github link
Accession IconGSE22935

Arginine utilization following mycobacteria infection in macrophages is dependent on autocrine-paracrine signaling

Organism Icon Mus musculus
Sample Icon 24 Downloadable Samples
Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Submitter Supplied Information

Description
Nitric oxide (NO) produced by macrophages (Ms) is toxic to both host tissues and invading pathogens and its regulation is therefore essential to suppress host cytotoxicity. M arginase 1 (Arg1) inhibits NO production by competing with NO synthases for arginine, the common substrate of NO synthases and arginases. Two signal transduction pathways control Arg1 expression in Ms. First, a MyD88-dependent pathway induces Arg1 in intracellular infections, while a second Stat6-dependent pathway is required for Arg1 expression in alternativelyactivated Ms. We found that mycobacteria-infected Ms produce soluble factors that induce Arg1 in an autocrine-paracrine manner via Stat3. We identify these factors as IL-6, IL-10 and GCSF. We further establish that Arg1 expression is controlled by the MyD88-dependent production of IL-6, IL-10 and G-CSF rather than cell intrinsic MyD88 signaling to Arg1. Our data reveal the MyD88-dependent pathway of Arg1induction following BCG infection requires Stat3 activation and may result in the development of an immunosuppressive niche in granulomas due to the induced Arg1 production in surrounding uninfected Ms
PubMed ID
Publication Title
No associated publication
Total Samples
24
Submitter’s Institution
Authors
No associated authors

Samples

Show of 0 Total Samples
Filter
Add/Remove
Accession Code
Title
Sex
Specimen part
Time
Processing Information
Additional Metadata
No rows found
Loading...