Insulin-like growth factor-I serum levels and their biological effects on Leishmania isolates from different clinical forms of American tegumentary leishmaniasis

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Citações na Scopus
6
Tipo de produção
article
Data de publicação
2016
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
BIOMED CENTRAL LTD
Autores
SOUZA, Luana Dias de
VENDRAME, Celia Maria Vieira
JESUS, Amelia Ribeiro de
CARVALHO, Marcia Dias Teixeira
MAGALHAES, Andrea Santos
SCHRIEFER, Albert
GUIMARAES, Luiz Henrique
CARVALHO, Edgar Marcelino de
Citação
PARASITES & VECTORS, v.9, article ID 335, 8p, 2016
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: American tegumentary leishmaniasis (ATL) in Brazil is mostly caused by Leishmania (Viannia) braziliensis, with known forms of the disease being cutaneous (CL), mucosal (ML) and disseminated (DL) leishmaniasis. The development of the lesion in ATL is related both to the persistence of the Leishmania in the skin and to the parasite-triggered immune and inflammatory responses that ensue lesions. In this context one factor with expected role in the pathogenesis is insulin-like growth factor (IGF)-I with known effects on parasite growth and healing and inflammatory processes. In the present study, we addressed the effect of IGF-I on intracellular amastigote isolates from CL, ML and DL patients within human macrophage and we evaluated the IGF-I and IGF-binding protein-3 (IGFBP3) serum levels in patients presenting different clinical forms and controls from the endemic area. Methods: We evaluated biological variability in the responses of intracellular amastigotes of Leishmania isolates derived from CL, ML, and DL patients from an area for ATL in response to IGF-I. Intracellular amastigote growth was evaluated using the human macrophage cell line THP-1. Arginase activity in infected cells was evaluated quantifying the generated urea concentration. Serum samples from patients and controls were assayed using chemiluminescent immunometric assay to determine IGF-I and IGFBP3 levels. Results: We observed an increase in intracellular parasitism upon IGF-I stimulus in 62.5 % of isolates from CL, in 85.7 % from ML and only 42.8 % from DL cases. In DL, the basal arginase activity was lower than that of CL. We then evaluated the IGF-I and IGFBP3 serum levels in patients, and we observed significantly lower levels in ML and DL than in CL and control samples. Conclusions: The data suggest that IGF-I is modulated distinctly in different clinical forms of tegumentary leishmaniasis. IGF-I seemingly exerts effect on parasite growth likely contributing to its persistence in the skin in earlier phase. In addition the decreased IGF-I serum levels may affect the modulation of inflammation and lesion healing in chronic phase. In view of potential role of IGF-I in the pathogenesis of ATL we can speculate on therapeutic procedures taking into account the local IGF-I level.
Palavras-chave
Leishmania braziliensis, Tegumentary leishmaniasis, THP-1, IGF-I level
URI
https://observatorio.fm.usp.br/handle/OPI/16293
Referências
  1. Aydin F, 2013, J DIABETES RES, DOI 10.1155/2013/567834
  2. Bacellar O, 2002, INFECT IMMUN, V70, P6734, DOI 10.1128/IAI.70.12.6734-6740.2002
  3. Blakytny Robert, 2000, Journal of Pathology, V190, P589, DOI 10.1002/(SICI)1096-9896(200004)190:5<589::AID-PATH553>3.0.CO;2-T
  4. Cantanhede LM, 2015, PLOS NEGLECT TROP D, V9, DOI 10.1371/journal.pntd.0004079
  5. Carvalho LP, 2007, PARASITE IMMUNOL, V29, P251, DOI 10.1111/j.1365-3024.2007.00940.x
  6. Carvalho LP, 2012, FRONT IMMUNOL, V3, DOI 10.3389/fimmu.2012.00301
  7. Castellucci LA, 2005, AM J TROP MED HYG, V73, P69
  8. CORRALIZA IM, 1994, J IMMUNOL METHODS, V174, P231, DOI 10.1016/0022-1759(94)90027-2
  9. Cunningham AC, 2002, EXP MOL PATHOL, V72, P132, DOI 10.1006/exmp.2002.2418
  10. CUPOLILLO E, 1994, AM J TROP MED HYG, V50, P296
  11. Da-Cruz AM, 2002, CLIN DIAGN LAB IMMUN, V9, P251, DOI 10.1128/CDLI.9.2.251-256.2002
  12. de Oliveira CI, 2004, MICROBES INFECT, V6, P977, DOI 10.1016/j.micinf.2004.05.009
  13. Elmlinger MW, 2004, CLIN CHEM LAB MED, V42, P654, DOI 10.1515/CCLM.2004.112
  14. Faria DR, 2005, INFECT IMMUN, V73, P7853, DOI 10.1128/IAI.73.12.7853-7859.2005
  15. Gollob KJ, 2014, PARASITE IMMUNOL, V36, P367, DOI 10.1111/pim.12100
  16. Gomes CMD, 2000, INT J EXP PATHOL, V81, P249, DOI 10.1046/j.1365-2613.2000.00157.x
  17. Goto H, 1998, P NATL ACAD SCI USA, V95, P13211, DOI 10.1073/pnas.95.22.13211
  18. Goto H, 2012, INFECT DIS CLIN N AM, V26, P293, DOI 10.1016/j.idc.2012.03.001
  19. Heller NM, 2008, SCI SIGNAL, V1, DOI 10.1126/scisignal.1164795
  20. KRATZ G, 1994, SCAND J PLAST RECONS, V28, P107
  21. Leopoldo PTG, 2006, BMC INFECT DIS, V6, DOI 10.1186/1471-2334-6-75
  22. Achar RAN, 2014, ACTA CIR BRAS, V29, P125, DOI 10.1590/S0102-86502014000200009
  23. Oliveira FS, 2013, PARASITE VECTOR, V6, DOI 10.1186/1756-3305-6-189
  24. Pereira-Carvalho R, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0081529
  25. Ribeiro-de-Jesus A, 1998, REV BRASILEIRA PESQU, V31, P143
  26. Rocha PN, 1999, J INFECT DIS, V180, P1731, DOI 10.1086/315071
  27. Saravia NG, 1998, AM J TROP MED HYG, V59, P86
  28. Schriefer A, 2004, INFECT IMMUN, V72, P508, DOI 10.1128/IAI.72.1.508-514.2004
  29. Sharp LL, 2005, NAT IMMUNOL, V6, P73, DOI 10.1038/ni1152
  30. Silveira FT, 2009, PARASITE IMMUNOL, V31, P423, DOI 10.1111/j.1365-3024.2009.01116.x
  31. Soong L, 2012, SEMIN IMMUNOPATHOL, V34, P735, DOI 10.1007/s00281-012-0350-8
  32. Sukhanov S, 2007, ARTERIOSCL THROM VAS, V27, P2684, DOI 10.1161/ATVBAHA.107.156257
  33. Tavakkol A, 1999, ARCH DERMATOL RES, V291, P643, DOI 10.1007/s004030050469
  34. TSUCHIYA S, 1982, CANCER RES, V42, P1530
  35. Turetz ML, 2002, J INFECT DIS, V186, P1829, DOI 10.1086/345772
  36. Vendrame CMV, 2007, SCAND J IMMUNOL, V66, P287, DOI 10.1111/j.1365-3083.2007.01950.x
  37. Vendrame CMV, 2010, T ROY SOC TROP MED H, V104, P566, DOI 10.1016/j.trstmh.2010.03.007
  38. Vendrame CM, 2014, MEDIAT INFLAMM, V2014

Coleções
Artigos e Materiais de Revistas Científicas - FM/MPR
Artigos e Materiais de Revistas Científicas - LIM/38