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Background: Trypanosoma rangeli is a haemoflagellate parasite that infects triatomine bugs and mammals in South and Central America. Trypanosoma cruzi, the etiological agent of Chagas disease, has a partially overlapping geographical distribution with T. rangeli, that leads to mixed human infections and cross-reactivity in immunodiagnosis. Although T. rangeli can be detected long after mammal infection, its multiplicative forms have not yet been described.
Objectives: To enhance our understanding of T. rangeli development in mammals, this study assessed various infection parameters in mice over time.
Methods: The parasitaemia, body temperature, and weight of Swiss Webster mice were monitored over 120 days after exposing them to the bites of Rhodnius prolixus nymphs containing metacyclic trypomastigotes in their salivary glands. On day 132 post-infection, spleens and mesenteric lymph nodes were analysed for T. rangeli DNA using polymerase chain reaction (PCR) and quantitative PCR (qPCR).
Findings: Parasites were detectable in mice blood since day 2 post-infection, detection peaking on day 5 and becoming undetectable by day 120. PCR and qPCR detected T. rangeli DNA in the spleens and mesenteric lymph nodes of infected mice. Infected mice showed higher body temperatures and a slower weight gain over time compared to controls.
Main Conclusions: The study confirmed that T. rangeli establishes a persistent infection in mice, detectable in lymphoid organs long after parasites had disappeared from blood. In addition, infected mice exhibited physiological changes, suggesting potential subclinical effects. These findings highlight the need for further studies on the immune response and potential impacts of T. rangeli infection in mammalian hosts.
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http://dx.doi.org/10.1590/0074-02760240138 | DOI Listing |
Angiogenesis
September 2025
Pathophysiology and Regenerative Medicine Group, Hospital Nacional de Parapléjicos, Servicio de Salud de Castilla la Mancha (SESCAM), 45071, Toledo, Spain.
Limited vascularization and ischemia are major contributors to the chronicity of wounds, such as ulcers and traumatic injuries, which impose significant medical, social, and economic burdens. These challenges are particularly pronounced in patients with spinal cord injury (SCI), a disabling condition associated with vascular dysfunction, infections, and impaired peripheral circulation, complicating the treatment of pressure injuries (PIs) and the success of reconstructive procedures like grafts and flaps. Regenerative medicine aims to address these issues by identifying effective cellular therapies to restore vascular beds.
View Article and Find Full Text PDFMol Ther Methods Clin Dev
June 2025
Université Paris-Saclay, University Evry, Inserm, Genethon, Integrare Research Unit UMR_S951, 91000 Evry, France.
Pompe disease is a glycogen storage disorder caused by mutations in the acid α-glucosidase (GAA) gene, leading to reduced GAA activity and glycogen accumulation in heart and skeletal muscles. Enzyme replacement therapy with recombinant GAA, the standard of care for Pompe disease, is limited by poor skeletal muscle distribution and immune responses after repeated administrations. The expression of GAA in muscle with adeno-associated virus (AAV) vectors has shown limitations, mainly the low targeting efficiency and immune responses to the transgene.
View Article and Find Full Text PDFCell Physiol Biochem
September 2025
Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institute of Biochemistry, 10117 Berlin, Germany.
Background/aims: The ubiquitin-like protein ISG15 and its covalent conjugation to substrates (ISGylation) represent a critical interferon (IFN)-induced antiviral mechanism. USP18 is an ISG15-specific isopeptidase and a key negative regulator of type I IFN signaling. While inactivation of USP18's catalytic activity enhances ISGylation and promotes viral resistance, its role in modulating inflammation and cardiac function during CVB3-induced myocarditis remains unclear.
View Article and Find Full Text PDFJ Biochem
September 2025
Division of Enzyme Pathophysiology, Institute for Enzyme Research, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Microglia, the central nervous system's resident macrophages, are critical for immune defense, protecting neurons during infection. Their role in postnatal brain development, particularly after injury, remains unclear. Nucling, a protein up-regulated during cardiac muscle differentiation, regulates NF-κB, influencing apoptosis and cell proliferation.
View Article and Find Full Text PDFACS Nano
September 2025
National Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Huazhong Agricultural University, Wuhan 430070, Hubei, China.
Foot-and-mouth disease virus (FMDV), a critical pathogen in the global livestock industry, has long been a focal point of international disease control strategies. This study developed a nanoparticle-based FMDV vaccine platform. We fused the FMDV immunodominant epitope (VP1-G-H-loop) and T-cell epitope (T) with the nanoparticle scaffold (LS), efficiently producing the T-LS-LOOP nanoparticle vaccine using the prokaryotic expression system (BL21).
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