Dataset Information

Candida albicans infection suppresses Lipopolysaccharide or Pseudomonas aeruginosa stimulated murine bone marrow derived macrophage (BMDM) responses

ABSTRACT: Candida albicans is a commensal fungi which populates most healthy individuals’ microflora, but can turn opportunistic in immunocompromised individuals. This opportunistic pathogen can cause severe disease and is linked with high rates of mortality. With limited therapeutic options and increasing resistance to antifungals, novel treatment strategies for C. albicans infections is paramount. Macrophages are a key immune cell which mount an immediate response to C. albicans infection. Macrophages physically sequester C. albicans through phagocytosis, trapping the pathogen in a harsh environment. Additionally, macrophages mount a signalling response, alerting other immune cells to the site of infection for quick removal. Here we utilise a discovery screen approach using DIA based total proteomics to describe murine bone marrow derived macrophage (BMDM) response to C. albicans infection as well as in response to co-infection with gram-negative bacterial plasma membrane component lipopolysaccharide (LPS) or live gram-negative bacteria Pseudomonas aeruginosa. We found C. albicans induced a surprisingly muted response in BMDMs compared to LPS or P. aeruginosa. Despite small measurable activation of BMDMs on single infection, upon co-infection with LPS or P. aeruginosa, C. albicans significantly suppressed BMDM proteome landscape. Additionally, C. albicans selectively suppressed BMDM secreted IL-6 and IL-12p40 cytokine response to P. aeruginosa. Thus, we describe C. albicans significant suppressive capabilities in host innate immune responses.

INSTRUMENT(S):

ORGANISM(S): Candida Albicans (yeast) Mus Musculus (mouse)

TISSUE(S): Bone Marrow Macrophage, Bone Marrow

SUBMITTER: Christa Baker

LAB HEAD: J Simon C Arthur

PROVIDER: PXD062689 | Pride | 2026-03-16

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	255_2022-260_2023-CB-mouse-candida-directDIA-high-stringency-no-normalization-v19_ConditionSetup.tsv	Tabular
	255_2022-260_2023-CB-mouse-candida-directDIA-high-stringency-no-normalization-v19_Report_Protein_pivot_FP.tsv	Tabular
	260_2023_CB-Sample-1.raw	Raw
	260_2023_CB-Sample-10.raw	Raw
	260_2023_CB-Sample-11.raw	Raw

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Publications

Candida albicans infection suppresses lipopolysaccharide or Pseudomonas aeruginosa stimulated murine bone marrow derived macrophage (BMDM) responses.

Baker Christa P CP Laba Stephanie S Warner Jordan J Shepherd Karen K Wilson Heather M HM Arthur J Simon C JSC

Scientific reports 20260213

PMID: 41688542

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Project description:BMDMs or iMACs were generated via differentiation of bone marrow cells or immortalized precursors, respectively, in culture media containing m-CSF for 7 day. Upon differentiation, BMDMs or iMacs were left untreated or stimulated as described below. 1) BMDM WT were stimulated with IFNa, LPS, PGE2, IL-4, IL-10, LPS+PGE2, LPS+IL-4, LPS+IL-10, IFNa+PGE2, IFNa+IL-10: each condition in duplicate. This experiment was performed to investigate transcriptional cross-antagonism in the concomitant presence of pro-inflammatory (LPS or IFNa) and anti-inflammatory stimuli (IL-4, IL-10, or PGE2). 2) BMDM WT were stimulated with LPS, in the presence or absence of PFI-1 (Brd2/4 inhibitor) or SGC-CBP30 (CBP/p300 inhibitor): each condition in triplicate. This experiment was performed to define pro-inflammatory genes dependent or not on chromatin remodeling for their induction. 3) BMDM Mef2C/D proficient (Vav-Cre) or BMDM Mef2C/D KO (obtained by crossing Mef2d-/- Mef2cfl/fl with Vav-Cre mice) were stimulated with LPS, PGE2, or LPS+PGE2: each condition in triplicate. This experiment was performed to investigate the role of MEF2C-D on LPS transcritptional response. 4) BMDM WT were pretreated for 40 minutes with an anti-IL10R antibody or the corresponding isotope control, and then left untreated or stimulated with LPS, PGE2 or LPS+PGE2: each condition in duplicate. This experiment was performed to investigate the crosstalk between IL-10 and PGE2. 5) BMDM WT were left untreated or stimulated with PGE2, LPS, LPS+PGE2, or LPS+PGE2+IFNb. In the latter condition, IFNb was added 1 hour after the beginning of the costimulation: each condition in triplicate. This experiment was performed to asses the impact of PGE2 into the LPS-mediated IFNb induction. 5) MEF2A-deficient iMac clones (D7, A7, A8, C7) and MEF2A-proficient (referred to as wild-type) iMac clones (NE, B3 and D10) were generated via CRISPR/Cas9 and stimulated or not with LPS: each condition in single. This experiment was performed to investigate the role of MEF2A on LPS transcritptional response.