The combination of high-fat diet-induced obesity and chronic ulcerative colitis reciprocally exacerbates adipose tissue and colon inflammation

<p>Abstract</p> <p>Background</p> <p>This study evaluated the relationship between ulcerative colitis and obesity, which are both chronic diseases characterized by inflammation and increases in immune cells and pro-inflammatory cytokines.</p> <p>Methods</p> <p>Mice with chronic ulcerative colitis induced by 2 cycles of dextran sodium sulfate (DSS) in the first and fourth week of the experiment were fed a high-fat diet (HFD) to induce obesity by 8 weeks. The animals were divided into 4 groups (control, colitis, HFD and colitis + HFD).</p> <p>Results</p> <p>Obesity alone did not raise histopathology scores, but the combination of obesity and colitis worsened the scores in the colon compared to colitis group. Despite the reduction in weight gain, there was increased inflammatory infiltrate in both the colon and visceral adipose tissue of colitis + HFD mice due to increased infiltration of macrophages, neutrophils and lymphocytes. Intravital microscopy of VAT microvasculature showed an increase in leukocyte adhesion and rolling and overexpression of adhesion molecules compared to other groups. Moreover, circulating lymphocytes, monocytes and neutrophils in the spleen and cecal lymph nodes were increased in the colitis + HFD group.</p> <p>Conclusion</p> <p>Our results demonstrated the relationship between ulcerative colitis and obesity as aggravating factors for each disease, with increased inflammation in the colon and adipose tissue and systemic alterations observed in the spleen, lymph nodes and bloodstream.</p

Depletion of neutrophils did not improve the metabolic alterations in antigen-induced arthritis mice.

<p>(A) Intensity of nociception. Inflammation in the knee cavity represented by (B) number of neutrophils and (C) myeloperoxidase activity. Metabolic features represented by (D) glucose, (E) triglyceride and total cholesterol levels, accompanied by the adipocytokines (F) adiponectin and leptin levels in the serum. (G) The PTX3 of mice that received an intra-articular injection in the knee cavity of PBS, mBSA or mBSA treated prior with RB6-8C5. The bars represent the mean values±SEM (n = 4–6), *<i>P</i><0.05 vs. PBS; #<i>P</i><0.05 vs. AIA of the respective time.</p

Pre-treatment with Etanercept improves the altered metabolic parameters of antigen-induced arthritis mice.

<p>(A) Intensity of nociception. (B) Neutrophils, (C) myeloperoxidase activity, (D) CXCL1 chemokine in the peri-articular tissue and (E) arthritis index. Systemic glucose metabolism showed by (F) glucose levels, (G) HOMA-IR index and (H) oral glucose tolerance test. The lipids, (I) triglyceride and total cholesterol levels. The adipocytokines, (J) adiponectin and leptin levels. (K) PTX3 levels of mice that received a knee intra-articular injection of PBS, mBSA or mBSA treated prior with Etanercept. Bars represent the mean values ±SEM (n = 6–8), *<i>P</i><0.05 vs. PBS; #<i>P</i><0.05 vs. AIA of the respective time.</p

Antigen-induced arthritis in mice is mainly associated with the presence of neutrophils.

<p>(A) Intensity of nociception. (B) Number of neutrophils, (C) myeloperoxidase activity, and (D) CXCL1 chemokine levels in the peri-articular tissue. (E) Representative photos of the morphologic alterations in the knee (x100 and x400) and (F) arthritis index. Arrows indicate the synovial and asterisks represent the inflammatory infiltrate. Adipose tissue and liver (G) myeloperoxidase activity, and (H) CXCL1 levels at 1, 3, 24 and 48 hours after the challenge with the antigen-induced arthritis (AIA). Bars represent the mean values±SEM (n = 6–8). Neutrophils number in (I) epididymal adipose tissue and liver accumulated in Lysm-eGFP mice and (J) representative confocal microscopy image, 3 and 24 hours after the challenge with the AIA (x100). Bars represent the mean values±SEM (n = 3–5), *<i>P</i><0.05 vs. PBS.</p

Pre-treatment with DF2156A contributes to metabolic alterations in antigen-induced arthritis mice.

<p>(A) Intensity of nociception. (B) Number of neutrophils, (C) myeloperoxidase activity, (D) CXCL1 chemokine in the peri-articular tissue and (E) arthritis index. Systemic glucose metabolism showed by (F) glucose levels, (G) HOMA-IR index and (H) oral glucose tolerance test. The lipids, (I) triglyceride and total cholesterol levels. The adipocytokines, (J) adiponectin and leptin levels. (K) PTX3 levels of mice that received a knee intra-articular injection of PBS, mBSA or mBSA treated prior with DF2156A. Bars represent the mean values±SEM (n = 6–8), *<i>P</i><0.05 vs. PBS; #<i>P</i><0.05 vs. AIA of the respective time.</p

Systemic metabolic alterations in antigen-induced arthritis mice at different time points.

<p>The metabolism of glucose showed by (A) glucose levels, (B) HOMA-IR index and (C) oral glucose tolerance test. The lipid metabolism represented by (D) triglyceride and (E) total cholesterol levels. Serum levels of the adipocytokines, (F) adiponectin and (G) leptin at 1, 3, 24 and 48 hours after the challenge with the antigen-induced arthritis (AIA). The bars represent the mean values ± SEM (n = 6–8), *<i>P</i><0.05 vs. PBS.</p

Characterisation of microbial attack on archaeological bone

As part of an EU funded project to investigate the factors influencing bone preservation in the archaeological record, more than 250 bones from 41 archaeological sites in five countries spanning four climatic regions were studied for diagenetic alteration. Sites were selected to cover a range of environmental conditions and archaeological contexts. Microscopic and physical (mercury intrusion porosimetry) analyses of these bones revealed that the majority (68%) had suffered microbial attack. Furthermore, significant differences were found between animal and human bone in both the state of preservation and the type of microbial attack present. These differences in preservation might result from differences in early taphonomy of the bones. © 2003 Elsevier Science Ltd. All rights reserved

NEOTROPICAL ALIEN MAMMALS: a data set of occurrence and abundance of alien mammals in the Neotropics

Biological invasion is one of the main threats to native biodiversity. For a species to become invasive, it must be voluntarily or involuntarily introduced by humans into a nonnative habitat. Mammals were among first taxa to be introduced worldwide for game, meat, and labor, yet the number of species introduced in the Neotropics remains unknown. In this data set, we make available occurrence and abundance data on mammal species that (1) transposed a geographical barrier and (2) were voluntarily or involuntarily introduced by humans into the Neotropics. Our data set is composed of 73,738 historical and current georeferenced records on alien mammal species of which around 96% correspond to occurrence data on 77 species belonging to eight orders and 26 families. Data cover 26 continental countries in the Neotropics, ranging from Mexico and its frontier regions (southern Florida and coastal-central Florida in the southeast United States) to Argentina, Paraguay, Chile, and Uruguay, and the 13 countries of Caribbean islands. Our data set also includes neotropical species (e.g., Callithrix sp., Myocastor coypus, Nasua nasua) considered alien in particular areas of Neotropics. The most numerous species in terms of records are from Bos sp. (n = 37,782), Sus scrofa (n = 6,730), and Canis familiaris (n = 10,084); 17 species were represented by only one record (e.g., Syncerus caffer, Cervus timorensis, Cervus unicolor, Canis latrans). Primates have the highest number of species in the data set (n = 20 species), partly because of uncertainties regarding taxonomic identification of the genera Callithrix, which includes the species Callithrix aurita, Callithrix flaviceps, Callithrix geoffroyi, Callithrix jacchus, Callithrix kuhlii, Callithrix penicillata, and their hybrids. This unique data set will be a valuable source of information on invasion risk assessments, biodiversity redistribution and conservation-related research. There are no copyright restrictions. Please cite this data paper when using the data in publications. We also request that researchers and teachers inform us on how they are using the data