Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23073000_1.fastq.gz | Fastqsanger.gz | |||
| SRR23073000_2.fastq.gz | Fastqsanger.gz | |||
| SRR23073100_1.fastq.gz | Fastqsanger.gz | |||
| SRR23073100_2.fastq.gz | Fastqsanger.gz | |||
| SRR23073001_1.fastq.gz | Fastqsanger.gz |
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Project description:Nasal vaccination elicits a humoral immune response that provides protection from airborne pathogens, yet the origins and specific immune niches of antigen-specific IgA-secreting cells in the upper airways remain unknown. Here, we define glandular acinus structures of the nasal turbinates as an immunological niche that recruits IgA-secreting plasma cells from the nasal-associated lymphoid tissues (NALT) in response to intranasal vaccination. Using intact organ imaging, we investigated the cellular events that support antibody-mediated immune responses in the mouse upper airways. Through visualization of antigen-specific T and B cells in the upper airways, we demonstrate that nasal vaccination induced extensive B cell expansion in the subepithelial dome (SED) of the NALT, followed by invasion into commensal bacteria-driven chronic germinal centers (GCs) in a T cell-dependent manner. Antigen-specific B cell response in the NALT required pre-expansion of cognate T cells, which initiate the immune response in the inter-follicular regions of the NALT, and occurred effectively in the presence of Monophosphoryl-Lipid A (MPLA), a synthetic, non-toxic TLR-4 agonist. NALT ablation and blockade of PSGL-1 demonstrated that intranasal vaccination generates IgA+ plasma cells that home to the nasal turbinates through the blood circulation where they are positioned primarily around glandular acinus structures. Thus, the glandular part of the nasal turbinate is an immunological niche that hosts NALT-derived IgA-secreting cells. These cellular events can be manipulated to design vaccines against inhaled pathogens or in the treatment of upper airway allergic responses.
2024-05-30 | GSE252018 | GEO
Project description:Nasal vaccination elicits a humoral immune response that provides protection from airborne pathogens, yet the origins and specific immune niches of antigen-specific IgA-secreting cells in the upper airways remain unknown. Here, we define glandular acinus structures of the nasal turbinates as an immunological niche that recruits IgA-secreting plasma cells from the nasal-associated lymphoid tissues (NALT) in response to intranasal vaccination. Using intact organ imaging, we investigated the cellular events that support antibody-mediated immune responses in the mouse upper airways. Through visualization of antigen-specific T and B cells in the upperairways, we demonstrate that nasal vaccination induced extensive B cell expansion in the subepithelial dome (SED) of the NALT, followed by invasion into commensal bacteria-driven chronic germinal centers (GCs) in a T cell-dependent manner. Antigen-specific B cell response in the NALT required pre-expansion of cognate T cells, which initiate the immune response in the inter-follicular regions of the NALT, and occurred effectively in the presence of Monophosphoryl-Lipid A (MPLA), a synthetic, non-toxic TLR-4 agonist. NALT ablation and blockade of PSGL-1 demonstrated that intranasal vaccination generates IgA+ plasma cells that home to the nasal turbinates through the blood circulation where they are positioned primarily around glandular acinus structures. Thus, the glandular part of the nasal turbinate is an immunological niche that hosts NALT-derived IgA-secreting cells. These cellular events can be manipulated to design vaccines against inhaled pathogens or in the treatment of upper airway allergic responses.
2024-08-17 | GSE264641 | GEO
Project description:Here we describe the dynamics underlying the generation of IgE-antibody secreting cells (ASC) in human nasal polyps (NP), mucosal tissues rich in ASC without germinal centers (GC). Using VH next generation sequencing, we identified an extrafollicular (EF) mucosal IgD+ naïve-like intermediate B cell population with high connectivity to the mucosal IgE ASC. Mucosal IgD+ B cells, express germline epsilon transcripts and predominantly co-express IgM. However, a small but significant fraction co-express IgG or IgA instead which also show connectivity to ASC IgE. Phenotypically, NP IgD+ B cells display an activated profile and molecular evidence of BCR engagement. Transcriptionally, mucosal IgD+ B cells reveal an intermediate profile between naïve B cells and ASC. Single cell IgE ASC analysis demonstrates lower mutational frequencies relative to IgG, IgA, and IgD ASC consistent with IgE ASC derivation from mucosal IgD+ B cell with low mutational load. In conclusion, we describe a novel mechanism of GC-independent, extrafollicular IgE ASC formation at the nasal mucosa whereby activated IgD+ naïve B cells locally undergo direct and indirect (through IgG and IgA), IgE class-switch.
2021-05-13 | GSE174349 | GEO
Project description:Purpose: Influenza virus infections affect millions of people annually. Current available vaccines provide varying rates of protection. There is a knowledge gap on how the nasal microbiota, particularly established pneumococcal colonization, shapes the response to influenza vaccination. Methods: In this study, we inoculated healthy adults with live S. pneumoniae and vaccinated them three days later with either TIV or LAIV. Vaccine-induced immune responses were assessed in nose, blood and lung. Results: Nasal pneumococcal colonization had no impact upon TIV-induced antibody responses to influenza, which manifested in all compartments. However, pre-existing pneumococcal colonization dampened LAIV-mediated mucosal antibody responses, primarily IgA in the nose and IgG in the lung. Pulmonary influenza-specific cellular responses were more apparent in the LAIV group compared to either TIV or an unvaccinated group. Conclusions: These results indicate that TIV and LAIV elicit differential immunity to adults and that LAIV immunogenicity is diminished by the nasal presence of S. pneumoniae. This important confounder should be considered when assessing LAIV efficacy.
2021-03-10 | GSE164649 | GEO
Project description:BACKGROUND. Coronavirus disease 2019 (COVID-19) is more benign in children compared with adults for unknown reasons. This contrasts with other respiratory viruses where disease manifestations are often more severe in children. We hypothesize that a more robust early innate immune response to SARS coronavirus 2 (SARS-CoV-2) protects against severe disease. METHODS. Clinical outcomes, SARS-CoV-2 viral copies, and cellular gene expression were compared in nasopharyngeal swabs obtained at the time of presentation to the emergency department from 12 children and 27 adults using bulk RNA sequencing and quantitative reverse-transcription PCR. Total protein, cytokines, and anti–SARS-CoV-2 IgG and IgA were quantified in nasal fluid. We used a subset of 21 samples for RNAseq analysis. RESULTS. SARS-CoV-2 copies, angiotensin-converting enzyme 2 (ACE2), and TMPRSS2 gene expression were similar in children and adults, but children displayed higher expression of genes associated with IFN signaling, NLRP3 inflammasome, and other innate pathways. Higher levels of IFN-α2, IFN-γ, IP-10, IL-8, and IL-1β protein were detected in nasal fluid in children versus adults. Children also expressed higher levels of genes associated with immune cells, whereas expression of those associated with epithelial cells did not differ in children versus adults. Anti–SARS-CoV-2 IgA and IgG were detected at similar levels in nasal fluid from both groups. None of the children required supplemental oxygen, whereas 7 adults did (P = 0.03); 4 adults died. CONCLUSION. These findings provide direct evidence of a more vigorous early mucosal immune response in children compared with adults and suggest that this contributes to favorable clinical outcomes.
2021-05-11 | GSE172274 | GEO
Project description:Nasal cavity is the main gateway for pathogen infection although it composed of many layers of defending barriers. Pathogens strongly willing to enter and infect from nasal cavity with the dominant form aerosol or respiratory droplets. However, the underlying mechanism of virus nasal infection and transmission are still unknown. Hence, a better understanding of this mechanism may provide insight into the pathogenesis of virus. In this study, IBDV was select as a model virus to study nasal infection and transmission for it could infect chicken from head (nasal) to tail (basal) and lead to massive destruction of bursal IgM+ B-lymphocytes. Initially, we found IBDV mostly entered and infected the interior of chicken’s nasal, where full of lymphoid tissue and easily for virus to transfer into blood. After passing nasal barriers, IBDV was subsequently transmit into blood and infected PBMCs. Following blood circulates, IBDV then infected bursal and hugely destroyed B-lymphocytes. However, the mechanism of how IBDV influenced the bursal cells, especially how virus destroyed B-lymphocytes were still unclear. With the help of single cells RNA sequence, we identified five vigorous clusters, including three immune cells types (B-cells: 64.70%, dendritic cells: 3.32% and T-cells: 6.33%) and two non-immune cell types (epithelial cells: 23.86% and fibroblast cells: 1.80% cells). Further analyses found that B-cells population were serious damaged, especially IgM+ B cells. However, the IgA+ B cells population hugely increased after IBDV infection. Interesting, we first demonstrated that basal cells and other non-immune cells in Bursa of Fabricius (BF) were the main target for IBDV infection and replication. Together, our study not only comprehensive elaborated the airborne IBDV and its transmission via intranasal route into the BF, but also explained its distribution in different immune and nonimmune cells and immunoglobulins rearrangement after immunosuppressive disorder on an age dependent infected organ.
2021-12-23 | GSE167377 | GEO
Project description:The nasal mucosa is frequently the initial site of respiratory viral infection, replication, and transmission, but the cellular composition at homeostasis, during infection, and during a memory response are poorly understood. Here, we generated a single-cell RNA-sequencing (scRNA-seq) atlas of the murine nasal mucosa sampling three distinct regions before and during primary and secondary influenza A virus (IAV) infection. Primary infection was largely restricted to respiratory mucosa and induced stepwise changes in immune and epithelial cell type, subset, and state composition over time. Following viral clearance (14 dpi), rare, previously undescribed Krt13+ nasal immune-interacting floor epithelial (KNIIFE) cells expressing multiple genes with immune communication potential increased concurrently with tissue-resident memory T (TRM)-like cells and early IgG+/IgA+ plasmablasts. Proportionality analysis coupled with cell-cell communication inference, alongside validation by in situ microscopy, underscored the CXCL16–CXCR6 signaling axis between MDMs and effector CD8 T cells 8dpi and KNIIFE cells and TRM cells 14 dpi. Secondary influenza challenge with a homologous or heterologous strain administered 60 dpi induced an accelerated and coordinated myeloid and lymphoid response without epithelial proliferation, illustrating how tissue-scale memory to natural infection engages both myeloid and lymphoid cells to reduce epithelial regenerative burden. Raw and processed single-cell counts matrices can be accessed and downloaded from the Broad Institute Single-Cell Portal from studies SCP2216 and SCP 2221.
2024-06-17 | GSE266469 | GEO
Project description:The interconnection between metabolic programming and chromatin remodeling during IgA class switching suggest that HIF-1a-dependent glycolytic flux may control the epigenetic modification at α class switching region (Sα) in the Igh locus. To test our hypothesis, histone acetylation was analyzed by chromatin immunoprecipitation sequencing (ChIP-seq) (H3K9ac and H3K27ac) in Hif-1a deficient and control B cell during IgA class switching. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modifications H3K27ac and H3K9ac in B cell from WT and HIF-1a deficient mice.
2025-01-08 | GSE228366 | GEO
Project description:The origins of IgA-secreting cells in the acinar structures of the nasal turbinates [scRNA-seq]
| PRJNA1057109 | ENA