Publications by authors named "Mônica Spadafora-Ferreira"

8 Publications

  • Page 1 of 1

Early Peritoneal CC Chemokine Production Correlates with Divergent Inflammatory Phenotypes and Susceptibility to Experimental Arthritis in Mice.

J Immunol Res 2019 26;2019:2641098. Epub 2019 Feb 26.

Immunogenetics Laboratory, Butantan Institute, Avenida Vital Brasil, 1500, São Paulo 05503-900, Brazil.

The inflammatory and autoimmune events preceding clinical symptoms in rheumatoid arthritis (RA) and other autoimmune diseases are difficult to study in human patients. Therefore, animal models that share immunologic and clinical features with human RA, such as pristane-induced arthritis (PIA), are valuable tools for assessing the primordial events related to arthritis susceptibility. PIA-resistant HIII and susceptible LIII mice were injected i.p. with pristane, and peritoneal lavage fluid was harvested in the early (7 days) and late (35 days) preclinical phases of PIA. Chemokine and cytokine levels were measured in lavage supernatant with ELISA, peritoneal inflammatory leukocytes were immunophenotyped by flow cytometry, and gene expression was determined by qRT-PCR. Leukocyte recruitment was quantitatively and qualitatively divergent in the peritoneum of HIII and LIII mice, with an early increase of CC chemokines (CCL2/CCL3/CCL5/CCL12/CCL22) in the susceptible LIII strain. Also, cytokines such as IL-12p40, IL-23, and IL-18 were elevated in LIII mice while IL-6 was increased in HIII animals. The results show that an early peritoneal CC chemokine response is an important feature of arthritis susceptibility and defines potential biomarkers in this model.
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http://dx.doi.org/10.1155/2019/2641098DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6413398PMC
July 2019

Mice Selected for Acute Inflammation Present Altered Immune Response during Pristane-Induced Arthritis Progression.

Biomed Res Int 2018 8;2018:1267038. Epub 2018 Oct 8.

Laboratório de Imunogenética, Instituto Butantan, São Paulo, Brazil.

Mouse lines selected for maximal (AIRmax) or minimal acute inflammatory reaction (AIRmin) were used to characterize the immune response and the influence of genetic background during pristane-induced arthritis (PIA). Susceptible AIRmax mice demonstrated exacerbated cellular profiles during PIA, with intense infiltration of lymphocytes, as well as monocytes/macrophages and neutrophils, producing higher levels of IL-1, IFN-, TNF-, IL-10, total IgG3, and chemokines. Resistant AIRmin mice controlled cell activation more efficiently than the AIRmax during arthritis progression. The weight alterations of the spleen and thymus in the course of PIA were observed. Our data suggest that selected AIRmax cellular and genetic immune mechanisms contribute to cartilage damage and arthritis severity, evidencing many targets for therapeutic actions.
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http://dx.doi.org/10.1155/2018/1267038DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197000PMC
February 2019

Crotalus durissus collilineatus Venom Induces TNF- α and IL-10 Production in Human Peripheral Blood Mononuclear Cells.

ISRN Inflamm 2014 19;2014:563628. Epub 2014 Jan 19.

Departamento de Biomedicina e Farmácia, Pontifícia Universidade Católica de Goiás, 74605-140 Goiania, GO, Brazil.

Snake venom has been the subject of numerous studies in an attempt to find properties and biological effects that may be beneficial to man. In this study we evaluated in vitro the effects of Crotalus durissus terrificus (Cdt) and Crotalus durissus collilineatus (Cdc) venom in human peripheral blood mononuclear cells (PBMCs). At 24 h, a significant decrease of viable cells was observed in cells stimulated with the Cdc venom at 0.0005 mg/mL and 0.005 mg/mL compared to the negative control. At 48 h, a significant decrease of viable cells was observed only in cells stimulated with Cdc venom at 0.005 mg/mL. A significant increase of TNF- α and IL-10 was detected 48 hours after culture of PBMC with Cdc, but not with Cdt venom. The expression of CD69 and PD1 (programmed death-1), activation and regulatory cell markers, on CD8+ and CD8- T cells did not change in the presence of Cdt and Cdc venom. Our results suggest the presence of proinflammatory and anti-inflammatory components in the Cdc venom. Further analysis should be done to identify those Cdc venom components as it has been done for the Cdt venom by other authors, indicating that modulatory components are found in the venom of different species of Crotalus snakes.
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http://dx.doi.org/10.1155/2014/563628DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3915804PMC
February 2014

Analysis of Spleen Cells in Susceptible and Resistant Mice with Experimental Lagochilascariosis.

ISRN Parasitol 2013 12;2013:180652. Epub 2012 Sep 12.

Department of Microbiology, Immunology, Parasitology and Pathology, Institute of Tropical Pathology and Public Health, Federal University of Goiás, Goiânia, GO, Brazil.

Lagochilascariosis is an emerging parasitic disease caused by the helminth Lagochilascaris minor. The experimental mouse model has been used to study the immune response against L. minor infection. In the present work, immunohistochemistry analysis of spleen cells populations was evaluated in susceptible (C57BL/6) and resistant (BALB/c) mice experimentally infected with L. minor. The BALB/c mice exhibited increased spleen cell indexes as follows: F4/80+ at 100 days after infection (DPI), CD4+ at 100 and 250 DPI, CD8+ at 35 and 100 DPI, and CD19+ at 100, 150, and 250 DPI. In the spleens of the infected C57BL/6 mice, increased indexes of the following spleen cells were observed: F4/80+ cells at 250 DPI, CD4+ cells at 150 DPI, CD8+ cells at 35, 150, and 250 DPI, and CD19+ cells at 150 to 250 DPI. The index of spleen cells confirmed the differences between the control and infected groups at several time points following the infection. These data demonstrate an association between a preferential increase in the number of CD4+ and CD19+ spleen cells and resistance to experimental lagochilascariosis in BALB/c mice and between a preferential increase in the number of CD8+ spleen cells and susceptibility in C57BL/6 mice.
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http://dx.doi.org/10.5402/2013/180652DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4890894PMC
June 2016

Contrasting roles of donor and recipient TGFB1 and IFNG gene polymorphic variants in chronic kidney transplant rejection.

Einstein (Sao Paulo) 2011 Mar;9(1):46-51

Instituto de Investigação em Imunologia, Institutos Nacionais de Ciência e Tecnologia, BR.

Objective: To assess the long-term impact (minimum of 3 years follow-up) of polymorphisms in cytokine genes in donor:recipient pairs on the results of the transplant.

Methods: We compared genetic cytokine polymorphisms and the primary factors of risk for the development of chronic rejection in paired groups of renal transplant patients with and without chronic allograft nephropathy [CAN].

Results: Multivariate analysis indicated that the presence of the high-production TT genotype (codon 10) of the transforming growth factor beta-1 (TGFB1) was protective in receptors (p=0.017), contrasting with the increased risk when present in donor samples (p=0.049). On the other hand, in the case of the gamma interferon studied, the greater frequency of the high production allele was protective in the analysis of the donor group (p=0.013), increasing the risk of chronic nephropathy of the allograft when present in the recipients (p=0.036).

Conclusion: Our results highlight the importance of TGFB1 genotyping in donors, and indicate that polymorphisms in the gene of this cytokine in donor cells might contribute to the development of chronic allograft nephropathy.
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http://dx.doi.org/10.1590/S1679-45082011AO1852DOI Listing
March 2011

Lagochilascaris minor: Susceptibility and Resistance to Experimental Infection in Mice Is Independent of H-2 Haplotype and Correlates with the Immune Response in Immunized Animals.

J Parasitol Res 2010 22;2010. Epub 2010 Jun 22.

Laboratory of Immunochemistry, Butantan Institute, 05503-900 São Paulo, Brazil.

Recently, we demonstrated that C57BL/6 mice are more susceptible to experimental lagochilascariosis than BALB/c mice. To investigate the pattern of infection and the role of the genetic background on susceptibility to infection, we studied experimental lagochilascariosis in H-2(a) identical B10.A and A/J mice. Infected B10.A mice had a lower survival ratio and more severe lesions in the lungs than did A/J mice. Splenocytes of A/J mice immunized with the crude extract of the parasite showed increased proliferation and produced a higher level of interleukin 10 and interferon-gamma in the presence of CE or concanavalin A when compared to B10.A mice. This suggests that resistance of A/J mice may be due to less severe lesions in lungs and other organs and a better immune response to parasite antigens. This paper provides evidence that major histocompatibility complex haplotype does not influence the survival to experimental infection with L. minor.
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http://dx.doi.org/10.1155/2010/610457DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2915754PMC
July 2011

Human complement activation and anaphylatoxins generation induced by snake venom toxins from Bothrops genus.

Mol Immunol 2010 Oct 31;47(16):2537-44. Epub 2010 Jul 31.

Immunochemistry Laboratory, Butantan Institute, Av. Prof. Vital Brazil, 1500, CEP 05503-900, São Paulo, Brazil.

Snake venoms are a complex mixture of components, which have a wide range of actions both on prey and human victims. The genus Bothrops causes the vast majority of snakebites in Central and South America, being responsible for 80% of snake envenomations in Brazil. Envenomations are characterized by prominent local effects, including oedema, haemorrhage and necrosis, which can lead to permanent disability. Systemic manifestations such as haemorrhage, coagulopathy, shock and acute renal failure may also occur. In the present study we have investigated the action of venoms from 19 species of snakes from the genus Bothrops, occurring in Brazil, on the complement system in in vitro studies. All venoms were able to activate the classical complement pathway, in the absence of sensitizing antibody. This activation was in part associated with the cleavage of C1-Inhibitor by proteases present in these venoms, which disrupts complement activation control. No modification of the membrane bound complement regulators, such as DAF, CR1 and CD59 was detected, after treatment of human erythrocytes with the snake venoms. Some of the Bothrops venoms were also able to activate alternative and lectin pathways, as measured in haemolytic and ELISA assays. C3a, C4a and C5a were generated in sera treated with the venoms, not only through C-activation, but also by the direct cleavage of complement components, as determined using purified C3 and C4. Metallo- and/or serine-protease inhibitors prevented cleavage of C3 and C4. These results suggest that Bothrops venoms can activate the complement system, generating a large amount of anaphylatoxins, which may play an important role in the inflammatory process presented in humans after snake envenomations, and they may also assist, due to their vasodilatory effects, to enhance the spreading of other venom components.
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http://dx.doi.org/10.1016/j.molimm.2010.07.003DOI Listing
October 2010

Lagochilascaris minor: experimental infection of C57BL/6 and BALB/c isogenic mice reveals the presence of adult worms.

Exp Parasitol 2008 Jul 26;119(3):325-31. Epub 2008 Mar 26.

Department of Microbiology, Immunology, Parasitology and Pathology (DMIPP), Institute of Tropical Pathology and Public Health (IPTSP), Federal University of Goiás (UFG), Goiânia, Goiás, Brazil.

The nematode Lagochilascaris minor is the causative agent of lagochilascariosis, a human disease that affects the neck region causing exudative abscesses with eggs, larvae, and adult parasites. Mice are currently considered intermediate hosts for the parasite. To determine the pattern of infection and the possibility of mice as definitive hosts for L. minor, experimental lagochilascariosis was studied in two distinct isogenic mouse strains: BALB/c and C57BL/6. Our results indicate that BALB/c mice are more resistant to L. minor infection than C57BL/6, having less intense lesions in the lungs, a lower number of nodules with encysted larvae and fewer adult worms, and displaying a higher serum level of IFN gamma. Both mouse strains had low levels of serum IL-10. We also observed adult parasites in both mouse strains, raising the possibility that mice are definitive hosts of L. minor. This is the first description of adult parasite development of L. minor in mice.
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http://dx.doi.org/10.1016/j.exppara.2008.03.009DOI Listing
July 2008