(Eh) y metanÃ³lico (Em) de Pera distichophylla sobre un aislado de ...

More documents

Recommendations

Info

M. T. GALáN-PUCHADES and A. OSUNA in an increase of T. cruzi parasitaemia, precisely one of the risks favouring vertical transmission. Additionally, helminths can also contribute to a lower IFN-g production via a predominant Th-2 response in pregnant women. Therefore, it would be interesting to evaluate the helminthological status of chagasic pregnant women and its possible influence on vertical transmission. 10 DISCUSSION In order to address the questions of whether helminth infection could affect the susceptibility to subsequent co-infection with T. cruzi, and whether a changing environment and cytokine profile induced by worms may influence the outcome of CD compared with hosts exclusively infected with T. cruzi, it was found that the presence of helminths modifies both the susceptibility and, in most cases, the course of CD. Concerning susceptibility, in all the studied hosts (humans, mice, dogs and primates) the presence of worms increases the likelihood to acquire CD mainly in the helminth chronic phase. In addition, co-infection seems to lengthen survivorship of coinfected hosts compared with those only harboring T. cruzi. The presence of helminths also tends to increase T. cruzi parasitaemia and certain helminths may even improve the health status of chagasic hosts. One of the main implications of these findings is that helminth co-infections could potentially modify the course of CD among patients with the same T. cruzi DTU (discrete typing units) (Monteiro et al., 2007). In the last two decades, studies explaining severe forms of CD have mainly been based on immunological findings (Dutra et al., 2005, Rodrigues et al., 2010). Chagasic myocarditis is thought to be due to the presence of parasites in the lesions. However, an unbalanced immune homeostasis can trigger parallel autoimmune phenomena which increase the immune response, thus worsening the outcome of the disease (Gutierrez et al., 2009). Several results evidence that an exacerbated Th1-like specific immune response against T. cruzi with high levels of IFN-γ and low levels of the anti-inflamatory cytokine IL-10 is established in T. cruzi-infected individuals present- ing cardiac disease (Gomes et al., 2003). In addition, there is some limited evidence regarding the role of Th17-mediated responses to T. cruzi. The IL-17 produced during the acute phase of CD controls cardiac inflammation by modulating the Th1 response, and this pro-inflammatory IL-17 is also required for the elimination of T. cruzi (Guedes et al., 2010; Miyazaki et al., 2010). In contrast IL- 27, which suppresses Th17 responses, is beneficial for the host during T. cruzi infection (Yoshida and Miyazaki, 2008). Surprisingly, there is no mention in the literature that evaluates the possible role of helminth infections in human CD when helminths are able to suppress all types (Th1, Th2, and Th17) of responses (see ref Osada and Kanazawa, 2010). Considering the classical Th1/Th2 paradigm, it is reasonable to speculate that a helminth-induced Th2 response with production of IL-4, IL-5, IL-6 and IL-10 skewing with downregulation of Th1 immune responses could result in an amelioration of Th1 diseases, such as CD. As IL-4 is known to suppress Th17 development (Romagnani, 2006), a Th17 response could also be suppressed as well as Th1 response in helminth-infected hosts. In fact, certain helminth infections reduce IL-17 mRNA by MLN cells and inhibit IL-17 production (Elliot et al., 2008). This is of relevance when considering persistent parasites such as helminths which are widely distributed in humans in developing countries (Maizels et al., 1993), where they coexist with T. cruzi. Wormy populations are exposed to two potential risks, namely an increased susceptibility to T. cruzi and a yet unresearched course of the disease. All of this should prompt research on the possible epidemiological relevance of helminth infections and the impact when controlling them on the incidence or the pathogenesis of CD. The presence of helminth co-infections may represent a much more important challenge for public health than recognized until now. In other co-infections of human parasites such as malaria and hookworms, it has been stated that it would be possible to define co-infection as a specific “disease”, separate from malaria by itself, or hookworm by itself (Payne et al., 2009), and this may also hold true for CD and helminths. Thus, gathering more reliable data on the true parasitological status of all chagasic patients would be desirable. Rev. Ibero-Latinoam. Parasitol. (2012); 71 (1): 5-13
CONCLUDING REMARKS Humans are exposed to a large number of pathogens interacting in a dynamic manner over time. Hence, the immunological networks activated as a result of these infections are multifactorial and complicated to study. Classical studies directed at one single parasite species are rather simplistic since they ignore the diverse outcome of the multiple interactions which result from co-infections by micro- and macroparasites. There are reasonable indications that coinfections with helminths and T. cruzi can interact and influence the immune responses to and clinical outcomes of CD. However, studies addressing these interactions are needed both in humans and animal models. A great number of people are likely to be co-infected with helminths and CD, and the influence of helminth infections on the course of the disease needs careful investigation in large populations. Each type of helminth infection should be studied separately, since each one of them may have different effects on the course of the disease. Treatment of helminth infections ensued by a detailed follow-up on the infection rate and on the symptoms of CD will be important to establish the precise effect of helminth infections on the outcome of T. cruzi parasitaemia and disease. Needless to say, the analysis of the immunological profiles will shed more light on the mechanisms that are involved and experimental murine co-infections will help to dissect the molecular immunological pathways involved. A better understanding of CD in a wormy world will not only improve the evaluation of T. cruzi vaccine trials and therapeutic measures but will also reveal the implications of anthelminthic treatment schemes in the course of CD and the risk of vertical transmission. REFERENCES 1. BRUTUS L, CASTILLO H, BERNAL C, SALAS NA, SCHNEIDER D, SANTALLA JA, CHIPPAUx JP. 2010. Detectable Trypanosoma cruzi parasitemia during pregnancy and delivery as a risk factor for congenital Chagas disease. Am J Trop Med Hyg 83: 1044-1047. 2. CARLIER Y, TRUYENS C. 2010. Maternal-Fetal Transmission of Trypanosoma cruzi. In: American Try- Rev. Ibero-Latinoam. Parasitol. (2012); 71 (1): 5-13 CHAGAS DISEASE IN A WORMY WORLD panosomiasis. Chagas Disease. One Hundred Years of Research (Telleria, J., Tybayrenc, M., Eds.). Elsevier, 539-581. 3. CRUZ-CHAN JV, QUIJANO-HERNáNDEZ I, RA- MÍREZ-SIERRA MJ, DUMONTEIL E. 2010. Dirofilaria immitis and Trypanosoma cruzi natural co-infection in dogs. Vet J 186: 399-401. 4. DUTRA WO, ROCHA MOC, TExEIRA MM. 2005. The clinical immunology of human Chagas disease. Trends Parasitol 21: 581-587. 5. ELLIOTT DE, METWALI A, LEUNG J, SETIAWAN T, BLUM AM. INCE MN, BAZZONE LE, STADEC- KER MJ, URBAN Jr JF, WEINSTOCK JV. 2008. Colonization with Heligmosomoides polygyrus Suppresses Mucosal IL-17 Production. J Immunol 181: 2414-2419. 6. EZENWA VO, ETIENNE RS, LUIKART G, BEJA- PEREIRA A, JOLLES AE. 2010. Hidden consequences of living in a wormy world: nematode - induced immune suppression facilitates tuberculosis invasion in African buffalo. Am Nat 176: 613-624. 7. EZENWA VO, JOLLES AE. 2011. From Host Immunity to Pathogen Invasion: The Effects of Helminth Coinfection on the Dynamics of Microparasites. Integr Comp Biol, 1-12 doi:10.1093/icb/icr058. 8. FALEIROS AC, LINO-JUNIOR R, LIMA V, CAVE- LLANI C, ROSA CORREA R, LLAGUNO M, REIS M, TEIxEIRA V. 2009. Análisis epidemiológico de pacientes coinfectados con enfermedad de Chagas y cisticercosis. Biomédica 29: 127-132. 9. GOMES JAS, BAHIA-OLIVEIRA LMG, ROCHA MOC, MARTINS-FILHO OA, GAZZINELLI G, CORREA-OLIVEIRA M. 2003. Evidence that Development of Severe Cardiomyopathy in Human Chagas’ Disease Is Due to a Th1-Specific Immune Response. Infect Immun 71: 1185-1193. 10. GRAHAM AL. 2008. Ecological rules governing helminth–microparasite coinfection. Proc Natl Acad Sci USA 15: 566-570. 11. GUEDES PMDM, GUTIÉRREZ FRS, MAIA FL, MILANEZI CM, SILVA GK, PAVANELLI WR, SILVA JS. 2010. IL-17 Produced during Trypanosoma cruzi Infection Plays a Central Role in Regulating Parasite- Induced Myocarditis. PLoS Negl Trop Dis 4: e604. doi:10.1371/journal.pntd.0000604. 12. GUTIÉRREZ FRS, GUEDES PMM, GAZZINELLI SILVA JS. 2009. The role of parasite persistence in pathogenesis of Chagas heart disease. Parasite Immunol 31: 673-685. 13. HARTGERS C, YAZDANBAKHSH M. 2006. Coinfection of helminths and malaria: modulation of the immune responses to malaria. Parasite Immunol 28: 497-506. 14. HELMBY H. 2009. Helminths and our immune system: Friend or foe? Parasitol Int 58: 121-127. 15. JONES JL, KRUSZON-MORAN D, WON K, WIL- SON M, SCHANTZ PM. 2008. Toxoplasma gondii and Toxocara spp. Co-infection. Am J Trop Med Hyg 78: 35-39. 16. KHAN IA, HAKAK R, EBERLE K, SAYLES P, WEISS LM, URBAN JF. Jr. 2008. Coinfection with Heligmosomoides polygyrus Fails To Establish CD8 T-Cell Immunity against Toxoplasma gondii. Infect Immun 76: 1305-1313. 11
Page 1: CONTINUACIÓN DE PARASITOLOGÍA LAT
Page 4 and 5: Producción: María Cristina Illane
Page 6 and 7: Contenido 4 Rev. Ibero-Latinoam. Pa
Page 8 and 9: M. T. GALáN-PUCHADES and A. OSUNA
Page 16 and 17: Artículo Original 14 Rev. Ibero-La
Page 18 and 19: A. MUÑOZ et al. cionalmente, exist
Page 20 and 21: A. MUÑOZ et al. Evaluación de la
Page 22 and 23: A. MUÑOZ et al. ta la máxima conc
Page 24 and 25: A. MUÑOZ et al. disease. In S Wend
Page 26 and 27: C. ZÚÑIGA et al. RESUMEN Ratones
Page 28 and 29: C. ZÚÑIGA et al. niveles de paras
Page 30 and 31: C. ZÚÑIGA et al. Figura 3. Tejido
Page 32 and 33: C. ZÚÑIGA et al. Figura 10. Tejid
Page 34 and 35: C. ZÚÑIGA et al. muerte súbita,
Page 38 and 39: I. NOVO-VELEIRO et al. zona norte d
Page 40 and 41: I. NOVO-VELEIRO et al. parte de los
Page 42 and 43: I. NOVO-VELEIRO et al. otras helmin
Page 46 and 47: A. DORLA et al. firme bajos y bosqu
Page 48 and 49: A. DORLA et al. en los campos obser
Page 50 and 51: A. DORLA et al. En la Figura 4, se
Page 52 and 53: A. DORLA et al. número de amibas n
Page 54 and 55: A. DORLA et al. el DMSO actúa como
Page 56 and 57: A. DORLA et al. temperature-II. Via
Page 58 and 59: C. M. WAGNER et al. el tratamiento
Page 60 and 61: C. M. WAGNER et al. Porcentaje (%)
Page 62 and 63:
C. M. WAGNER et al. estudiada es ti
Page 64 and 65:
Artículo Original 62 Rev. Ibero-La
Page 66 and 67:
R. H. QUIROZ et al. Productos exper
Page 68 and 69:
R. H. QUIROZ et al. peso el Grupo 1
Page 70 and 71:
R. H. QUIROZ et al. géneros el res
Page 72 and 73:
Page 74 and 75:
A. J. TORRES et al. pazes de trocar
Page 76 and 77:
A. J. TORRES et al. 74 Figura 1. Es
Page 78 and 79:
A. J. TORRES et al. infestações.
Page 80 and 81:
Page 82 and 83:
A. MORALES et al. el descarte de he
Page 84 and 85:
A. MORALES et al. Seroprevalence, R
Page 86 and 87:
C. MEDINA et al. la presencia de Cr
Page 88 and 89:
C. MEDINA et al. la metodología de
Page 90 and 91:
C. MEDINA et al. Tabla 2. Valor má
Page 92 and 93:
Page 94 and 95:
A. da S. BARBOSA et al. animals as
Page 96 and 97:
A. da S. BARBOSA et al. Table 3. Co
Page 98 and 99:
A. da S. BARBOSA et al. Diagnóstic
Page 100 and 101:
C. N. VALENCIA et al. (NFx) y benzn
Page 102 and 103:
C. N. VALENCIA et al. Tabla 3. Ante
Page 104 and 105:
C. N. VALENCIA et al. Tabla 5. Regi
Page 106 and 107:
C. N. VALENCIA et al. en los dos pe
Page 108 and 109:
C. N. VALENCIA et al. boliza abunda
Page 110 and 111:
C. N. VALENCIA et al. mox en pacien
Page 112 and 113:
NORMAS DE PUBLICACIóN 1. Los traba
Page 114:
NORMAS DE PUBLICACIÓN clock (e.g.
show all

(Eh) y metanÃ³lico (Em) de Pera distichophylla sobre un aislado de ...

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?