190 research outputs found
INI879997 Supplemental Material3 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material3 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material5 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material5 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material6 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material6 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material4 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material4 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material2 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material2 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
INI879997 Supplemental Material1 - Supplemental material for Unmethylated CpG motif-containing genomic DNA fragment of <i>Bacillus calmette-guerin</i> promotes macrophage functions through TLR9-mediated activation of NF-<b>κ</b>B and MAPKs signaling pathways
No full textSupplemental material, INI879997 Supplemental Material1 for Unmethylated CpG motif-containing genomic DNA fragment of Bacillus calmette-guerin promotes macrophage functions through TLR9-mediated activation of NF-κB and MAPKs signaling pathways by Junli Li, Lili Fu, Guozhi Wang, Selvakumar Subbian, Chuan Qin and Aihua Zhao in Innate Immunity</p
Supplementary data for Communication Biology manuscript
No full textData used for figures in the Aggregation state of Mycobacterium tuberculosis impacts host immunity and augments
pulmonary disease pathology Afsal
Kolloli1, Ranjeet Kumar1, Pooja Singh1,2,
Anshika Narang1, Gilla Kaplan3, Alex Sigal4,5,6,
Selvakumar Subbian1,*</p
Nutritional markers and proteome in patients undergoing treatment for pulmonary tuberculosis differ by geographic region
No full textIntroductionContemporary phase 2 TB disease treatment clinical trials have found that microbiologic treatment responses differ between African versus non-African regions, the reasons for which remain unclear. Understanding host and disease phenotypes that may vary by region is important for optimizing curative treatments.MethodsWe characterized clinical features and the serum proteome of phase 2 TB clinical trial participants undergoing treatment for smear positive, culture-confirmed TB, comparing host serum protein expression in clinical trial participants enrolled in African and Non-African regions. Serum samples were collected from 289 participants enrolled in the Centers for Disease Control and Prevention TBTC Study 29 (NCT00694629) at time of enrollment and at the end of the intensive phase (after 40 doses of TB treatment).ResultsAfter a peptide level proteome analysis utilizing a unique liquid chromatography IM-MS platform (LC-IM-MS) and subsequent statistical analysis, a total of 183 core proteins demonstrated significant differences at both baseline and at week 8 timepoints between participants enrolled from African and non-African regions. The majority of the differentially expressed proteins were upregulated in participants from the African region, and included acute phase proteins, mediators of inflammation, as well as coagulation and complement pathways. Downregulated proteins in the African population were primarily linked to nutritional status and lipid metabolism pathways.ConclusionsWe have identified differentially expressed nutrition and lipid pathway proteins by geographic region in TB patients undergoing treatment for pulmonary tuberculosis, which appear to be associated with differential treatment responses. Future TB clinical trials should collect expanded measures of nutritional status and further evaluate the relationship between nutrition and microbiologic treatment response
Systems Analysis of Early Host Gene Expression Provides Clues for Transient Mycobacterium avium ssp avium vs. Persistent Mycobacterium avium ssp paratuberculosis Intestinal Infections.
No full textIt has long been a quest in ruminants to understand how two very similar mycobacterial species, Mycobacterium avium ssp. paratuberculosis (MAP) and Mycobacterium avium ssp. avium (MAA) lead to either a chronic persistent infection or a rapid-transient infection, respectively. Here, we hypothesized that when the host immune response is activated by MAP or MAA, the outcome of the infection depends on the early activation of signaling molecules and host temporal gene expression. To test our hypothesis, ligated jejuno-ileal loops including Peyer's patches in neonatal calves were inoculated with PBS, MAP, or MAA. A temporal analysis of the host transcriptome profile was conducted at several times post-infection (0.5, 1, 2, 4, 8 and 12 hours). When comparing the transcriptional responses of calves infected with the MAA versus MAP, discordant patterns of mucosal expression were clearly evident, and the numbers of unique transcripts altered were moderately less for MAA-infected tissue than were mucosal tissues infected with the MAP. To interpret these complex data, changes in the gene expression were further analyzed by dynamic Bayesian analysis. Bayesian network modeling identified mechanistic genes, gene-to-gene relationships, pathways and Gene Ontologies (GO) biological processes that are involved in specific cell activation during infection. MAP and MAA had significant different pathway perturbation at 0.5 and 12 hours post inoculation. Inverse processes were observed between MAP and MAA response for epithelial cell proliferation, negative regulation of chemotaxis, cell-cell adhesion mediated by integrin and regulation of cytokine-mediated signaling. MAP inoculated tissue had significantly lower expression of phagocytosis receptors such as mannose receptor and complement receptors. This study reveals that perturbation of genes and cellular pathways during MAP infection resulted in host evasion by mucosal membrane barrier weakening to access entry in the ileum, inhibition of Ca signaling associated with decreased phagosome-lysosome fusion as well as phagocytosis inhibition, bias toward Th2 cell immune response accompanied by cell recruitment, cell proliferation and cell differentiation; leading to persistent infection. Contrarily, MAA infection was related to cellular responses associated with activation of molecular pathways that release chemicals and cytokines involved with containment of infection and a strong bias toward Th1 immune response, resulting in a transient infection
Gut microbiome dysbiosis and correlation with blood biomarkers in active-tuberculosis in endemic setting.
No full textTuberculosis (TB) is the largest infectious disease with 10 million new active-TB patients and1.7 million deaths per year. Active-TB is an inflammatory disease and is increasingly viewed as an imbalance of immune responses to M. tb. infection. The mechanisms of a switch from latent infection to active disease is not well worked out but a shift in the immune responses is thought to be responsible. Increasingly, the role of gut microbiota has been described as a major influencer of the immune system. And because the gut is the largest immune organ, we aimed to analyze the gut microbiome in active-TB patients in a TB-endemic country, Pakistan. The study revealed that Ruminococcacea, Enetrobactericeae, Erysipelotrichaceae, Bifidobacterium, etc. were the major genera associated with active-TB, also associated with chronic inflammatory disease. Plasma antibody profiles against several M. tb. antigens, as specific biomarkers for active-TB, correlated closely with the patient gut microbial profiles. Besides, bcoA gene copy number, indicative of the level of butyrate production by the gut microbiome was five-fold lower in TB patients compared to healthy individuals. These findings suggest that gut health in TB patients is compromised, with implications for disease morbidity (e.g., severe weight loss) as well as immune impairment
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