Lipopolysaccharide inhalation recruits monocytes and dendritic cell subsets DC2,3 and DC5 to the alveolar airspace
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ABSTRACT:
PROVIDER: PRJNA523739 | ENA |
REPOSITORIES: ENA
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Project description:Using lipopolysaccharide inhalation to induce acute inflammation in healthy volunteers and examine the impact on bronchoalveolar lavage (BAL) fluid and blood MP repertoire. This study defines the characteristics of human DCs and monocytes recruited into bronchoalveolar space immediately following localised acute inflammatory stimulus in vivo.
2019-02-23 | GSE126923 | GEO
Project description:Mononuclear phagocytes (MPs) including monocytes, macrophages and dendritic cells (DCs) are critical innate immune effectors and initiators of the adaptive immune response. MPs are present in the alveolar airspace at steady state, however little is known about DC recruitment in acute pulmonary inflammation. Here we use lipopolysaccharide inhalation to induce acute inflammation in healthy volunteers and examine the impact on bronchoalveolar lavage fluid and blood MP repertoire. Classical monocytes and two DC subsets (DC2/3 and DC5) are expanded in bronchoalveolar lavage fluid 8?h after lipopolysaccharide inhalation. Surface phenotyping, gene expression profiling and parallel analysis of blood indicate recruited DCs are blood-derived. Recruited monocytes and DCs rapidly adopt typical airspace-resident MP gene expression profiles. Following lipopolysaccharide inhalation, alveolar macrophages strongly up-regulate cytokines for MP recruitment. Our study defines the characteristics of human DCs and monocytes recruited into bronchoalveolar space immediately following localised acute inflammatory stimulus in vivo.
| S-EPMC6491485 | biostudies-literature
Project description:Murine Pulmonary Interstitial Macrophage Subsets after Lipopolysaccharide
| PRJNA906080 | ENA
Project description:Rationale: Lipopolysaccharide (LPS) is ubiquitous in the environment. Inhalation of LPS has been implicated in the pathogenesis and/or severity of several lung diseases, including pneumonia, chronic obstructive pulmonary disease and asthma. Alveolar macrophages are the main resident leukocytes exposed to inhaled antigens. Objectives: To obtain insight into which innate immune pathways become activated within human alveolar macrophages upon exposure to LPS in vivo.
2012-09-15 | GSE40885 | GEO
Project description:We sought to characterize pulmonary interstitial macrophage (IM) origin, subsets, and transcriptomic profiles during homeostasis and lipopolysaccharide (LPS) induced acute lung inflammation. During homeostasis, we used three complementary methods: spectral flow cytometry, single-cell RNA-sequencing, and gene regulatory network enrichment to demonstrate that IMs can be divided into two core subsets distinguished by surface and transcriptional expression of folate receptor β (Folr2/FRβ). Within FRβ+ IMs we identified a subpopulation marked by co-expression of LYVE1. During acute LPS-induced inflammation, lung IM numbers expand. Lineage tracing revealed IM expansion was due to recruitment of monocyte-derived IMs. At the peak of inflammation, recruited IMs were comprised of two unique subsets defined by expression of genes associated with interferon signaling and glycolytic pathways. As recruited IMs matured, they adopted the overall transcriptional state of FRβ- resident IMs but retained expression in several origin-specific genes. FRβ+ IMs were of near-pure resident origin.
2023-03-17 | GSE218884 | GEO
Project description:Rationale: Lipopolysaccharide (LPS) is ubiquitous in the environment. Inhalation of LPS has been implicated in the pathogenesis and/or severity of several lung diseases, including pneumonia, chronic obstructive pulmonary disease and asthma. Alveolar macrophages are the main resident leukocytes exposed to inhaled antigens. Objectives: To obtain insight into which innate immune pathways become activated within human alveolar macrophages upon exposure to LPS in vivo. In seven healthy humans sterile saline was instilled into a lung segment by bronchoscope, followed by instillation of LPS into the contralateral lung. Six hours later a bilateral bronchoalveolar lavage was performed and whole-genome transcriptional profiling was done (Affymetrix HG-U133 Plus 2.0) on purified alveolar macrophages, comparing cells exposed to saline or LPS from the same individuals.
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Project description:Cigarette smoke exposure is associated with an increased risk of the acute respiratory distress syndrome (ARDS); however, the mechanisms underlying this relationship remain largely unknown.To assess pathways of lung injury and inflammation in smokers and non-smokers with and without lipopolysaccharide (LPS) inhalation using established biomarkers.We measured plasma and bronchoalveolar lavage (BAL) biomarkers of inflammation and lung injury in smokers and non-smokers in two distinct cohorts of healthy volunteers, one unstimulated (n=20) and one undergoing 50??g LPS inhalation (n=30).After LPS inhalation, cigarette smokers had increased alveolar-capillary membrane permeability as measured by BAL total protein, compared with non-smokers (median 274 vs 208??g/mL, p=0.04). Smokers had exaggerated inflammation compared with non-smokers, with increased BAL interleukin-1? (p=0.002), neutrophils (p=0.02), plasma interleukin-8 (p=0.003), and plasma matrix metalloproteinase-8 (p=0.006). Alveolar epithelial injury after LPS was more severe in smokers than non-smokers, with increased plasma (p=0.04) and decreased BAL (p=0.02) surfactant protein D. Finally, smokers had decreased BAL vascular endothelial growth factor (VEGF) (p<0.0001) with increased soluble VEGF receptor-1 (p=0.0001).Cigarette smoke exposure may predispose to ARDS through an abnormal response to a 'second hit,' with increased alveolar-capillary membrane permeability, exaggerated inflammation, increased epithelial injury and endothelial dysfunction. LPS inhalation may serve as a useful experimental model for evaluation of the acute pulmonary effects of existing and new tobacco products.
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Project description:Pulmonary dendritic cells are heterogenous cells comprise four distinct subsets including two conventional dendritic cell subsets, CD103+ and CD11bhiCD14lo cells, and two monocyte-derived dendritic cell subsets. Their functions in terms of migration and T cell activation are distinct, but genes regulating their features are to be determined. We used microarrays to identify a select set of genes that are expressed in conventinal dendritic cells and in monocyte-derived dendriti cells. Four distinct lung DC subsets were purified by flow cytometry-based sorting after inhalation of lipopolusaccharide and ovalbumin. Each subset has three replicates.
2015-04-02 | E-GEOD-64896 | biostudies-arrayexpress
Project description:LC-IMS-CID-MS lipidomics of BALF and plasma from severe smoke inhalation and NIST SRM 1950.
2021-11-12 | MSV000088372 | MassIVE
Project description:We set out to test the hypothesis that formaldehyde inhalation exposure significantly alters miRNA expression profiles within the nasal epithelium of nonhuman primates. Here, cynomolgus macaques were exposed to 0, 2, and 6 ppm formaldehyde for 6 hours/day across two consecutive days. RNA was extracted from the nasal maxilloturbinate region, a direct target of formaldehyde inhalation exposure. Genome-wide miRNA expression levels were assessed using microarrays. Cynomolgus macaques (Macaca fascicularis) were exposed to 0, 2 and 6 ppm formaldehyde for 6 hours/day across two consecutive days using whole body exposure chambers. RNA was extracted from the nasal maxilloturbinate region, a direct target of formaldehyde inhalation exposure. Genome-wide miRNA expression levels were assessed using microarrays.
2012-09-01 | E-GEOD-34978 | biostudies-arrayexpress