named entity '3B8' named entity 'NITRIC OXIDE' named entity 'FOUND' named entity 'EXPRESSION' named entity 'THERAPEUTIC' named entity 'SEVERE ANEMIA' named entity 'CYTOKINE ' named entity 'INGEST' named entity 'PARTIALLY' named entity 'PHENOTYPES' named entity 'DOCUMENTED' named entity 'TYPES' named entity 'R M' named entity 'AT THE END' named entity 'SIGNALING PATHWAYS' named entity 'CCL17' named entity 'INDUCED' named entity 'REVERSED' named entity 'PHENOTYPE' named entity 'REVERSED' named entity 'ACTIVATION' named entity 'CHLOROQUINE' named entity 'ARGINASE ACTIVITY' named entity 'POTENTIAL' named entity 'CONSIDERING' named entity 'FORMS' named entity 'MARKERS' named entity 'MACROPHAGES' named entity 'COMPLICATIONS' named entity 'LIKE' named entity 'SECRETED' named entity 'INFECTIOUS DISEASES' named entity 'LIMITATIONS' named entity 'REPORT'

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