B-1 Cells May Drive Macrophages Susceptibility to Trypanosoma cruzi Infection

Rocha, Raphael Francisco Dutra Barbosa da; LaRocque-de-Freitas, Isabel Ferreira; Arcanjo, Angélica; Logullo, Jorgete; Nunes, Marise P.; Freire-de-Lima, Célio Geraldo; Decotè-Ricardo, Débora

doi:10.3389/fmicb.2019.01598

Cited by 6 publications

(5 citation statements)

References 48 publications

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“…The trypomastigote forms when phagocytosed by macrophages differ from amastigote forms, with the macrophage state being the determinant for their survival. IFN-γ-activated macrophages are able to partially destroy the parasites [44,45,66,67]. The results obtained in our study corroborate the previous studies since the presence of collagen I did not alter the activation of the macrophages by IFN-γ and LPS, which still were able to control the intracellular replication of T. cruzi [68].…”

Section: Discussionsupporting

confidence: 90%

Increased Trypanosoma cruzi Growth during Infection of Macrophages Cultured on Collagen I Matrix

Logullo

Diniz-Lima

Rocha

et al. 2023

Life

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The interactions between cell and cellular matrix confers plasticity to each body tissue, influencing the cellular migratory capacity. Macrophages rely on motility to promote their physiological function. These phagocytes are determinant for the control of invasive infections, and their immunological role largely depends on their ability to migrate and adhere to tissue. Therefore, they interact with the components of the extracellular matrix through their adhesion receptors, conferring morphological modifications that change their shape during migration. Nevertheless, the need to use in vitro cell growth models with the conditioning of three-dimensional synthetic matrices to mimic the dynamics of cell-matrix interaction has been increasingly studied. This becomes more important to effectively understand the changes occurring in phagocyte morphology in the context of infection progression, such as in Chagas disease. This disease is caused by the intracellular pathogen Trypanosoma cruzi, capable of infecting macrophages, determinant cells in the anti-trypanosomatid immunity. In the present study, we sought to understand how an in vitro extracellular matrix model interferes with T. cruzi infection in macrophages. Using different time intervals and parasite ratios, we evaluated the cell morphology and parasite replication rate in the presence of 3D collagen I matrix. Nevertheless, microscopy techniques such as scanning electron microscopy were crucial to trace macrophage-matrix interactions. In the present work, we demonstrated for the first time that the macrophage-matrix interaction favors T. cruzi in vitro replication and the release of anti-inflammatory cytokines during macrophage infection, in addition to drastically altering the morphology of the macrophages and promoting the formation of migratory macrophages.

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Section: Discussionsupporting

confidence: 90%

Increased Trypanosoma cruzi Growth during Infection of Macrophages Cultured on Collagen I Matrix

Logullo

Diniz-Lima

Rocha

et al. 2023

Life

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“…Studies using B-1 cells of deficient mice (XID mice), suggested an important role for these cells during the immune responses against infections 29 , 30 , 34 , 35 . This led us to investigate if the B-1 cells would be implyed in the response against C. gattii infection on this animal model.…”

Section: Resultsmentioning

confidence: 99%

“…The role of B-1 lymphocytes in antibody production has been characterized. However, these cells also have other characteristics that can play important mechanisms in protecting against different pathogens, and one of these mechanisms is their ability to differentiate into phagocytes called B-1 cell-derived phagocytes (B-1CDP) 30 , 34 , 72 – 74 . It was also shown that B-1 cells migrate to the inflammatory/infectious focus and differentiate into macrophage-like cells 75 .…”

Section: Discussionmentioning

confidence: 99%

X-linked immunodeficient (XID) mice exhibit high susceptibility to Cryptococcus gattii infection

Diniz-Lima

Rosa

Silva-Junior

et al. 2021

Sci Rep

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Cryptococcosis is an opportunistic disease caused by the fungus Cryptococcus neoformans and Cryptococcus gattii. It starts as a pulmonary infection that can spread to other organs, such as the brain, leading to the most serious occurrence of the disease, meningoencephalitis. The humoral response has already been described in limiting the progression of cryptococcosis where the B-1 cell seems to be responsible for producing natural IgM antibodies, crucial for combating fungal infections. The role of the B-1 cell in C. neoformans infection has been initially described, however the role of the humoral response of B-1 cells has not yet been evaluated during C. gattii infections. In the present study we tried to unravel this issue using XID mice, a murine model deficient in the Btk protein which compromises the development of B-1 lymphocytes. We use the XID mice compared to BALB/c mice that are sufficient for the B-1 population during C. gattii infection. Our model of chronic lung infection revealed that XID mice, unlike the sufficient group of B-1, had early mortality with significant weight loss, in addition to reduced levels of IgM and IgG specific to GXM isolated from the capsule of C. neoformans. In addition to this, we observed an increased fungal load in the blood and in the brain. We described an increase in the capsular size of C. gattii and the predominant presence of cytokines with a Th2 profile was also observed in these animals. Thus, the present study strongly points to a higher susceptibility of the XID mouse to C. gattii, which suggests that the presence of B-1 cells and anti-GXM antibodies is fundamental during the control of infection by C. gattii.

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“…Consistently, higher NO levels were observed in C57BL/6 mice during acute infection with T. cruzi , and iNOS KO mice showed a higher susceptibility to T. cruzi ( Holscher et al., 1998 ). Furthermore, insufficient NO causes a higher susceptibility to T. cruzi in BALB/c mice than in XID mice, which is negatively related to excessive IL-10 secreted by B-1 cells ( da Rocha et al., 2019 ). In addition, parasite-specific IgG and sex differences are also involved in parasite-host adaptation, but further investigation of the underlying mechanisms is needed ( Perez et al., 2005 ; Micucci et al., 2010 ).…”

Section: Main Textmentioning

confidence: 99%

Host genetic backgrounds: the key to determining parasite-host adaptation

Zhang

Tang

et al. 2023

Front. Cell. Infect. Microbiol.

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Parasitic diseases pose a significant threat to global public health, particularly in developing countries. Host genetic factors play a crucial role in determining susceptibility and resistance to infection. Recent advances in molecular and biological technologies have enabled significant breakthroughs in understanding the impact of host genes on parasite adaptation. In this comprehensive review, we analyze the host genetic factors that influence parasite adaptation, including hormones, nitric oxide, immune cells, cytokine gene polymorphisms, parasite-specific receptors, and metabolites. We also establish an interactive network to better illustrate the complex relationship between host genetic factors and parasite-host adaptation. Additionally, we discuss future directions and collaborative research priorities in the parasite-host adaptation field, including investigating the impact of host genes on the microbiome, developing more sophisticated models, identifying and characterizing parasite-specific receptors, utilizing patient-derived sera as diagnostic and therapeutic tools, and developing novel treatments and management strategies targeting specific host genetic factors. This review highlights the need for a comprehensive and systematic approach to investigating the underlying mechanisms of parasite-host adaptation, which requires interdisciplinary collaborations among biologists, geneticists, immunologists, and clinicians. By deepening our understanding of the complex interactions between host genetics and parasite adaptation, we can develop more effective and targeted interventions to prevent and treat parasitic diseases. Overall, this review provides a valuable resource for researchers and clinicians working in the parasitology field and offers insights into the future directions of this critical research area.

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B-1 Cells May Drive Macrophages Susceptibility to Trypanosoma cruzi Infection

Cited by 6 publications

References 48 publications

Increased Trypanosoma cruzi Growth during Infection of Macrophages Cultured on Collagen I Matrix

Increased Trypanosoma cruzi Growth during Infection of Macrophages Cultured on Collagen I Matrix

X-linked immunodeficient (XID) mice exhibit high susceptibility to Cryptococcus gattii infection

Host genetic backgrounds: the key to determining parasite-host adaptation

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