Dataset Information

Microvesicles Derived from Human Bronchial Epithelial Cells Regulate Macrophage Activation During Mycobacterium abscessus Infection

ABSTRACT: Intercellular communication is important for host immunity in response to bacterial infections. Nontuberculous mycobacterium (NTM), such as Mycobacterium abscessus (M.ab), is a group of environmental bacteria that can cause severe lung infections in individuals with pre-existing lung conditions, including cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). There is limited knowledge understanding the interaction between airway epithelial cells and immune cells during NTM infections. In this study, we characterized microvesicles (MVs) released from M.ab-infected human bronchial epithelial cells and investigated the effect of these MVs on the activation and polarization of THP-1-derived macrophages in cell culture. Our results indicate that MVs released by M.ab-infected human bronchial epithelial cells stimulated the activation of M2-polarized macrophages in cell culture. Additionally, the proteomic analysis for isolated MVs showed that the proteins involved in the cell adhesion pathway were enriched in MVs from M.ab-infected human bronchial epithelial cells compared to the uninfected cells. Among those, the cell surface protein, intercellular adhesion molecule 1 (ICAM-1), regulated the MV internalization by recipient macrophages. In conclusion, our data suggests that in response to M.ab infection, human airway epithelial cells release MVs to modulate the activation of macrophages, which are key cells for mycobacterial intracellular survival in the host.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human) Mycobacterium Abscessus (strain Atcc 19977 / Dsm 44196 / Cip 104536 / Jcm 13569 / Nctc 13031 / Tmc 1543)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Cystic Fibrosis

SUBMITTER: Steven Hartson

LAB HEAD: Yong Cheng

PROVIDER: PXD056025 | Pride | 2026-03-30

REPOSITORIES: Pride

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Microvesicles Derived from Human Bronchial Epithelial Cells Regulate Macrophage Activation During Mycobacterium abscessus Infection.

Guthrie Carlyn M CM Meeker Amber C AC Self Ashton E AE Ramos-Leyva Aidaly A Clark Olivia L OL Kotey Stephen K SK Hartson Steven D SD Liang Yurong Y Liu Lin L Tan Xuejuan X Cheng Yong Y

Journal of proteome research 20250328 5

Intercellular communication is important for host immunity in response to bacterial infections. Nontuberculous mycobacterium (NTM), such as Mycobacterium abscessus (M. ab), is a group of environmental bacteria that can cause severe lung infections in individuals with pre-existing lung conditions, including cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). There is limited knowledge understanding the interaction between airway epithelial cells and immune cells d ...[more]

PMID: 40153482

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Project description:Microvesicles (MV) are small membrane-bound particles comprised of exosomes and various sized extracellular vesicles. These are released by a number of cell types. Microvesicles have a variety of cellular functions from communication to mediating growth and differentiation. Microvesicles contain proteins and nucleic acids. Previously, we showed that plasma microvesicles contain microRNAs (miRNAs). Based on our previous report, the majority of peripheral blood microvesicles are derived from platelets while mononuclear phagocytes, including macrophages, are the second most abundant population. Here, we characterized macrophage-derived microvesicles and whether they influenced the differentiation of naM-CM-/ve monocytes. We also identified the miRNA content of the macrophage-derived microvesicles. We found that RNA molecules contained in the macrophage-derived microvesicles were transported to target cells, including monocytes, endothelial cells, epithelial cells and fibroblasts. Furthermore, we found that miR-223 was transported to target cells and was functionally active. Based on our observations, we hypothesize that microvesicles bind to and activate target cells. Furthermore, we find that microvesicles induce the differentiation of macrophages. Thus, defining key components of this response may identify novel targets to regulate host defense and inflammation. We used GeneChip microarrays to examine changes in gene expression induced by MV in primary monocyte-derived macrophages (MDM) and in THP1 cells, and compare this to cells treated with GM-CSF and PMA, respectively. All experiments were done in triplicates. Primary monocytes were collected from buffy coats (BC). The freshly isolated monocytes from three donors (Mono1-3) were either treated with GM-CSF or subjected to RNA isolation. Following treatment, MVs were isolated from the GM-CSF-treated macrophage cultures. RNA was isolated from the remaining cells for profiling (GM1-3). The isolated MVs were then used to treat new BC monocytes for 24 h (BC-GMCSF-MV24). A fraction of the new BC monocytes was subjected to RNA extraction for profiling (BC1-3). For THP1 cells, they were treated with either DMSO or PMA to produce MVs. The MVs were collected and the remaining cells lyzed for RNA extraction and profiling (DMSO1-3 and PMA1-3). The collected MVs from the DMSO or PMA-treated THP1 cells were incubated with new THP1 for 24 h and designated DMSO-MV24 or PMA-MV24. We had a total of 24 samples.

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Dataset Information

Microvesicles Derived from Human Bronchial Epithelial Cells Regulate Macrophage Activation During Mycobacterium abscessus Infection

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Microvesicles Derived from Human Bronchial Epithelial Cells Regulate Macrophage Activation During <i>Mycobacterium abscessus</i> Infection.

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Dataset Information

Microvesicles Derived from Human Bronchial Epithelial Cells Regulate Macrophage Activation During Mycobacterium abscessus Infection

Dataset's files

Publications

Microvesicles Derived from Human Bronchial Epithelial Cells Regulate Macrophage Activation During &lt;i&gt;Mycobacterium abscessus&lt;/i&gt; Infection.

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OmicsDI is part of the ELIXIR infrastructure

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Microvesicles Derived from Human Bronchial Epithelial Cells Regulate Macrophage Activation During <i>Mycobacterium abscessus</i> Infection.