Understanding hypergammaglobulinemia in experimental or natural visceral leishmaniasis

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Tipo de produção
article
Data de publicação
2024
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ISSN da Revista
Título do Volume
Editora
WILEY
Citação
PARASITE IMMUNOLOGY, v.46, n.1, article ID e13021, 9p, 2024
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Unidades Organizacionais
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Resumo
Nonspecific hypergammaglobulinemia (HGG) occurs in symptomatic human visceral leishmaniasis (VL) caused by L. L. infantum. This study assessed this finding in experimental infection in hamsters and natural infection in dogs. The serum concentration of proteins, albumin and globulins was determined through the biuret and bromocresol green reaction, where the HGG was better expressed through the albumin/globulin (A/G) ratio. HGG was associated with a higher concentration of specific anti-glycan antibodies (BSA-G)/promastigote soluble extract (PSE) and the presence of circulating immune complexes (IC) by dissociative enzyme-linked immunoassay (ELISA). The study found monovalent IC in 37.9% (PSE) and 50% (BSA-G) of sera from infected hamsters, with increased frequency as the disease progressed. HGG was found in >60% of the samples in dogs with VL, associated with higher levels of specific immunoglobulin (Ig)A and IgM, but not IgG, determined using the PSE and BSA-G ELISA. HGG was associated with the presence of monovalent IC in 58.9% (PSE) and 63.4% (BSA-G) positive dog samples. HGG may result not only from the nonspecific activation of B cells, with greater production of specific and nonspecific antibodies, but also due to lower IgG excretion due to the presence of soluble monovalent IC. HGG correlates to the progression of VL and may be a marker for manifested disease.
Palavras-chave
dogs, hamsters, hypergammaglobulinemia, immune complexes, Leishmania L. infantum, visceral leishmaniasis
Referências
  1. Almeida MAO, 2005, VET IMMUNOL IMMUNOP, V106, P151, DOI 10.1016/j.vetimm.2004.08.024
  2. Baneth G, 2008, TRENDS PARASITOL, V24, P324, DOI 10.1016/j.pt.2008.04.001
  3. Baneth G, 2022, VET CLIN N AM-SMALL, V52, P1359, DOI 10.1016/j.cvsm.2022.06.012
  4. Batista LFS, 2020, VET PARASITOL, V288, DOI 10.1016/j.vetpar.2020.109276
  5. Beuvon C, 2021, EUR J INTERN MED, V90, P119, DOI 10.1016/j.ejim.2021.05.023
  6. BUNNMORENO MM, 1985, CLIN EXP IMMUNOL, V59, P427
  7. Medeiros FAC, 2021, CAD SAUDE PUBLICA, V37, DOI [10.1590/0102-311X00041320, 10.1590/0102-311x00041320]
  8. de Carvalho CA, 2020, PARASITOL RES, V119, P3881, DOI 10.1007/s00436-020-06851-9
  9. de Carvalho CA, 2019, IMMUNOLOGY, V158, P314, DOI 10.1111/imm.13118
  10. de Carvalho CA, 2013, ACTA TROP, V125, P128, DOI 10.1016/j.actatropica.2012.10.010
  11. ELASSAD AMS, 1994, CLIN EXP IMMUNOL, V95, P294, DOI 10.1111/j.1365-2249.1994.tb06526.x
  12. GALVAOCASTRO B, 1984, CLIN EXP IMMUNOL, V56, P58
  13. Gautam S, 2014, J INFECT DIS, V209, P290, DOI 10.1093/infdis/jit401
  14. Giunchetti RC, 2019, VET PARASITOL, V271, P87, DOI 10.1016/j.vetpar.2019.05.006
  15. Malatesha G, 2007, Trop Gastroenterol, V28, P28
  16. Mansueto P, 2007, INT J IMMUNOPATH PH, V20, P435, DOI 10.1177/039463200702000302
  17. Montes CL, 2007, J LEUKOCYTE BIOL, V82, P1027, DOI 10.1189/jlb.0407214
  18. Morales-Yuste M, 2022, VET SCI, V9, DOI 10.3390/vetsci9080387
  19. Osuna C, 2022, VET IMMUNOL IMMUNOP, V254, DOI 10.1016/j.vetimm.2022.110518
  20. Rombolà P, 2021, PLOS ONE, V16, DOI 10.1371/journal.pone.0244923
  21. Saporito L, 2013, INT J INFECT DIS, V 17, pE572, DOI 10.1016/j.ijid.2012.12.024
  22. Silva-Barrios S, 2019, EUR J IMMUNOL, V49, P1082, DOI 10.1002/eji.201847917
  23. Singh S, 2006, INDIAN J MED RES, V123, P311
  24. van Griensven J, 2012, INFECT DIS CLIN N AM, V26, P309, DOI 10.1016/j.idc.2012.03.005
  25. Villanueva-Saz S, 2022, ACTA TROP, V229, DOI 10.1016/j.actatropica.2022.106371
  26. Yadav P, 2023, PATHOGENS, V12, DOI 10.3390/pathogens12020297
  27. Zhao EJ, 2021, LANCET HAEMATOL, V8, pE365, DOI 10.1016/S2352-3026(21)00056-9