Details

Autor(en) / Beteiligte

• Quixabeira, Valéria Bernadete Leite
• Pereira, Ledice Inacia de Araújo
• Veras, Poliana Ribeiro Valadares
• da Costa, Ana Carolina Vieira
• Fonseca, Larissa Gomides
• Galdino Jr, Hélio
• da Silva Jr, Ildefonso Alves
• Morato, Camila Imai
• Pinto, Sebastião Alves
• Pereira, Ana Joaquina Cohen Serique
• Dorta, Miriam Leandro
• Oliveira, Milton Adriano Pelli de
• Gomes, Rodrigo Saar
• Ribeiro‐Dias, Fátima

Titel

Alterations in monocyte subsets and cytokine production after TLR activation in American Cutaneous Leishmaniasis

Ist Teil von

• Parasite immunology, 2019-05, Vol.41 (5), p.e12623-n/a

Ort / Verlag

England: Wiley Subscription Services, Inc

Erscheinungsjahr

2019

Quelle

Wiley-Blackwell Journals

Beschreibungen/Notizen

• Phenotypic and functional aspects of monocytes from Localized Cutaneous Leishmaniasis (LCL) patients were evaluated. The frequencies of monocyte subsets and TLR2/TLR4 expression were evaluated in fresh peripheral blood whereas cytokine production was evaluated in whole blood cell cultures stimulated with TLR agonists or Leishmania braziliensis antigen (Ag). CD16+ monocytes frequency was increased in patients compared with controls. A TLR4 agonist (LPS) induced expression of TNF and IL‐10 in monocyte subsets of patients and controls. The CD14+CD16+ monocytes expressed higher levels of these cytokines than CD14+CD16− cells. The levels of secreted TNF were higher in whole blood cell cultures from patients than controls after LPS/TLR4 or Ag stimulation. Whereas in controls there was a positive correlation between TNF and IL‐10 levels, this was not observed in stimulated cell cultures from patients. The high levels of LPS‐induced TNF were associated with the number of lesions and the percentages of CD14hiCD16+ monocytes. The levels of TLR2‐induced TNF were also associated with number of lesions. All monocyte subsets from patients expressed higher levels of TLR2 and TLR4 than controls. Data suggest that systemically activated monocytes contribute for an imbalance in pro‐ and anti‐inflammatory cytokine production during LCL, participating in the immunopathogenesis of the disease.