Pro-inflammatory cytokine Interleukin-1β (IL-1β) controls Leishmania infection
Autor: | Tejaswini Patil, Arup Sarkar, Vasundhara More, Ashok Patidar, Arkajyoti Mukherjee, David M. Mosser, Rahul Suresh, Deepti Rane, Jagneshwar Dandapat, Neelam Bodhale |
---|---|
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
medicine.medical_treatment Interleukin-1beta Immunology Inflammation Biology Nitric Oxide Biochemistry Monocytes Nitric oxide Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Immune system Bone Marrow medicine Animals Humans Immunology and Allergy Leishmaniasis Molecular Biology Leishmania Mice Inbred BALB C Macrophages Intracellular parasite Hematology biology.organism_classification Interleukin-10 Mice Inbred C57BL Interleukin 10 030104 developmental biology Cytokine medicine.anatomical_structure chemistry Female Bone marrow medicine.symptom 030215 immunology |
Zdroj: | Cytokine. 112:27-31 |
ISSN: | 1043-4666 |
DOI: | 10.1016/j.cyto.2018.06.033 |
Popis: | Leishmania is an obligate intracellular parasite uses low pH phagolysosomal compartments of host macrophages as their final abode. IL-1β is a pro inflammatory cytokine, which is secreted by immune cells to trigger inflammation and this has been found profoundly in the lesions caused by Leishmania pathogens. But the specific role of this cytokine on host cell macrophages during infection has not been fully explored. Here in, we have showed that prolonged exposure of IL-1β on macrophages increases the parasite burden. Pre-treatment of bone marrow derived macrophages (BMDM) with IL-1β also generates significantly higher amount of anti-inflammatory cytokine IL-10. As IL-10 plays crucial role in the establishment of infection, enhanced production of IL-10 observed upon IL-1β treatment could contribute to the progression of the disease. By quantifying the production of Nitric oxide (NO), we further report that the pretreatment of IL-1β fails to produce the nitric oxide. By measuring the footpad thickness in two different mice strains of differential susceptibility we showed IL-1β treatment increases parasitic burden. As our results shows that the exposure of IL-1β helps in disease progression, IL-1β signalling may be an attractive target for future therapeutic intervention. |
Databáze: | OpenAIRE |
Externí odkaz: |