Peripheral blood monocytes show morphological pattern of activation and decreased nitric oxide production during acute Chagas’ disease in rats

Fabrino, Daniela Leite; Leon, Leonor L.; Parreira, Gleydes G.; Genestra, Marcelo; Almeida, Patrícia E. de; Melo, Rossana C. N.

doi:10.1016/j.niox.2004.07.010

Cited by 19 publications

(38 citation statements)

References 46 publications

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“…Semi-serial 5-m-thick sections were cut on a microtome (RM 2155; Leica) stained by hematoxylin and eosin or toluidine blue-basic fuchsin as before [6,20] and examined for qualitative evaluation of the inflammatory and degenerative processes and quantification of parasitism. The number of amastigote nests in the myocardium and skeletal muscles was evaluated at 70-m intervals in order to avoid parasite recounting [21] .…”

Section: Histological Methods and Histoquantitative Analysesmentioning

confidence: 99%

“…Peripheral blood monocytes (PBM) were washed twice in phosphate-buffered saline (PBS) at 280 g for 10 min at 4 ° C and resuspended in RPMI 1640 medium. The cell viability was assessed by Trypan blue test as before [6] , and was higher than 95%.…”

Section: Peripheral Blood Monocyte and Macrophage Isolation And Viabimentioning

confidence: 99%

“…Arginase activity was evaluated in cells as before [6] . Briefly, to 10 6 cells previously washed with RPMI (Sigma), 0.5 ml of 0.1% Triton X-100 in buffer containing 0.1 m M /l phenimethilsufonyl fluoride, 0.01%W/V Leupeptin, 0.2 mg/ml trypsin inhibitor and 1 m M /l of benzamidine in 0.25 M sucrose and 5 M KCl were added.…”

Section: Arginase Assaymentioning

confidence: 99%

“…In order to control parasite replication, cells of the monocytic lineage are remarkably recruited and have a pivotal role in the parasite clearance in both human beings and experimental models [for review, see 5 ]. Activated macrophages are able to produce high levels of proinflammatory cytokines and microbicidal products such as hydrogen peroxide (H 2 O 2 ) [6] , peroxinitrite [7] and nitric oxide (NO) [8] . However, despite extensive experimental investigations, the mechanisms used by activated macrophages to kill T. cruzi are not fully understood.…”

mentioning

confidence: 99%

“…For instance, the production of high amounts of NO through the inducible NO synthase (iNOS) by macrophages has been claimed as one of the main biochemical pathways to kill the parasite during the murine infection [8][9][10][11][12] . On the other hand, there are controversial data about the importance of this molecule in the control of parasite multiplication [6,13,14] . In fact, it has also been demonstrated that neither NO production [15] nor iNOS [16] are essential for the in vivo control of T. cruzi in mice.…”

mentioning

confidence: 99%

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Rat Models to Investigate Host Macrophage Defense against <i>Trypanosoma cruzi</i>

Fabrino

Leon²,

Genestra³

et al. 2010

J Innate Immun

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Trypanosoma cruzi is the causal agent of Chagas’ disease, an infection with a great impact on public health in Latin America. One of the challenges to understand Chagas’ disease lies on the complex host-parasite interaction. The understanding of this interaction requires the use of appropriate experimental models that mimic the human disease. Here, we have used two lineages of rats (Wistar and Holtzman) to comparatively evaluate the course of the acute infection (Y strain). Infection was monitored by parasitemia, cardiac and skeletal muscle parasitism and inflammation, heart ultrastructure, recruitment of monocytes/macrophages and nitric oxide, and arginase production by these cells. Although both rats were able to infect, only Holtzman rats developed a marked infection in the cardiac and skeletal muscles, in parallel to a high recruitment of first-line defense cells. A high number of inflammatory macrophages directed parasite clearance. By the end of the acute phase, Holtzman rats showed consistent disease control. Interestingly, parasite killing was not related to nitric oxide production likely inhibited by an arginase-dependent mechanism. Our work demonstrates differential responses of Holtzman and Wistar rats to T. cruzi, and highlights the use of Holtzman rats as useful models for further studies of cardiac/skeletal muscle tropism and innate immune responses that protect the host against parasite replication. This is important for the development of proper therapeutic interventions.

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Section: Histological Methods and Histoquantitative Analysesmentioning

confidence: 99%

Section: Peripheral Blood Monocyte and Macrophage Isolation And Viabimentioning

confidence: 99%

Section: Arginase Assaymentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Rat Models to Investigate Host Macrophage Defense against <i>Trypanosoma cruzi</i>

Fabrino

Leon²,

Genestra³

et al. 2010

J Innate Immun

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Histological Approaches to Study Tissue Parasitism During the Experimental Trypanosoma cruzi Infection

Fabrino

Ribeiro

Teixeira

et al. 2010

Methods in Molecular Biology

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During acute infection with the parasite Trypanosoma cruzi, the causal agent of Chagas' disease, tissue damage is related to intense tissue parasitism. Here we discuss histological approaches for an optimal visualization and quantification of T. cruzi nests in the heart, the main target organ of the parasite. These analyses are important to evaluate the course of the infection in different experimental models and also can be used to investigate parasite colonization and inflammatory processes in other infected tissues and biopsies.

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Lipid bodies: structural markers of inflammatory macrophages in innate immunity

et al. 2006

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Peripheral blood monocytes show morphological pattern of activation and decreased nitric oxide production during acute Chagas’ disease in rats

Cited by 19 publications

References 46 publications

Rat Models to Investigate Host Macrophage Defense against <i>Trypanosoma cruzi</i>

Rat Models to Investigate Host Macrophage Defense against <i>Trypanosoma cruzi</i>

Histological Approaches to Study Tissue Parasitism During the Experimental Trypanosoma cruzi Infection

Lipid bodies: structural markers of inflammatory macrophages in innate immunity

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