RGD Reference Report - MicroRNA 155 Contributes to Host Immunity against Leishmania donovani but Is Not Essential for Resolution of Infection. - Rat Genome Database

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MicroRNA 155 Contributes to Host Immunity against Leishmania donovani but Is Not Essential for Resolution of Infection.

Authors: Varikuti, Sanjay  Natarajan, Gayathri  Volpedo, Greta  Singh, Bhawana  Hamza, Omar  Messick, Gretchen V  Guerau-de-Arellano, Mireia  Papenfuss, Tracey L  Oghumu, Steve  Satoskar, Abhay R 
Citation: Varikuti S, etal., Infect Immun. 2019 Jul 23;87(8). pii: IAI.00307-19. doi: 10.1128/IAI.00307-19. Print 2019 Aug.
RGD ID: 21081525
Pubmed: PMID:31182615   (View Abstract at PubMed)
PMCID: PMC6652779   (View Article at PubMed Central)
DOI: DOI:10.1128/IAI.00307-19   (Journal Full-text)

CD4+ T helper 1 (Th1) cells producing interferon gamma (IFN-γ) are critical for the resolution of visceral leishmaniasis (VL). MicroRNA 155 (miR155) promotes CD4+ Th1 responses and IFN-γ production by targeting suppressor of cytokine signaling-1 (SOCS1) and Src homology-2 domain-containing inositol 5-phosphatase 1 (SHIP-1) and therefore could play a role in the resolution of VL. To determine the role of miR155 in VL, we monitored the course of Leishmania donovani infection in miR155 knockout (miR155KO) and wild-type (WT) C57BL/6 mice. miR155KO mice displayed significantly higher liver and spleen parasite loads than WT controls and showed impaired hepatic granuloma formation. However, parasite growth eventually declined in miR155KO mice, suggesting the induction of a compensatory miR155-independent antileishmanial pathway. Leishmania antigen-stimulated splenocytes from miR155KO mice produced significantly lower levels of Th1-associated IFN-γ than controls. Interestingly, at later time points, levels of Th2-associated interleukin-4 (IL-4) and IL-10 were also lower in miR155KO splenocyte supernatants than in WT mice. On the other hand, miR155KO mice displayed significantly higher levels of IFN-γ, iNOS, and TNF-α gene transcripts in their livers than WT mice, indicating that distinct organ-specific antiparasitic mechanisms were involved in control of L. donovani infection in miR155KO mice. Throughout the course of infection, organs of miR155KO mice showed significantly more PDL1-expressing Ly6Chi inflammatory monocytes than WT mice. Conversely, blockade of Ly6Chi inflammatory monocyte recruitment in miR155KO mice significantly reduced parasitic loads, indicating that these cells contributed to disease susceptibility. In conclusion, we found that miR155 contributes to the control of L. donovani but is not essential for infection resolution.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
MIR155Humanvisceral leishmaniasis  ISOMir155 (Mus musculus) RGD 
Mir155Mousevisceral leishmaniasis  IMP  RGD 
Mir155Ratvisceral leishmaniasis  ISOMir155 (Mus musculus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mir155  (microRNA 155)

Genes (Mus musculus)
Mir155  (microRNA 155)

Genes (Homo sapiens)
MIR155  (microRNA 155)


Additional Information