NAIURA VIEIRA PEREIRA
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/53 - Laboratório de Micologia, Hospital das Clínicas, Faculdade de Medicina
LIM/53 - Laboratório de Micologia, Hospital das Clínicas, Faculdade de Medicina
6 resultados
Resultados de Busca
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- Lichen planus: altered AIM2 and NLRP1 expression in skin lesions and defective activation in peripheral blood mononuclear cells(2019) DOMINGUES, R.; PIETROBON, A. J.; CARVALHO, G. C.; PEREIRA, N. Z.; PEREIRA, N. V.; SOTTO, M. N.; AOKI, V.; DUARTE, A. J. S.; SATO, M. N.Background Lichen planus (LP) is an inflammatory skin disease with unknown aetiology. Activation by pathogen-associated molecular patterns or environmental stimuli may activate some components of inflammasomes that contribute to the inflammatory process in LP lesions. Aim To characterize the inflammasomes in skin lesions and peripheral blood mononuclear cells (PBMCs) of patients with LP under Toll-like receptor (TLR) activation. Methods In total, 15 patients with LP and 14 healthy controls (HCs) were enrolled in the study. Inflammasome expression in skin was evaluated by real-time PCR and immunohistochemistry, while ELISA was used to assess the production of interleukin (IL)-1 beta by PBMCs under stimulation with TLR4 and TLR7/TLR8 agonists and adenosine triphosphate (ATP). Results Compared with the levels in HC samples, increased expression of the inflammasome AIM2 was verified in both epidermal and dermal sections of LP skin lesions, whereas NLRP1 and IL-beta expression levels were enhanced in the dermis. LP skin lesion samples exhibited higher AIM2 transcript levels, similar NLRP1 levels and lower pro-IL-1 beta mRNA levels compared with HC samples. We verified that, compared with PBMCs from HC subjects, PBMCs from patients with LP produced similar amounts of IL-1 beta after induction by TLR4 agonists but lower IL-1 beta levels after induction by TLR7/TLR8 agonists, regardless of the addition of ATP. Conclusion Alterations in innate immunity, such as inflammasome component expression in skin lesions and PBMCs, were observed in patients with LP. Further investigations of dysfunctional inflammasome activation and the chronic inflammatory status of LP are required.
- Up-regulation of Proinflammatory Genes and Cytokines Induced by S100A8 in CD8(+) T Cells in Lichen Planus(2016) CARVALHO, Gabriel Costa de; DOMINGUES, Rosana; NOGUEIRA, Marcelle Almeida de Sousa; BRANCO, Anna C. Calvielli Castelo; MANFRERE, Kelly C. Gomes; PEREIRA, Naiura Vieira; AOKI, Valeria; SOTTO, Mirian Nacagami; DUARTE, Alberto J. da Silva; SATO, Maria NotomiLichen planus (LP) is a chronic inflammatory mucocutaneous disease. The inflammatory status of LP may be related to S100A8 (myeloid-related protein 8; MRP8) activation of cytotoxic cells. The aims of this study were to evaluate S100A8 expression in skin lesions and the in vitro effects of S100A8 on CD8(+) T cells and natural killer (NK) cells in LP. Increased levels of S100A8/S100A9 were detected in the skin lesions as well as in the sera of subjects with LP. S100A8 expression induced an increased cytotoxic response by peripheral blood CD8(+)CD107a(+) T cells as well as by NK CD56(bright) cells in patients with LP. Increased expression of interleukin (1L)-1 beta, tumour necrosis factor (TNF) and IL-6 in the CD8(+) T cells of patients with LP was induced by S100A8, in contrast to the control group that produced IL- 10 and interferon type I genes. These data suggest that, in individuals with LP, S100A8 may exert distinct immunomodulatory and cytotoxicity functions.
- Staphylococcus aureus enterotoxins modulate IL-22-secreting cells in adults with atopic dermatitis(2018) ORFALI, Raquel Leao; OLIVEIRA, Luanda Mara da Silva; LIMA, Josenilson Feitosa de; CARVALHO, Gabriel Costa de; RAMOS, Yasmim Alefe Leuzzi; PEREIRA, Natalli Zanete; PEREIRA, Naiura Vieira; ZANIBONI, Mariana Colombini; SOTTO, Mirian Nacagami; DUARTE, Alberto Jose da Silva; SATO, Maria Notomi; AOKI, ValeriaAtopic dermatitis (AD) is a chronic inflammatory immune-mediated skin disease characterized by skin colonization by Staphylococcus aureus. Interleukin (IL)-22, in cooperation with IL-17, triggers antimicrobial peptide elaboration and enhances certain immunological responses. In AD, IL-22 is related to epidermal hyperplasia, keratinocyte apoptosis, and inhibition of antimicrobial peptide (AMP) production. We aimed to evaluate the impact of staphylococcal enterotoxins on the Tc22/Th22 induction in the peripheral blood of AD patients and on CD4(+/)CD8(+)T cells expressing IL-22 in AD skin. Our study showed inhibition of the staphylococcal enterotoxins A and B (SEA and SEB) response by Th22 (CD4(+)IL22(+)IL-17A(-)IFN-gamma(-)) cells in AD patients. In contrast, Tc22 (CD8(+)IL-22(+)IL-17A(-)IFN-gamma(-)) cells were less susceptible to the inhibitory effects of staphylococcal enterotoxins and exhibited an enhanced response to the bacterial stimuli. In AD skin, we detected increased IL-22 transcript expression and T lymphocytes expressing IL-22. Together, our results provide two major findings in response to staphylococcal enterotoxins in adults with AD: dysfunctional CD4(+)IL-22 secreting T cells and increased Tc22 cells. Our hypothesis reinforces the relevance of CD8 T cells modulated by staphylococcal enterotoxins as a potential source of IL-22 in adults with AD, which is relevant for the maintenance of immunological imbalance.
- Increased Expression on Innate Immune Factors in Placentas From HIV-Infected Mothers Concurs With Dampened Systemic Immune Activation(2020) PEREIRA, Natalli Zanete; BRANCO, Anna Claudia Calvielli Castelo; MANFRERE, Kelly Cristina Gomes; LIMA, Josenilson Feitosa de; YOSHIKAWA, Fabio Seiti Yamada; MILANEZ, Helaine Maria Besteti Pires Mayer; PEREIRA, Naiura Vieira; SOTTO, Miriam Nacagami; DUARTE, Alberto Jose da Silva; SATO, Maria NotomiInnate immunity is one of the main protection mechanisms against viral infections, but how this system works at the maternal-fetal interface, especially during HIV infection, is still poorly known. In this study, we investigated the relationship between pregnancy and innate mechanisms associated with HIV immunity by evaluating the expression of DAMPs, inflammasome components and type I/III IFNs in placenta and serum samples from HIV-infected mothers and exposed newborns. Our results showed that most of these factors, including HMGB1, IL-1, and IFN, were increased in placental villi from HIV-infected mothers. Curiously, however, these factors were simultaneously repressed in serum from HIV-infected mothers and their exposed newborns, suggesting that pregnancy could restrict HIV immune activation systemically but preserve the immune response at the placental level. An effective local antiviral status associated with a suppressed inflammatory environment can balance the maternal immune response, promoting homeostasis for fetal development and protection against HIV infection in neonates.
- Up-regulation of HMGB1 and TLR4 in skin lesions of lichen planus(2018) CARVALHO, Gabriel Costa de; HIRATA, Fabiana Yasumoto Araujo; DOMINGUES, Rosana; FIGUEIREDO, Cristina Adelaide; ZANIBONI, Mariana Colombini; PEREIRA, Naiura Vieira; SOTTO, Mirian Nacagami; AOKI, Valeria; DUARTE, Alberto Jose da Silva; SATO, Maria NotomiLichen planus (LP) is a chronic, mucocutaneous inflammatory disease of an unknown aetiology. The disease has been associated with certain viruses, and the factors such as DAMPs (damage-associated molecular patterns) and PAMPs (pathogen-associated molecular patterns) may also contribute to the inflammatory response in LP. HMGB1 (high mobility group box 1 protein) is one of the major DAMPs that induces inflammation and could trigger LP disease. The present study was aimed to examine TLR4, RAGE and HMGB1 production in epidermis or dermis by immunohistochemistry and the respective expression of these targets in the skin lesions of patients with LP. Moreover, we measured HMGB1 serum levels by ELISA. The results showed similar profile of expression by HMGB1 and TLR4, which are decreased at epidermis and up-regulated at dermis of skin lesions of LP patients that was sustained by intense cellular infiltration. RAGE expression was also increased in dermis of LP. Although there is increased RAGE protein levels, a decreased RAGE transcript levels was detected. Similar HMGB1 serum levels were detected in the LP and control groups. This study demonstrates that HMGB1 and TLR4 could contribute to the inflammatory LP process in skin.
- Obesity Induces an Impaired Placental Antiviral Immune Response in Pregnant Women Infected with Zika Virus(2023) BRANCO, Anna Claudia Calvielli Castelo; OLIVEIRA, Emily Araujo De; PEREIRA, Natalli Zanete; ALBERCA, Ricardo Wesley; DUARTE-NETO, Amaro Nunes; SILVA, Luiz Fernando Ferraz Da; LUIZ, Fernanda Guedes; PEREIRA, Naiura Vieira; SOTTO, Mirian Nacagami; DEJANI, Naiara Naiana; RONDO, Patricia Helen Carvalho; AVVAD-PORTARI, Elyzabeth; VASCONCELOS, Zilton Farias Meira De; DUARTE, Alberto Jose da Silva; AZAMOR, Tamiris; SATO, Maria NotomiObesity is increasing in incidence worldwide, especially in women, which can affect the outcome of pregnancy. During this period, viral infections represent a risk to the mother, the placental unit, and the fetus. The Zika virus (ZIKV) outbreak in Brazil has been the cause of congenital Zika syndrome (CZS), with devastating consequences such as microcephaly in newborns. Herein, we analyzed the impact of maternal overweight/obesity on the antiviral factors' expression in the placental tissue of Zika-infected mothers. We accessed placentas from women with and without obesity from 34 public health units (Sao Paulo) and from Zika-infected mothers with and without obesity from the Clinical Cohort Study of ZIKV pregnant women (Rio de Janeiro, Brazil). We first verified that obesity, without infection, did not alter the constitutive transcriptional expression of antiviral factors or IFN type I/III expression. Interestingly, obesity, when associated with ZIKV infection, showed a decreased transcriptional expression of RIG-I and IFIH1 (MDA-5 protein precursor gene). At the protein level, we also verified a decreased RIG-I and IRF-3 expression in the decidual placenta from the Zika-infected obese group, regardless of microcephaly. This finding shows, for the first time, that obesity associated with ZIKV infection leads to an impaired type I IFN downstream signaling pathway in the maternal-fetal interface.