About: IRAK-M alters the polarity of macrophages to facilitate the survival of Mycobacterium tuberculosis

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About: IRAK-M alters the polarity of macrophages to facilitate the survival of Mycobacterium tuberculosis Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	IRAK-M alters the polarity of macrophages to facilitate the survival of Mycobacterium tuberculosis
Creator	Li, Jianrong Huang, Hanju Li, Quan Ma, Jilei Shen, Pei Shi, Chunwei Tian, Maopeng Zhai, Xinjie Fei, Hong
Source	Medline; PMC
abstract	BACKGROUND: Intracellular bacterium, Mycobacterium tuberculosis (M. tb), infects specifically macrophages as host cells. IRAK-M, a member of IRAK family, is a negative regulator in TLR signaling and specifically expresses in monocytes and macrophages. The role of IRAK-M in intracellular growth of M. tb and macrophage polarization was explored, for deeply understanding the pathogenesis of M. tb, the significance of IRAK-M to innate immunity and pathogen-host interaction. METHODS: IRAK-M expression was detected in M. tb infected macrophages and in human lung tissue of pulmonary tuberculosis with immunofluorescence staining, Western blot and immunohistochemistry. IRAK-M knock-down and over-expressing cell strains were constructed and intracellular survival of M. tb was investigated by acid-fast staining and colony forming units. Molecular markers of M1-type (pSTAT1 and iNOS) and M2-type (pSTAT6 and Arg-1) macrophages were detected using Western blot in IRAK-M knockdown U937 cells infected with M. tb H37Rv. U937 cells were stimulated with immunostimulant CpG7909 into M1 status and then infected with M. tb H37Rv. Expression of IRAK-M, IRAK-4 and iNOS was detected with immunofluorescence staining and Western blot, to evaluate the effect of IRAK-M to CpG directed M1-type polarization of macrophages during M. tb infection. Molecules related with macrophage’s bactericidal ability such as Hif-1 and phosphorylated ERK1/2 were detected with immunohistochemistry and Western blot. RESULTS: IRAK-M increased in M. tb infected macrophage cells and also in human lung tissue of pulmonary tuberculosis. IRAK-M over-expression resulted in higher bacterial load, while IRAK-M interference resulted in lower bacterial load in M. tb infected cells. During M. tb infection, IRAK-M knockdown induced M1-type, while inhibited M2-type polarization of macrophage. M1-type polarization of U937 cells induced by CpG7909 was inhibited by M. tb infection, which was reversed by IRAK-M knockdown in U937 cells. IRAK-M affected Hif-1 and MAPK signaling cascade during M. tb infection. CONCLUSIONS: Conclusively, IRAK-M might alter the polarity of macrophages, to facilitate intracellular survival of M. tb and affect Th1-type immunity of the host, which is helpful to understanding the pathogenesis of M. tb.
has issue date	2017-08-23(xsd:dateTime)
bibo:doi	10.1186/s12866-017-1095-2
bibo:pmid	28835201
has license	cc-by
sha1sum (hex)	41743a48f1acec724d627f76e02e85137debc076
schema:url	https://doi.org/10.1186/s12866-017-1095-2
resource representing a document's title	IRAK-M alters the polarity of macrophages to facilitate the survival of Mycobacterium tuberculosis
has PubMed Central identifier	PMC5569470
has PubMed identifier	28835201
schema:publication	BMC Microbiol
resource representing a document's body	covid:41743a48f1acec724d627f76e02e85137debc076#body_text
is schema:about of	named entity 'intracellular' named entity 'reversed' named entity 'staining' named entity 'infected' named entity 'host' named entity 'macrophage' named entity 'type' named entity 'Methods' named entity 'bacterium' named entity 'expresses' named entity 'infection' named entity 'inhibited' named entity 'MYCOBACTERIUM TUBERCULOSIS' named entity 'INVESTIGATED' named entity '27S' named entity 'IRAK-M' named entity 'PULMONARY TUBERCULOSIS' named entity 'STIMULATED' named entity 'TH1' named entity 'UNDERSTANDING' named entity 'INTERFERENCE' named entity 'MACROPHAGES' named entity 'INFECTION' named entity 'BACTERIAL LOAD' named entity 'IS A' named entity 'INDUCED' named entity 'MAPK SIGNALING' named entity 'RELATED' named entity 'PATHOGEN-HOST INTERACTION' named entity 'CONCLUSIONS' named entity 'USING' named entity 'IMMUNITY' named entity 'INNATE IMMUNITY' named entity 'IRAK-4' named entity 'STATUS' named entity 'IMMUNOHISTOCHEMISTRY' named entity 'DIRECTED' named entity 'CELL' named entity 'EVALUATE' named entity 'SURVIVAL' named entity 'AFFECT' named entity 'TLR' named entity 'ALTER' named entity 'IMMUNOSTIMULANT' named entity 'ROLE' named entity 'POLARIZATION' named entity 'HIF-1' named entity 'POLARITY' named entity 'MYCOBACTERIUM TUBERCULOSIS' named entity 'CONSTRUCTED' named entity 'AFFECTED' named entity 'DETECTED' named entity 'INTRACELLULAR' named entity 'ACID-FAST STAINING' named entity 'LUNG TISSUE' named entity 'SIGNIFICANCE' named entity 'RESULTS' named entity 'HIGHER' named entity 'POLARITY' named entity 'MACROPHAGES' named entity 'PHOSPHORYLATED' named entity 'HOST CELLS' named entity 'CELLS' named entity 'EXPRESSION' named entity 'STRAINS' named entity 'MONOCYTES' covid:arg/41743a48f1acec724d627f76e02e85137debc076 named entity 'MEMBER OF' named entity 'GROWTH' named entity 'HUMAN LUNG' named entity 'KNOCK-DOWN' named entity 'SURVIVAL' named entity 'IRAK-M'

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