Project description:Qiita ID 13241 - The Association Between Milk Feedings in the Preterm Population, the Microbiome and Risk of Atopic Disease: Microbiome, Atopic Disease, and Prematurity (MAP Study) - Data was acquired using a Bruker Maxis Impact and C18 RP-UHPLC. Positive polarity acquisition of LC-MS/MS.
2020-10-07 | MSV000086246 | GNPS
Project description:The Association Between Milk Feedings in the Preterm Population, the Microbiome and Risk of Atopic Disease: Microbiome, Atopic Disease, and Prematurity (MAP Study)
Project description:Characteization host-microbiome interactions in patients with allergic (model: atopic dermatitis) and autoimmune (model: psoriasis) diseases by integration of microarray transcriptome data with 16S microbial profiling. 6mm punch biopsies were collected from the skin of atopic dermatitis and psoriasis patients alongside healthy volunteers, and subjected to analysis using Affymetrix Human Gene ST 2.1 arrays.
Project description:We explore whether a low-energy diet intervention for Metabolic dysfunction-associated steatohepatitis (MASH) improves liver disease by means of modulating the gut microbiome. 16 individuals were given a low-energy diet (880 kcal, consisting of bars, soups, and shakes) for 12 weeks, followed by a stepped re-introduction to whole for an additional 12 weeks. Stool samples were obtained at 0, 12, and 24 weeks for microbiome analysis. Fecal microbiome were measured using 16S rRNA gene sequencing. Positive control (Zymo DNA standard D6305) and negative control (PBS extraction) were included in the sequencing. We found that low-energy diet improved MASH disease without lasting alterations to the gut microbiome.
Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
Project description:The aim of this study was to find disease-associated genes in atopic eczema. Experiment Overall Design: Skin biopsies were analyzed from ten patients with active atopic eczema and ten healthy controls.
Project description:Periostin is a matricellular protein known to be alternatively spliced to produce isoforms with a molecular weight of 78-91 kDa. In the extracellular matrix, periostin attach to cell surfaces and induce signaling via integrin-binding and participates in fibrillogenesis to organize collagen in the extracellular space. In the atopic diseases atopic dermatitis and asthma, periostin is known to participate in driving the disease-causing type 2 inflammation. The periostin isoforms expressed in these diseases and the implication of the alternative splicing events are unknown. Here we present two universal assays to map the expression of periostin isoforms on both the transcriptional (RT-qPCR) and translational (PRM-based mass spectrometry) level. We use these assays to study the splice profile of periostin in atopic dermatitis lesions from patients in active treatment vs. normal skin and in in vitro models of atopic dermatitis and asthma. All isoforms expect isoform 3 show decreased expression at the transcriptional level in AD lesions from patients treated with corticosteroids compared to normal skin. The isoforms display an elevated amount at the translational level indicating a delayed response in periostin level during treatment. Expression of the isoforms were upregulated in the in vitro models of atopic dermatitis and asthma at both the transcriptional and translational level with isoform 3 and 5 displaying the highest level of overexpression. Interestingly, the often overlooked isoform 9 and 10 behaved opposite to the other isoforms as they were equally or even less abundant in the disease models compared to the control, and they were identified in the normal skin samples but not in atopic dermatitis lesions. With the assays and findings presented in the publication connected to this dataset we can take further steps in mapping and understanding the role of periostin isoforms.
Project description:Children who grow up on farms have a lower risk of developing childhood atopic disease. Although human milk proteins are heavily glycosylated, there is a lack of studies investigating the milk glycoproteome. In this study, we have used label-free quantitative proteomics to analyze milk samples from Rochester and Older Order Mennonite mothers, two populations with different lifestyles, exposures, and risk of allergic disease. We identified multiple N-glycopeptides with significantly different abundances between the two communities and four N-glycopeptides that may have a protective effect against the development of atopic disease. The findings of this study indicate that the differential glycosylation of milk proteins may affect the development of atopic disease, something previously uninvestigated.