2,012 research outputs found
Influence of Oral and Gut Microbiota in the Health of Menopausal Women
Sex differences in gut microbiota are acknowledged, and evidence suggests that gut microbiota may have a role in higher incidence and/or severity of autoimmune diseases in females. Additionally, it has been suggested that oral, vaginal, and gut microbiota composition can be regulated by estrogen levels. The association of vaginal microbiota with vulvovaginal atrophy at menopause is well described in the literature. However, the relevance of oral and gut microbiota modulation in the immune system during estrogen deficiency and its effect on inflammatory diseases is not well explored. Estrogen deficiency is a condition that occurs in menopausal women, and it can last approximately 30 years of a woman’s life. The purpose of this mini- review is to highlight the importance of alterations in the oral and gut microbiota during estrogen deficiency and their effect on oral and inflammatory diseases that are associated with menopause. Considering that hormone replacement therapy is not always recommended or sufficient to prevent or treat menopause-related disease, we will also discuss the use of probiotics and prebiotics as an option for the prevention or treatment of these diseases
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Genetic Interactions between Chromosomes 11 and 18 Contribute to Airway Hyperresponsiveness in Mice
We used two-dimensional quantitative trait locus analysis to identify interacting genetic loci that contribute to the native airway constrictor hyperresponsiveness to methacholine that characterizes A/J mice, relative to C57BL/6J mice. We quantified airway responsiveness to intravenous methacholine boluses in eighty-eight (C57BL/6J X A/J) F2 and twenty-seven (A/J X C57BL/6J) F2 mice as well as ten A/J mice and six C57BL/6J mice; all studies were performed in male mice. Mice were genotyped at 384 SNP markers, and from these data two-QTL analyses disclosed one pair of interacting loci on chromosomes 11 and 18; the homozygous A/J genotype at each locus constituted the genetic interaction linked to the hyperresponsive A/J phenotype. Bioinformatic network analysis of potential interactions among proteins encoded by genes in the linked regions disclosed two high priority subnetworks - Myl7, Rock1, Limk2; and Npc1, Npc1l1. Evidence in the literature supports the possibility that either or both networks could contribute to the regulation of airway constrictor responsiveness. Together, these results should stimulate evaluation of the genetic contribution of these networks in the regulation of airway responsiveness in humans.</p
Angiotensin-(1-7) and angiotensin-(1-9): function in cardiac and vascular remodeling
The renin angiotensin system (RAS) is integral to cardiovascular physiology, however, dysregulation of this system largely contributes to the pathophysiology of cardiovascular disease (CVD). It is well established that angiotensin II (Ang II), the main effector of the RAS, engages the angiotensin type 1 receptor and promotes cell growth, proliferation, migration and oxidative stress, all processes which contribute to remodeling of the heart and vasculature, ultimately leading to the development and progression of various CVDs including heart failure and atherosclerosis. The counter-regulatory axis of the RAS, which is centered on the actions of angiotensin converting enzyme 2 (ACE2) and the resultant production of angiotensin-(1-7) (Ang-(1-7) from Ang II, antagonizes the actions of Ang II via the receptor Mas, thereby providing a protective role in CVD. More recently, another ACE2 metabolite, Ang-(1-9), has been reported to be a biologically active peptide within the counter-regulatory axis of the RAS. This review will discuss the role of the counter-regulatory RAS peptides, Ang-(1-7) and Ang-(1-9) in the cardiovascular system, with a focus on their effects in remodeling of the heart and vasculature
Ictiose Arlequim: Caso Clínico
Harlequin ichthyosis is a rare autosomal recessive congenital disease in which neonates present generalized hyperkeratotic plaques and deep fissures, ectropion, eclabium, malformation of the auricular pavilion and typical facies. Although several complications related to the skin restriction may occur, support in intensive care and early introduction of systemic retinoids, such as acitretin, have significantly contributed to patients' survival and improved prognosis. The purpose of this report is to present a rare case of harlequin ichthyosis and to discuss strategies for early diagnosis and first supportive care.Ictiose arlequim é uma doença congênita autossómica recessiva rara, na qual os recém-nascidos apresentam placas de hiperqueratose generalizadas e fissuras profundas, ectrópio, eclábio, malformação do pavilhão auricular e fácies típicas. Embora várias complicações relacionadas à restrição cutânea possam ocorrer, o suporte em terapia intensiva e a introdução precoce de retinóides sistémicos, como a acitretina, têm contribuído significativamente para a melhoria da sobrevida e do prognóstico dos doentes. O objetivo deste relato é apresentar um raro caso de ictiose arlequim e discutir estratégias para o diagnóstico precoce e o primeiro tratamento de suporte
Insights Into the Effects of Mucosal Epithelial and Innate Immune Dysfunction in Older People on Host Interactions With Streptococcus pneumoniae
In humans, nasopharyngeal carriage of Streptococcus pneumoniae is common and although primarily asymptomatic, is a pre-requisite for pneumonia and invasive pneumococcal disease (IPD). Together, these kill over 500,000 people over the age of 70 years worldwide every year. Pneumococcal conjugate vaccines have been largely successful in reducing IPD in young children and have had considerable indirect impact in protection of older people in industrialized country settings (herd immunity). However, serotype replacement continues to threaten vulnerable populations, particularly older people in whom direct vaccine efficacy is reduced. The early control of pneumococcal colonization at the mucosal surface is mediated through a complex array of epithelial and innate immune cell interactions. Older people often display a state of chronic inflammation, which is associated with an increased mortality risk and has been termed ‘Inflammageing’. In this review, we discuss the contribution of an altered microbiome, the impact of inflammageing on human epithelial and innate immunity to S. pneumoniae, and how the resulting dysregulation may affect the outcome of pneumococcal infection in older individuals. We describe the impact of the pneumococcal vaccine and highlight potential research approaches which may improve our understanding of respiratory mucosal immunity during pneumococcal colonization in older individuals
Implicações técnicas e ecossistêmicas do manejo inadequado da arborização urbana: o caso das podas drásticas em oitis na cidade de Ilha Solteira - SP
Oiti is a large species, recommended for urban afforestation. However, it is often implemented in inappropriate places, which can cause conflicts with some factors in cities and with the population in general. Thus, inadequate pruning is carried out, causing great damage to the plant and to public management. The objective of this work was to analyze the drastic pruning performed on Oiti trees used in urban afforestation in the municipality of Ilha Solteira - SP. Oiti specimens diagnosed with drastic pruning were diagnosed and data related to location, presence of electriclal cables and pruning order were collected from the City Hall. The reasons for pruning were listed, the trees were registered using digital photos, which were compared to images from Google Street View® prior to the pruning. It was concluded that Oiti trees received drastic pruning in several neighborhoods in the city of Ilha Solteira, which were carried out with no justification nor request/consent from the City Hall, resulting in some cases in the death of the tree and consequent loss of urban green.O Oiti é uma espécie de grande porte, recomendada para arborização urbana. Contudo, muitas vezes é implantada em locais inadequados, o que pode ocasionar conflitos com alguns fatores nas cidades e com a população em geral. Assim, podas inadequadas são realizadas, ocasionando grandes prejuízos na planta e para a gestão pública. O objetivo deste trabalho foi analisar as podas drásticas realizadas em árvores de Oiti utilizadas na arborização urbana no município de Ilha Solteira - SP. Foram diagnosticados exemplares de Oiti consideradas com poda drástica e coletados dados referentes à localização, presença de fiação e pedido de poda junto a Prefeitura Municipal. Foram elencados os motivos para a realização da poda, o registro das árvores por fotos digitais, que foram comparadas com imagens do Google Street View® anteriores à realização da poda. Concluiu-se que árvores de Oiti receberam poda drástica em diversos bairros da cidade de Ilha Solteira, sendo estas realizadas sem justificativa e solicitação/anuência da Prefeitura Municipal, resultando em alguns casos na morte da árvore e consequente perda do verde urbano
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ICOS-Expressing Lymphocytes Promote Resolution of CD8-Mediated Lung Injury in a Mouse Model of Lung Rejection
Acute rejection, a common complication of lung transplantation, may promote obliterative bronchiolitis leading to graft failure in lung transplant recipients. During acute rejection episodes, CD8+ T cells can contribute to lung epithelial injury but the mechanisms promoting and controlling CD8-mediated injury in the lung are not well understood. To study the mechanisms regulating CD8+ T cell–mediated lung rejection, we used a transgenic model in which adoptively transferred ovalbumin (OVA)-specific cytotoxic T lymphocytes (CTL) induce lung injury in mice expressing an ovalbumin transgene in the small airway epithelium of the lungs (CC10-OVA mice). The lung pathology is similar to findings in humans with acute lung transplant. In the presence of an intact immune response the inflammation resolves by day 30. Using CC10-OVA.RAG-/- mice, we found that CD4+ T cells and ICOS+/+ T cells were required for protection against lethal lung injury, while neutrophil depletion was not protective. In addition, CD4+Foxp3 + ICOS+ T cells were enriched in the lungs of animals surviving lung injury and ICOS+/+ Tregs promoted survival in animals that received ICOS-/- T cells. Direct comparison of ICOS-/- Tregs to ICOS+/+ Tregs found defects in vitro but no differences in the ability of ICOS-/- Tregs to protect from lethal lung injury. These data suggest that ICOS affects Treg development but is not necessarily required for Treg effector function
Allergen Exposure in Lymphopenic Fas-Deficient Mice Results in Persistent Eosinophilia Due to Defects in Resolution of Inflammation
Asthma is characterized by chronic airway type-2 inflammation and eosinophilia, yet the mechanisms involved in chronic, non-resolving inflammation remain poorly defined. Previously, our group has found that when Rag-deficient mice were reconstituted with Fas-deficient B6 LPR T cells and sensitized and challenged, the mice developed a prolonged type-2-mediated airway inflammation that continued for more than 6 weeks after the last antigen exposure. Surprisingly, no defect in resolution was found when intact B6 LPR mice or T cell specific Fas-conditional knockout mice were sensitized and challenged. We hypothesize that the homeostatic proliferation induced by adoptive transfer of T cells into Rag-deficient mice may be an important mechanism involved in the lack of resolution. To investigate the role of homeostatic proliferation, we induced lymphopenia in the T cell-specific Fas-conditional knockout mice by non-lethal irradiation and sensitized them when T cells began to repopulate. Interestingly, we found that defective Fas signaling on T cells plus antigen exposure during homeostatic proliferation was sufficient to induce prolonged eosinophilic airway inflammation. In conclusion, our data show that the combination of transient lymphopenia, abnormal Fas-signaling, and antigen exposure leads to the development of a prolonged airway eosinophilic inflammatory phase in our mouse model of experimental asthma
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