Microbial Translocation Induces an Intense Proinflammatory Response in PatientsWith Visceral Leishmaniasis and HIV Type 1 Coinfection
Carregando...
Citações na Scopus
32
Tipo de produção
article
Data de publicação
2013
Título da Revista
ISSN da Revista
Título do Volume
Editora
OXFORD UNIV PRESS INC
Autores
SANTOS-OLIVEIRA, Joanna R.
REGIS, Eduardo G.
GIACOIA-GRIPP, Carmem B. W.
VALVERDE, Joanna G.
ALEXANDRINO-DE-OLIVEIRA, Priscilla
OLIVEIRA-NETO, Manoel P.
GUERRA, Jorge O.
GRINSZTEJN, Beatriz
Citação
JOURNAL OF INFECTIOUS DISEASES, v.208, n.1, p.57-66, 2013
Resumo
Background. Leishmania infection is a cofactor in the heightened cellular activation observed in patients with American visceral leishmaniasis and human immunodeficiency virus type 1 (HIV) infection, with or without progression to AIDS (AVL/HIV). Thus, the persistence of a high parasite load despite antileishmanial therapy could be responsible for the continued immune stimulation. Methods. CD8(+) T cells expressing CD38, parasite load, lipopolysaccharide (LPS), soluble CD14, macrophage migration inhibitory factor (MIF), intestinal fatty acid-binding protein (IFABP), and proinflammatory cytokines (interleukin 1 beta, interleukin 6, interleukin 8, interleukin 17, interferon gamma, and tumor necrosis factor) were measured in 17 patients with AVL/HIV, 16 with HIV, and 14 healthy subjects (HS). Results. Lower Leishmania parasitemia was observed after antileishmanial and antiretroviral therapies. However, higher levels of CD38(+) on CD8(+) T cells were observed in both clinical phases of leishmaniasis, compared with HIV cases. AVL/HIV and HIV patients showed higher levels of LPS and IFABP than HS. Proinflammatory cytokine levels were significantly augmented in patients with active coinfection, as well as those with remission of Leishmania infection. LPS levels and Leishmania infection were positively correlated with CD38 expression on CD8(+) T cells and with IL-6 and IL-8 levels. Conclusions. LPS levels along with the immune consequences of Leishmania infection were associated with elevated cellular activation in coinfected patients. As a consequence, secondary chemoprophylaxis for leishmaniasis or even the use of antiinflammatory drugs or antibiotics may be considered for improving the prognosis of AVL/HIV.
Palavras-chave
visceral leishmaniasis-HIV/AIDS coinfection, microbial translocation, inflammatory cytokines
Referências
- Alexandrino-de-Oliveira P, 2010, MEM I OSWALDO CRUZ, V105, P692, DOI 10.1590/S0074-02762010000500016
- Alexandrino-de-Oliveira P, 2010, BMC INFECT DIS, V10, P35863
- Alvar J, 2008, CLIN MICROBIOL REV, V21, P334, DOI 10.1128/CMR.00061-07
- Antinori S, 2007, CLIN INFECT DIS, V44, P1602, DOI 10.1086/518167
- Appay V, 2008, J PATHOL, V214, P231, DOI 10.1002/path.2276
- Balkhair A, 2008, INT J INFECT DIS, V12, P111, DOI 10.1016/j.ijid.2007.04.009
- Barreto-De-Souza V, 2006, J INFECT DIS, V194, P846, DOI 10.1086/506618
- Bernier R, 1998, J IMMUNOL, V160, P2881
- Brasil Ministerio da Saude Departamento de DST Aids e hepatites virais, PROT CLIN DIR TER AD
- Brasil Ministerio da Saude Secretaria de Vigilancia em Saude Departamento de Vigilancia Epidemiologica, 2006, MAN VIG CONTR LEISHM
- Brenchley JM, 2012, ANNU REV IMMUNOL, V30, P149, DOI 10.1146/annurev-immunol-020711-075001
- Brenchley JM, 2004, J EXP MED, V200, P749, DOI 10.1084/jem.20040874
- Brenchley JM, 2006, NAT MED, V12, P1365, DOI 10.1038/nm1511
- Calandra T, 2003, NAT REV IMMUNOL, V3, P791, DOI 10.1038/nri1200
- Caradonna L, 2000, J ENDOTOXIN RES, V6, P205, DOI 10.1179/096805100101532063
- Casado JL, 2001, EUR J CLIN MICROBIOL, V20, P202, DOI 10.1007/s10096-001-8082-z
- Connolly NC, 2005, AIDS REV, V7, P168
- Cooke KR, 2002, J ENDOTOXIN RES, V8, P441, DOI 10.1179/096805102125001046
- Cota GF, 2011, PLOS NEGLECT TROP D, V5, DOI 10.1371/journal.pntd.0001153
- Doisne JM, 2004, J IMMUNOL, V173, P2410
- Douek DC, 2009, ANNU REV MED, V60, P471, DOI 10.1146/annurev.med.60.041807.123549
- Estes JD, 2010, PLOS PATHOG, V6, DOI 10.1371/journal.ppat.1001052
- Giorgi JV, 1999, J INFECT DIS, V179, P859, DOI 10.1086/314660
- Gonzalez VD, 2009, J VIROL, V83, P11407, DOI 10.1128/JVI.01211-09
- Goto H, 2009, REV I MED TROP, V51, P241, DOI 10.1590/S0036-46652009000500002
- Hicks L, 2009, EUR J GASTROEN HEPAT, V21, P117, DOI 10.1097/MEG.0b013e32830e6fdb
- Rodrigues Denise do Socorro S., 2003, Braz J Infect Dis, V7, P161, DOI 10.1590/S1413-86702003000200010
- Lee PI, 2009, J INFECT DIS, V199, P1664, DOI 10.1086/598953
- Lieberman JM, 1997, SURGERY, V121, P335, DOI 10.1016/S0039-6060(97)90363-9
- Liu ZY, 1997, J ACQ IMMUN DEF SYND, V16, P83
- Baba Chalamalasetty Sreenivasa, 2006, Indian J Gastroenterol, V25, P309
- McCoy JJ, 1998, MOL BIOCHEM PARASIT, V95, P251, DOI 10.1016/S0166-6851(98)00112-1
- Medrano FJ, 1998, CLIN EXP IMMUNOL, V114, P403, DOI 10.1046/j.1365-2249.1998.00733.x
- Mehandru S, 2004, J EXP MED, V200, P761, DOI 10.1084/jem.20041196
- Miller SI, 2005, NAT REV MICROBIOL, V3, P36, DOI 10.1038/nrmicro1068
- Mock DJ, 2012, PLOS PATHOG, V8, DOI 10.1371/journal.ppat.1002635
- Nazli A, 2010, PLOS PATHOG, V6, DOI 10.1371/journal.ppat.1000852
- Rabello A, 2003, ANN TROP MED PARASIT, V97, P17, DOI 10.1179/000349803225002507
- Saha S, 2006, INDIAN J MED RES, V123, P245
- Sandler NG, 2011, GASTROENTEROLOGY, V141, P1220, DOI 10.1053/j.gastro.2011.06.063
- Santos-Oliveira JR, 2011, PLOS NEGLECT TROP D, V5, DOI 10.1371/journal.pntd.0001198
- Senent SG, 2009, GASTROENTEROL HEPATO, V32, P176, DOI 10.1016/j.gastrohep.2008.09.021
- Peruhype-Magalhaes V, 2006, CLIN EXP IMMUNOL, V146, P124, DOI 10.1111/j.1365-2249.2006.03171.x
- Sinha PK, 2006, INDIAN J MED RES, V123, P197
- Sousa-Gomes ML, 2011, EPIDEMIOL SERV SAUDE, V20, P519
- Weirather JL, 2011, J CLIN MICROBIOL, V49, P3892, DOI 10.1128/JCM.r00764-11
- Wolday D, 1998, SCAND J INFECT DIS, V30, P29
- Zhao CQ, 2004, CLIN IMMUNOL, V113, P81, DOI 10.1016/j.clim.2004.06.003
- Nylen S, 2007, J EXP MED, V204, P805, DOI 10.1084/jem.20061141