A ética do silêncio racial no contexto urbano: políticas públicas e desigualdade social no Recife, 1900-1940

Mais de meio século após o preconceito racial ter se tornado o principal alvo dos movimentos urbanos pelos direitos civis nos Estados Unidos e na África do Sul, e décadas depois do surgimento dos movimentos negros contemporâneos no Brasil, o conjunto de ferramentas legislativas criado no Brasil para promover o direito à cidade ainda adere à longa tradição brasileira de silêncio acerca da questão racial. Este artigo propõe iniciar uma exploração das raízes históricas desse fenômeno, remontando ao surgimento do silêncio sobre a questão racial na política urbana do Recife, Brasil, durante a primeira metade do século XX. O Recife foi eé um exemplo paradigmático do processo pelo qual uma cidade amplamente marcada por traços negros e africanos chegou a ser definida política e legalmente como um espaço pobre, subdesenvolvido e racialmente neutro, onde as desigualdades sociais originaram na exclusão capitalista, e não na escravidão e nas ideologias do racismo científico. Neste sentido, Recife lança luzes sobre a política urbana que se gerou sob a sombra do silêncio racial.More than half a century after racial prejudice became central to urban civil rights movements in the United States and South Africa, and decades after the emergence of Brazil’s contemporary Black movements, Brazil's internationally recognized body of rights-to-the-city legislation still adheres to the country's long historical tradition of racial silence. This article explores the historical roots of this phenomenon by focusing on the emergence of racial silence in Recife, Brazil during the first half of the 20th Century. Recife was and remains a paradigmatic example of the process through which a city marked by its Black and African roots came to be legally and politically defined as a poor, underdeveloped and racially neutral space, where social inequalities derived from capitalist exclusion rather than from slavery and scientific racism. As such, Recife'sexperience sheds light on the urban policies that were generated in the shadow of racial silence

Pratos e mais pratos: louças domésticas, divisões culturais e limites sociais no Rio de Janeiro, século XIX

Reply to ten comments on a paper published in the last issue of this journal. The discussion follows along six main lines: History museums, identity, ideology and the category of nation; the need of material collections and their modalities: patrimonial, operational, virtual; theater versus laboratory; visitors and their ambiguities; Public History: the museum and the academy.Resposta aos comentários de dez especialistas que contribuíram no debate de texto publicado no último número desta revista. A discussão orientou-se segundo seis tópicos principais: museus históricos, identidade, ideologia e a categoria de nação; a necessidade de acervos materiais e suas modalidades: acervo patrimonial, operacional, virtual; teatro versus laboratório; o público e suas ambigüidades; História Pública: o museu e a Academia

Maternal treatment with short-chain fatty acids modulates the intestinal microbiota and immunity and ameliorates type 1 diabetes in the offspring.

We recently hypothesized that the intestinal microbiota and the innate immune system play key roles in the mechanism of Kilham Rat Virus-induced type 1 diabetes in the LEW1.WR1 rat. We used this animal model to test the hypothesis that maternal therapy with short-chain fatty acids can modulate the intestinal microbiota and reverse virus-induced proinflammatory responses and type 1 diabetes in rat offspring. We observed that administration of short-chain fatty acids to rat breeders via drinking water prior to pregnancy and further treatment of the offspring with short-chain fatty acids after weaning led to disease amelioration. In contrast, rats that were administered short-chain fatty acids beginning at weaning were not protected from type 1 diabetes. Short-chain fatty acid therapy exerted a profound effect on the intestinal microbiome in the offspring reflected by a reduction and an increase in the abundances of Firmicutes and Bacteroidetes taxa, respectively, on day 5 post-infection, and reversed virus-induced alterations in certain bacterial taxa. Principal component analysis and permutation multivariate analysis of variance tests further revealed that short-chain fatty acids induce a distinct intestinal microbiota compared with uninfected animals or rats that receive the virus only. Short-chain fatty acids downregulated Kilham Rat Virus-induced proinflammatory responses in the intestine. Finally, short-chain fatty acids altered the B and T cell compartments in Peyer's patches. These data demonstrate that short-chain fatty acids can reshape the intestinal microbiota and prevent virus-induced islet autoimmunity and may therefore represent a useful therapeutic strategy for disease prevention

Median abundance of bacterial communities in LEW1.WR1 rats treated with SCFAs.

<p>Median abundance of bacterial communities in LEW1.WR1 rats treated with SCFAs.</p

Bacterial taxa in animals treated with SCFAs.

<p>Rats were divided into eight groups and were left untreated (n = 6); administered KRV only (n = 6); or administered KRV plus 250 mM of butyrate (n = 6), formate (n = 6), or propionate (n = 6); or butyrate (n = 6), formate (n = 4), or propionate (n = 3) only. Fecal DNA was extracted from feces collected on day 5 post-infection and analyzed for bacterial composition. Panel A: Stacked bar chart of median percent counts of Operational Taxonomic Units (OTU) representing bacterial genera with a frequency of ≥1% of total counts in fecal samples from rats treated with SCFAs as indicated in the figure using Protocol 1 as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0183786#pone.0183786.g001" target="_blank">Fig 1</a>. Panel B: Results of PERMANOVA tests across all treatment groups (under the “Overall” heading) and pairs of treatment groups (table). Panel C: The PCA scores are displayed for each sample. The different colors and shapes correspond to the various treatment groups as indicated in the figure and described in <i>Materials and Methods</i>. Vectors corresponding to the indicated top 10 genera with the highest loadings are displayed. The magnitude and direction correspond to the weights. Panel D: The distribution of Sobs and Shannon diversity indices across groups. The area inside each box represents the interquartile range (IQR: 25th to 75th percentiles), the median is denoted by a line. The whiskers extend 1.5 IQR from the box, the observations outside of this range are displayed as points.</p

Kaplan-Meier analysis of virus-induced T1D in LEW1.WR1 rats treated with SCFAs.

<p>LEW1.WR1 rat breeders were treated with 250 mM of the various SCFAs beginning at the age of 6 weeks prior to any pregnancy (Protocol 1). The offspring were injected with 1 x 10⁷ PFU of KRV at 21–25 days of age and continued to receive SCFAs after weaning for 40 days following virus inoculation as shown in Fig 1A. A second animal group was injected with KRV and treated with 250 mM of sodium butyrate in the drinking water beginning at weaning (Protocol 2). Another group was administered with KRV only. Diabetes was defined as the presence of plasma glucose concentrations >250 mg/dl (11.1 mmol/L) on 2 consecutive days. Survival was analyzed using the Kaplan-Meier method as shown in Fig 1B. Statistical analyses among groups were performed using the log rank test (<i>p</i> = 0.001 for formate; <i>p</i> = 0.005 for propionate; and <i>p</i> = 0.006 for butyrate versus KRV only). Shown are paraffin sections of hematoxylin- and eosin-stained sections of pancreatic tissue isolated from uninfected control rats, KRV-infected rats at 21 days following infection (insulitis), KRV- plus SCFA-treated animals at 40 days following infection as indicated, and KRV-infected rats at diabetes onset (Panel C).</p

Gene expression in the Peyer’s patches from SCFA-treated LEW1.WR1 rats.

<p>LEW1.WR1 rats were treated with KRV plus formate (A), Propionate (B), or Butyrate (C) using Protocol 1. RNA was extracted from Peyer’s patches 5 days after virus infection and the expression levels of the indicated genes were assessed using quantitative RT-PCR. The results are expressed as the mRNA expression of the gene of interest relative to the expression of β-actin. Shown are data from individual rats. The lines represent the mean and SD. The numbers in brackets indicate the animal number. Statistical analyses were performed using an ANOVA with Bonferroni's multiple comparison adjustments. *<i>p</i> < 0.001; **<i>p</i> < 0.01; ***<i>p</i> < 0.05.</p

T and B cell frequencies and numbers in the Peyer’s patches from LEW1.WR1 rats treated with SCFAs.

<p>Rats were treated with SCFAs and were infected with KRV using Protocol 1. On day 5, cells from the Peyer’s patches were harvested, counted, and stained with fluorochrome-conjugated mAbs directed against CD4, CD25, Foxp3, and CD45R, followed by flow cytometry analysis. Panel A includes representative histograms of lymphocyte subsets in the Peyer’s patches from rats treated with sodium butyrate. The shaded areas show staining with the isotype control. The frequency of cells stained is indicated in the upper right corner. Data shown in Panel B represent the frequency and cell number of the indicated subsets found in Peyer’s patches from individual rats. The lines in Panel B represent the mean and SD. The numbers in brackets indicate the animal number. Statistical analyses were performed using an ANOVA with Bonferroni's multiple comparison adjustments. *<i>p</i> < 0.001; **<i>p</i> < 0.01; ***<i>p</i> < 0.05.</p

Implication of the intestinal microbiome as a potential surrogate marker of immune responsiveness to experimental therapies in autoimmune diabetes

<div><p>Type 1 diabetes (T1D) is an autoimmune proinflammatory disease with no effective intervention. A major obstacle in developing new immunotherapies for T1D is the lack of means for monitoring immune responsiveness to experimental therapies. The LEW1.WR1 rat develops autoimmunity following infection with the parvovirus Kilham rat virus (KRV) via mechanisms linked with activation of proinflammatory pathways and alterations in the gut bacterial composition. We used this animal to test the hypothesis that intervention with agents that block innate immunity and diabetes is associated with a shift in the gut microbiota. We observed that infection with KRV results in the induction of proinflammatory gene activation in both the spleen and pancreatic lymph nodes. Furthermore, administering animals the histone deacetylase inhibitor ITF-2357 and IL-1 receptor antagonist (Anakinra) induced differential STAT-1 and the p40 unit of IL-12/IL-23 gene expression. Sequencing of bacterial 16S rRNA genes demonstrated that both ITF-2357 and Anakinra alter microbial diversity. ITF-2357 and Anakinra modulated the abundance of 23 and 8 bacterial taxa in KRV-infected animals, respectively, of which 5 overlapped between the two agents. Lastly, principal component analysis implied that ITF-2357 and Anakinra induce distinct gut microbiomes compared with those from untreated animals or rats provided KRV only. Together, the data suggest that ITF-2357 and Anakinra differentially influence the innate immune system and the intestinal microbiota and highlight the potential use of the gut microbiome as a surrogate means of assessing anti-inflammatory immune effects in type 1 diabetes.</p></div

Treatment of LEW1.WR1 rats with Anakinra and ITF-2357.

<p>LEW1.WR1 rats at the age of 21–25 days were left untreated or infected with KRV. They were left with no further treatment of administered Anakinra or ITF-2357 on 5 consecutive days as described in Materials and Methods. The gut microbiome and KRV-induced innate immunity were analyzed on day 5 post-infection.</p