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Transcriptional comparison of alveolar macrophages from patients with RA-ILD. IIM-ILD and DI-ILD.

ABSTRACT: To examine the differences of AMs by disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE142540 | GEO | 2021/12/31

REPOSITORIES: GEO

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Transcriptional comparison of alveolar macrophages from patients with RA-ILD. IIM-ILD and DI-ILD.

Project description:Transcriptional comparison of alveolar macrophages from patients with RA-ILD. IIM-ILD and DI-ILD.

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Project description:Respiratory infections, like the current pandemic SARS-CoV-2 virus, target the epithelial cells in the respiratory tract. However, alveolar macrophages (AMs) are tissue-resident macrophages located within the alveoli of the lung and they play a key role in the early phases of an immune response to respiratory infections. We expect that AMs are the first immune cells to encounter the SARS-CoV-2 and therefore their reaction to SARS-CoV-2 infection will have a profound impact upon the outcome of the infection. Interferons (IFNs) are antiviral cytokines and the first cytokine produced upon viral infection. Here, we challenge AMs with SARS-CoV-2 and to our surprise find that the AMs are incapable of recognising SARS-CoV-2 and produce IFN. This is in contrast to respiratory pathogens, such as influenza A virus and Sendai virus. Callenge of AMs with those viruses resulted in a robust IFN response. The absence of IFN production by AMs upon challenge could explain the initial asymptotic phase of SARS-CoV-2 infections and argues against the AMs as the source of proinflamatory cytokines later in infection.

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Alveolar macrophages from tuberculosis patients display an altered inflammatory gene expression profile

Project description:Alveolar macrophages (AMs) are major targets of Mycobacterium tuberculosis (Mtb) infection, critical during the progression of active tuberculosis (TB). The complex immunopathology of TB generates diverse microenvironments in the lung, which shape immune responses by AMs. In the current study, we perform whole genome microarray transcriptional profiling on RNA isolated from AMs from TB patients (AMsTB) compared to AMs from control subjects (AMsCT) using bronchoalveolar lavage (BAL). Our hypothesis was that systemic effects on the local lung microenvironment during TB affect the transcriptional response of AMsTB. We found a unique gene expression profile of 51 genes, including up-regulated CHIT1, CHI3L1, CCL5, CCL22, CCL8, CXCL9, MMP9, MMP7 and MMP12, associated with a robust pro-inflammatory response, cell recruitment and tissue damage, and genes of the cyclin family (CCND1, CCND2, and CCNA1) associated with cell proliferation. These expression profiles may account for the inflammatory condition in the lungs of TB patients. CXCL5, IL1B, CAMP, and TGFB1 were down-regulated, suggesting an altered control of Mtb infection. Also, MARCO and COLEC12, affecting phagocytosis, and CES1, associated with an increase in free cholesterol, were down-regulated. The observed changes in mRNA expression profiles may partially account for the inability of AMsTB to effectively control Mtb infection, suggesting that a balanced control of pro- and anti-inflammatory immune responses is crucial for infection control.

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The Lung Microenvironment Instructs Gene Transcription in Neonatal and Adult Alveolar Macrophages

Project description:Immaturity of alveolar macrophages (AMs) around birth contributes to the susceptibility of newborns to lung disease. However, the molecular features differentiating neonatal and mature, adult AMs are poorly understood. Here we identify the unique transcriptomes and enhancer landscapes of neonatal and adult AMs. While the core AM signature was similar, adult AMs expressed higher levels of genes involved in lipid metabolism, while neonatal AMs expressed a largely proinflammatory gene profile. Open enhancer regions identified by ATAC-seq contained motifs for nuclear receptors, MITF, and STAT in adult AMs and AP-1 and NF-kB in neonatal AMs. Intranasal LPS activated a similar innate immune response in both neonates and adults, with higher basal expression of inflammatory genes in neonates. The lung microenvironment drove many of the distinguishing gene expression and open chromatin characteristics of neonatal and adult AMs. Neonatal AMs retained high expression of some proinflammatory genes, suggesting the differences in neonatal AMs result from both inherent cell properties and environmental influences.

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RNA-seq of mouse alveolar macrophages sorted from CD11cCre/+ Tgfbr2fl/fl and control Tgfbr2fl/fl neonatal mice

Project description:Alveolar macrophages (AMs) are lung resident phagocytes. They derive from fetal liver monocytes, which colonize the lung during embryonic development and give rise to fully mature AMs perinatally. We have identified TGF- signaling as an indispensible regulator during this process. To analyze the impact of TGF- on the entire transcriptome of AMs, we performed RNA-seq on AMs deficient of Tgfbr2 in CD11cCre/+ Tgfbr2fl/fl mice at P3 with Tgfbr2fl/fl littermates as a control.

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Mycobacterium tuberculosis induced interferon pathways distinguish responses of Human Alveolar Macrophages from Monocyte-Derived Macrophages

Project description:Alveolar macrophages (AMs) and recruited monocyte-derived macrophages (MDMs) mediate early lung immune responses to Mycobacterium tuberculosis (Mtb). Using paired human AMs and MDMs from 6 healthy volunteers, we investigated transcriptional profiles in responses to Mtb. We found 681 genes that were Mtb-dependent in AMs compared to MDMs, 107 that were induced in both cell types but in different directions, and 4538 that were Mtb-dependent in MDMs but not AMs (FDR < 0.05). We found that IFNA Response and IFNG Response were the top two gene sets selectively induced in Mtb-infected AM. Thus, a second experiment utilized MDMs treated with IFNA1, IFNA8, IFNE, or IFNL1 found that IFNA8 modulated Mtb-induced pro-inflammatory cytokines and, compared to other interferons,stimulated unique transcriptional profiles.

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Project description:The aim of this study was to measure the immune response of alveolar macrophages (AMs) to intracellular Mtb infection in vivo. We characterized the transcriptional profile of murine Mtb-infected AMs after aerosol infection by sorting cells from bronchoalveolar lavage fluid and performing low-input RNA-sequencing. To determine the effect of the transcription factor Nrf2 on this response we also measured the transcriptional profiles of AMs from mice lacking Nrf2.

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