Expression data from mouse crypt
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE108132 | GEO | 2018/09/03
REPOSITORIES: GEO
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Project description:Paneth cells of intestinal crypts contribute to host defense by producing antimicrobial peptides that are packaged as granules for secretion into the crypt lumen. Here, we provide evidence using light and electron microscopy that postsecretory Paneth cell granules undergo limited dissolution and accumulate within the intestinal crypts of cystic fibrosis (CF) mice. On the basis of this finding, we evaluated bacterial colonization and expression of two major constituents of Paneth cells, i.e., {alpha}-defensins (cryptdins) and lysozyme, in CF murine intestine. Paneth cell granules accumulated in intestinal crypt lumens in both untreated CF mice with impending intestinal obstruction and in CF mice treated with an osmotic laxative that prevented overt clinical symptoms and mucus accretion. Ultrastructure studies indicated little change in granule morphology within mucus casts, whereas granules in laxative-treated mice appear to undergo limited dissolution. Protein extracts from CF intestine had increased levels of processed cryptdins compared with those from wild-type (WT) littermates. Nonetheless, colonization with aerobic bacteria species was not diminished in the CF intestine and oral challenge with a cryptdin-sensitive enteric pathogen, Salmonella typhimurium, resulted in greater colonization of CF compared with WT intestine. Modest downregulation of cryptdin and lysozyme mRNA in CF intestine was shown by microarray analysis, real-time quantitative PCR, and Northern blot analysis. Based on these findings, we conclude that antimicrobial peptide activity in CF mouse intestine is compromised by inadequate dissolution of Paneth cell granules within the crypt lumens. Keywords: other
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Project description:To investigate the response of S. pneumoniae to three distinct antimicrobial peptides (AMPs), i.e. bacitracin, nisin and LL-37, transcriptome analysis of challenged bacteria was performed. Only a limited number of genes was found to be up- or down-regulated in all cases. Several of these common highly induced genes were chosen for further analysis, i.e. SP0385-0387, SP0912-0913, SP0785-0787, SP1714-1715 and the blp cluster. Deletion of these genes in combination with MIC determinations showed that several putative transporters, i.e. SP0785-0787 and SP0912-0913, were indeed involved in resistance to lincomycin, LL-37 and to bacitracin, nisin, lincomycin, respectively. Mutation of blp-bacteriocin production and its immunity genes resulted in an increased of sensitivity to LL-37. Interestingly, a putative ABC transporter (SP1715) protected against bacitracin and Hoechst 33342, but confered sensitivity to LL-37. A GntR-like regulator, SP1714, was identified as a negative regulator of itself and two of the putative transporters. In conclusion, we show that resistance to three different AMPs in S. pneumoniae is mediated by several putative ABC transporters, some of which have not been associated with antimicrobial resistance in this organism before. In addition, a GntR-like regulator was identified, which regulates two of these transporters. Our findings extend the undertstanding of defense mechanisms of this important human pathogen against antimicrobial compounds and points toward novel proteins, i.e. putative ABC transporters, which can be used as targets for the development of new antimicrobials.
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Project description:Nod2 has been extensively characterized as a bacterial sensor that induces an antimicrobial and inflammatory gene expression program. Therefore, it is unclear why Nod2 mutations that disrupt bacterial recognition are paradoxically among the highest risk factors for Crohn’s disease, which involves an exaggerated immune response directed at intestinal bacteria. Previous studies from our lab have shown that mice deficient in Atg16L1, another Crohns disease susceptibility gene, develop abnormalities in Paneth cells, specialized epithelial cells in the small intestine involved in antimicrobial responses. The goal of our study is to determine whether Nod2 deficiency leads to differences in the transcriptional profile of Paneth cells, ultimately leading to small intestinal inflammation. Small intestinal sections (ileum) of 8 week old WT and Nod2-/- mice were fixed in methacarn and embedded in paraffin. The Leica LMD6000 Laser Microdissection system was used to capture crypt base epithelial cells to enrich for Paneth cells. RNA was extracted from these cells, followed by cDNA synthesis and qPCR to confirm enrichment of Paneth cells using unique markers (a-defensins).
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Project description:Expression data from mouse crypt
| PRJNA422533 | ENA