Iriane Eger

Prof. Dr. Iriane Eger

orcid

Research Focus & Metrics

Academic Career Length

16Years (2011-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
1 August 2011 in The Journal of Infectious Diseases
Verified
Journal Article
Open access
PDF file
DPDarlene A. Pena
Darlene A. Pena
IEIriane Eger
Iriane Eger
LNLucas de Lima Nogueira
Lucas de Lima Nogueira
NHNicoli Heck
Nicoli Heck
ÁMÁlvaro Menin
Álvaro Menin
MSMário Steindel
Mário Steindel
Background. Chagas disease is caused by the protozoan parasite Trypanosoma cruzi, which exhibits a high genetic variability. TcI, TcII, or mixed TcI/TcII strains may be found during acute human infection while mainly TcII parasites are present at the chronic stage of disease. In a previously studied Chagas disease outbreak, we identified mixed TcI/TcII strains in the vector Triatoma tibiamaculata and only TcII strains in infected humans, indicating that T. cruzi populations may be selected within the human host. Methods. Utilizing molecular typing and cell biology techniques, we investigated the interaction of TcI, TcII, and mixed TcI/TcII strains with macrophages, an important cell population implicated in controlling protozoan infection. Results. TcII but not TcI strains were selected by both human and murine macrophages in vitro and by peritoneal cavity cells in vivo. Biological analysis revealed that, compared with TcI, TcII strains display higher infective and multiplicative ability as well as lower doubling time inside macrophages. However, TcI and TcII strains present similar susceptibility to interferon-γ–activated macrophages in vitro. Conclusions. Taken together, our results reveal the existence of an intracellular selection process in macrophages that favors TcII, but not TcI, when infection occurs with vector-derived mixed TcI/TcII strains.

14 February 2013 in PLOS ONE
Verified
Journal Article
Open access
PDF file
MMMariel Asbury Marlow
Mariel Asbury Marlow
MMMarise da Silva Mattos
Marise da Silva Mattos
MMMaria Ernestina Makowiecky
Maria Ernestina Makowiecky
IEIriane Eger
Iriane Eger
ARAndre Luiz Rossetto
Andre Luiz Rossetto
MSMário Steindel
Mário Steindel
Although known to be highly endemic in the Amazon regions of Brazil, the presence of cutaneous leishmaniasis (CL) in the subtropical southern part of the country has largely been ignored. This study was conducted to demonstrate CL is emerging in the Brazilian state of Santa Catarina, as well as to characterize the epidemiological profile and Leishmania species involved. For this cross-sectional study, data from all CL cases from Santa Catarina, Brazil, reported to the Brazilian National Notifiable Diseases Information System from 2001 to 2009 were investigated. Amplification of the kDNA minicircle conserved region followed by restriction fragment length polymorphism (PCR-RFLP) was conducted to screen for Leishmania species present in patient biopsy. Overall, 542 CL cases were reported, with majority resulting from autochthonous transmission (n = 401, 73.99%) and occurring in urban zones (n = 422, 77.86%). Age, gender, zone of residence, origin of case, clinical form and case outcome were found to differ significantly by region. Imported cases were over seven times more likely to relapse (95% CI 2.56–21.09). Mapping of cases revealed new endemic areas in northeastern Santa Catarina with two species present. With the exception of three L. (Leishmania) amazonensis cases (1.20%), majority of PCR positive samples were found to be L. (Viannia) braziliensis (n = 248, 98.80%). CL is now endemic in the state of Santa Catarina, Brazil, with case profiles varying significantly by region. L. (V.) braziliensis has been identified as the predominant species in the region.

Verified
Journal Article
Open access
PDF file
JAJuliana Bernardi Aggio
Juliana Bernardi Aggio
VVVerônica Vitória Vedam
Verônica Vitória Vedam
LNLindice Mitie Nisimura
Lindice Mitie Nisimura
RSRosiane Valeriano da Silva
Rosiane Valeriano da Silva
MLMaria Izabel Lovo-Martins
Maria Izabel Lovo-Martins
PWPryscilla Fanini Wowk
Pryscilla Fanini Wowk
Chagas disease remains a significant public health concern, with limited treatment options and an urgent need for novel preventive strategies. Extracellular vesicles (EVs) from Trypanosoma cruzi have been shown to modulate host immune responses, often favoring parasite persistence. In this study, we characterized EVs derived from the non-pathogenic trypanosomatids Trypanosoma rangeli and Phytomonas serpens and evaluated their potential as immunogens capable of inducing cross-protection against T. cruzi infection. Isolated EVs were characterized by Nanoparticle Tracking Analysis (NTA) and electron microscopy. A comparative proteomic analysis of EVs was performed using Mass Spectrometry-Based Proteomic Analysis (LC-MS/MS). The effects of EVs on immunomodulation and T. cruzi infection were assessed through in vitro and in vivo assays, using peripheral blood mononuclear cells (PBMCs) and BALB/c mice. The proteomic analysis identified shared proteins between the EVs of T. rangeli, P. serpens, and T. cruzi, including immunogenic candidates such as calpain-like cysteine peptidase and elongation factor 2. In vitro, pre-stimulation with the T. rangeli EVs reduced infection rates of the host cells by T. cruzi. In vivo, immunization with the EVs from T. rangeli and P. serpens led to a significant reduction in parasitemia in the BALB/c mice challenged with T. cruzi, though this did not translate into improved survival compared to controls. Interestingly, the EVs from T. cruzi also reduced parasitemia but did not confer protection against mortality. These findings suggest that while non-pathogenic trypanosomatid EVs exhibit potential immunogenic properties and can reduce parasitic load, their efficacy in preventing disease progression remains limited. Further research is needed to explore the mechanisms underlying these effects and to optimize EV-based strategies for protective immunity against Chagas disease.

1 January 2024 in Memórias do Instituto Oswaldo Cruz
Verified
Journal Article
Open access
PDF file
CDCleyson Mathias Morais Delvoss
Cleyson Mathias Morais Delvoss
AIAlexandre Haruo Inoue
Alexandre Haruo Inoue
RSRosiane Valeriano da Silva
Rosiane Valeriano da Silva
SFStênio Perdigão Fragoso
Stênio Perdigão Fragoso
IEIriane Eger
Iriane Eger
American trypanosomiasis, also known as Chagas disease (CD), is a zoonotic illness caused by the protozoan Trypanosoma cruzi. Endemic to the Americas and trivialised by society due to its predominant impact on poor and vulnerable populations,1 1. Damasceno RF, Sabino EC, Ferreira AM, Ribeiro ALP, Moreira HF, Prates TEC, et al. Challenges in the care of patients with Chagas disease in the Brazilian public health system: a qualitative study with primary health care doctors. PLoS Negl Trop Dis. 2020; 14(11): e0008782. this parasitic infection is classified as a neglected disease by the World Health Organization (WHO).2 2. Dias JCP, Ramos Jr AN, Gontijo ED, Luquetti A, Shikanai-Yasuda MA, Coura JR, et al. Brazilian Consensus on Chagas disease, 2015. Epidemiol Serv Saude. 2016; 25: 7-86. The primary transmission mechanism of T. cruzi is through the vector pathway, but alternative routes of transmission include blood transfusion, organ transplantation, laboratory accidents, congenital, and oral infections. Oral transmission is particularly noteworthy in the medical scenario of CD due to its characteristic outbreak nature, clinical severity, and higher parasite inoculum compared to the classic vector transmission.3 3. Coura JR. The main sceneries of Chagas disease transmission. The vectors, blood and oral transmissions - A comprehensive review. Mem Inst Oswaldo Cruz. 2015; 110(3): 277-82. These transmission mechanisms, combined with human migration between the Americas and other regions, have elevated CD to a global health concern.4 4. Guggenbühl Noller JM, Froeschl G, Eisermann P, Jochum J, Theuring S, Reiter-Owona I, et al. Describing nearly two decades of Chagas disease in Germany and the lessons learned: a retrospective study on screening, detection, diagnosis, and treatment of Trypanosoma cruzi infection from 2000 - 2018. BMC Infect Dis. 2020; 20(1): 919.

7 August 2026 in Preprints.org
Verified
Preprint
Open access
PDF file
SQSuelen Queiroz
Suelen Queiroz
IEIriane Eger
Iriane Eger
ECEurico Cleto Ribeiro de Campos
Eurico Cleto Ribeiro de Campos
EMEdmar Miyoshi
Edmar Miyoshi
Diabetes mellitus affects over 537 million adults worldwide, yet the impact of hyperglycemia on absorbable suture degradation remains poorly understood. This study evaluated the in vitro degradation of polyglycolic acid (PGA) and PGLA 910 copolymer sutures under glucose concentrations of 0, 300, and 600 mg/dL over 28 days. A total of 120 sutures (60 per material) were incubated at 37°C in phosphate-buffered saline with different glucose concentrations. Mechanical properties were assessed at baseline and at 7, 14, 21, and 28 days via tensile testing. Medium pH was monitored weekly, and surface morphology was characterized by scanning electron microscopy. PGLA 910 demonstrated higher baseline strength than PGA (14.56 ± 1.11 N vs. 13.37 ± 1.00 N; p < 0.001). Both materials maintained strength during the first 7 days (p = 0.080), but progressive loss occurred from day 14 onward. At day 28 in a glucose-free medium (0 mg/dL), PGA retained only 1.12 N (8.4% of initial strength), while PGLA 910 retained 3.81 N (26.2%; p < 0.001). SEM revealed more severe surface degradation in PGA than in PGLA 910. We conclude that PGLA 910 offers superior resistance to hydrolytic degradation, making it a more suitable choice for diabetic patients when extended mechanical integrity is required. However, both materials degrade extensively within 4 weeks and are unsuitable for applications requiring support beyond 3 weeks. The strong pH–strength correlation confirms the autocatalytic nature of the degradation mechanism.