Dataset Information

Proteome and Secretome of Denatonium-treated Mouse Trachea Cells

ABSTRACT: The peptide-level analysis of proteome and secretome changes of mouse trachea cells upon denatonium treatment (in comparison to Ringer lactate solution control).

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Epithelium Of Trachea, Tracheal Epithelium

DISEASE(S): Disease Free

SUBMITTER: Alexey Stukalov

LAB HEAD: Andreas Pichlmair

PROVIDER: PXD018170 | Pride | 2022-08-11

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20150916_QEp5_AnGe_SA_SN_Denatorium_10.raw	Raw
	20150916_QEp5_AnGe_SA_SN_Denatorium_10_161013181111.raw	Raw
	20150916_QEp5_AnGe_SA_SN_Denatorium_11.raw	Raw
	20150916_QEp5_AnGe_SA_SN_Denatorium_12.raw	Raw
	20150916_QEp5_AnGe_SA_SN_Denatorium_7.raw	Raw

Items per page:

1 - 5 of 61

Publications

Bitter taste signaling in tracheal epithelial brush cells elicits innate immune responses to bacterial infection.

Hollenhorst Monika I MI Nandigama Rajender R Evers Saskia B SB Gamayun Igor I Abdel Wadood Noran N Salah Alaa A Pieper Mario M Wyatt Amanda A Stukalov Alexey A Gebhardt Anna A Nadolni Wiebke W Burow Wera W Herr Christian C Beisswenger Christoph C Kusumakshi Soumya S Ectors Fabien F Kichko Tatjana I TI Hübner Lisa L Reeh Peter P Munder Antje A Wienhold Sandra-Maria SM Witzenrath Martin M Bals Robert R Flockerzi Veit V Gudermann Thomas T Bischoff Markus M Lipp Peter P Zierler Susanna S Chubanov Vladimir V Pichlmair Andreas A König Peter P Boehm Ulrich U Krasteva-Christ Gabriela G

The Journal of clinical investigation 20220701 13

Constant exposure of the airways to inhaled pathogens requires efficient early immune responses protecting against infections. How bacteria on the epithelial surface are detected and first-line protective mechanisms are initiated are not well understood. We have recently shown that tracheal brush cells (BCs) express functional taste receptors. Here we report that bitter taste signaling in murine BCs induces neurogenic inflammation. We demonstrate that BC signaling stimulates adjacent sensory ner ...[more]

PMID: 35503420

Similar Datasets

Project description:Scnn1b-Tg mice overexpress the beta subunit of the epithelial sodium channel (Scnn1b) in airway Club cells. The general phenotype of these mice is described in three published manuscripts (Mall et al. 2004, Nature Medicine, 10(5):487-93; Mall et al. 2008, Am J Respir Crit Care Med. 177(7):730-42; Livraghi-Butrico et al. 2012, Physiol. Genomics 44(8):470-84; and Livraghi-Butrico et al. 2012, Mucosal Immunology 5(4):397-408). Briefly, overexpression of the Scnn1b transgene in airway Club cells leads to hyperabsorption of sodium from the airway surface liquid, which causes airway surface liquid and mucus dehydration, resulting in reduced mucus clearance and airway mucus obstruction. The data provided here represents mRNA expression data from dissected whole trachea (distal and proximal ends were cut 3-4 cartilage rings below the larynx and just above the bifurcation, respectively) from male WT and Scnn1b-Tg littermates (C57Bl/6N Tac background) at 4 time points [postnatal days (PND) 0, 3, 10, and 42]. Histologically, PND 0 trachea are normal, a tracheal mucus plug/obstruction develops around PND 3 and typically recedes to the intrapulmonary airways after PND 10, and the trachea is again histologically normal by PND 42. The data from the WT mice provides a global look at mRNA post-natal developmental changes, while the data from the Scnn1b-Tg line provides mRNA data that allows differential gene expression due to airway mucus obstruction to be queried. The data presented for the trachea is part of a larger body of work evaluating gene expression in whole lung, trachea, and purified macrophages. 24 Total tracheal samples were analyzed; three from each timepoint. In our manuscript, we were most interested in changes between WT and Scnn1b-Tg mice, however, the data can also be used to evaluate changes in gene expression across time (PND 0, 3, 10, and 42). It should be noted that a significant difference in RNA expression quality parameters was noted for the 10 day trachea data.

Project description:Lower respiratory tract infections (LRTI) from human Respiratory Syncytial Virus (RSV) are a significant cause of morbidity in children. A component of LRTI pathogenesis is due to signals generated by infected lower airway cells that alter lymphocyte populations and trigger airway remodeling. To obtain insights into this process, we applied an unbiased quantitative proteomics analysis of the RSV-induced epithelial secretory response in cells representative of the trachea (hBECs) vs small airway bronchiolar cells (hSAECs). A workflow was standardized initially using telomerase immortalized human epithelial cells that showed high reproducibility and cell-type differences in proteomic signatures of both secreted proteins and isolated nanoparticles (exosomes). Over half of secretome proteins were contained within exosomal, with the remainder originating from lysosomal and vaculolar compartments. We applied this workflow to three independently derived primary human cultures. 577 differentially expressed proteins from control supernatants and 966 differentially expressed proteins from RSV-infected cell supernatants were identified at a 1% false discovery rate (FDR). 15 proteins were unique to RSV-infected hBECs regulated by epithelial-specific ets homology factor (EHF). 106 proteins were unique to RSV-infected hSAECs enriched in proteins regulated by the NFB transcription factor. In this latter group, we independently validated the differential expression of Chemokine (C-C Motif) Ligand 20 (CCL20)/macrophage inducible protein (MIP)3, Thymic Stromal Lymphopoietin (TSLP) and chemokine (CC) ligand 3-like 1(CCL3-L1). CCL20/MIP3 is the most active mucin inducing factor in the RSV infected hSAEC secretome, and is differentially expressed in smaller airways in a mouse model of RSV infection. These studies provide insight into role of exosomal production in innate responses and regional differences in epithelial secretomes that participate in pathogenesis of RSV LRTI-induced airway remodeling.