Inflammatory mediators from monocytes down-regulate cellular proliferation and enhance cytokines production in patients with polar clinical forms of Chagas disease.
Exposure to Trypanosoma cruzi parasites induces monocytes and macrophages to produce various endogenous mediators, including prostaglandins and cytokines. To clarify the involvement of monocytes as an important source of inflammatory mediators in Chagas disease patients, we evaluated PBMC before and after depletion of adherent cells (monocytes) from patients with indeterminate (IND) and cardiac (CARD) clinical forms and from non-infected individuals (NI). We demonstrated that after the partial depletion of adherent cells, production of PGE2 was slightly decreased in patients with Chagas disease. Inhibition of the cells by indomethacin increased the proliferation in PBMC cells from patients after antigen stimulation. Pro-inflammatory cytokines as IL-2 and IFN-γ also had a greater decrease after partial depletion of adherent cells in both clinical forms of Chagas disease. IL-10 and IL-5 levels were also reduced after partial depletion of adherent cells both in IND and CARD patients. In addition, we evaluated the APC potential of B cells and observed that the MHCII and CD80 molecules had an increased expression after partial depletion of most monocytes in all groups. Thus, inflammatory mediators produced by monocytes seem to be important to modulate immune responses in Chagas disease by regulating the processes of inflammation and antigen presentation.
Department of Morphology, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil; School of Medicine, Postgraduate Program in Health Sciences: Infectology in Tropical Medicine, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 30130-100, Brazil; René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil. Electronic address: estanislau.juliana@gmail.com.
Juliana Assis Silva
JA
Gomes
School of Medicine, Postgraduate Program in Health Sciences: Infectology in Tropical Medicine, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 30130-100, Brazil; René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil.
Andreia Maria
AM
Molica
Department of Molecular and Cellular Biology, Federal University of Paraíba, João Pessoa, Paraíba, Brazil.
Tatjana Souza Lima
TS
Keesen
René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil.
Maria José Ferreira
MJ
Morato
René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil.
Fernanda Fortes
FF
de Araujo
René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil.
Rafaelle Christine Gomes
RC
Fares
René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil.
Jacqueline Araujo
JA
Fiuza
René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil.
Ana Thereza
AT
Chaves
School of Medicine, Postgraduate Program in Health Sciences: Infectology in Tropical Medicine, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 30130-100, Brazil; René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil.
Vladimir
V
Pinheiro
School of Medicine, Postgraduate Program in Health Sciences: Infectology in Tropical Medicine, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 30130-100, Brazil.
Maria do Carmo Pereira
Mdo C
Nunes
René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil; National Institute of Science and Technology on Tropical Diseases - INCT-DT, Salvador, Bahia, Brazil.
Rodrigo
R
Correa-Oliveira
School of Medicine, Postgraduate Program in Health Sciences: Infectology in Tropical Medicine, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 30130-100, Brazil.
Manoel Otávio
MO
da Costa Rocha
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D000953:Antigens, Protozoan / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D002598:Chagas Cardiomyopathy / Q000276:immunology / Q000378:metabolism; D014355:Chagas Disease / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D016207:Cytokines / Q000096:biosynthesis*; D015232:Dinoprostone / Q000096:biosynthesis; D015870:Gene Expression; D006684:HLA-DR Antigens / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D018836:Inflammation Mediators / Q000378:metabolism* / Q000494:pharmacology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D009000:Monocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D014349:Trypanosoma cruzi / Q000276:immunology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000953:Antigens, Protozoan; D016207:Cytokines; D006684:HLA-DR Antigens; D018836:Inflammation Mediators; D015232:Dinoprostone; D007213:Indomethacin
CARD; CD; HLA-DR; IL; IND; MHC class II cell surface receptor; NI; PGE2; Prostagladin E2; TRYPO; cluster of differentiation; interleukin; non-infected individuals; patients with indeterminate clinical form of Chagas disease; patients with the cardiac clinical form of Chagas disease; tryposmastigotes antigen