Journal: Frontiers in Toxicology

Article Title: Microplastics amplify the pro-inflammatory response to fungal mycelial fragments and spores in neutrophil-like cells

doi: 10.3389/ftox.2026.1718466

Figure Lengend Snippet: Bar plots of the fold changes following submerged exposure of reporter cells to test materials that include AFMHDPE (AFM (10 6 /mL) + HDPE (100 μg/mL)), AFM (10 6 /mL), AFSHDPE [AFS (10 6 /mL) + HDPE (100 μg/mL)], AFS (10 6 /mL) particles, H 2 O as the negative control, and positive controls [LPS (100 ng/mL) for TLR4 and LTA (100 ng/mL) for TLR2]. The blank control served as the background response without cells. The red stippled line indicates fold change level 2, which was considered the activation threshold. Data from two independent experiments are shown.

Article Snippet: In brief, TLR2 (InvivoGen #hkb-htlr2 Toulouse, France) and TLR4 (InvivoGen #hkb-htlr4) HEK-Blue reporter cells were grown in Dulbecco’s modified Eagle’s medium (DMEM; Gibco #31966) supplemented with 10% heat-inactivated endotoxin-free fetal bovine serum (FBS; Biowest #S1860), 100 U/mL penicillin (Biowest #L0022 Nuaillé, France), 100 μg/mL streptomycin (Biowest #L0022), 100 μg/mL normocin (InvivoGen #ant-zn), and 1xHEK Selection-Blue (InvivoGen #hb-sel).

Techniques: Negative Control, Control, Activation Assay

Journal: bioRxiv

Article Title: Mitochondrial COX4I2 drives pericyte-dependent inflammation and emphysema

doi: 10.64898/2026.02.09.703513

Figure Lengend Snippet: a-c) Migration of neutrophils in response to conditioned medium from pericytes isolated from Cox4i2 −/− and WT mice, following stimulation with the TLR4 agonist LPS-EB and treatment with the CXCL1 inhibitor 10µM SX-517 (a, n =3) and from WT mice treated with different doses of MitoQ/DecylTPP + (b, n =4) or S3QEL (c, n =4). d, e) mRNA expression of Cxcl1 in pericytes isolated from Cox4i2 −/− and WT mice and exposed to the TLR4 agonist LPS-EB (d, n =3) or CXCL1 protein in the cell culture supernatant (e, n=3). f, g) mRNA expression of Cxcl1 in pericytes isolated from WT mice and stimulated with the TLR4 agonist LPS-EB following treatment with MitoQ/DecylTPPLJ (f, n = 4) or S3QEL (g, n =3). h-j) Protein expression of ANG1 (i) and VEGFR2 (j) in the lung tissues of Cox4i2 −/− and WT mice exposed to CS for 8 months. n = 3 per group. h: Representative images. k, l) Pulmonary vessel casting of mice exposed to CS for 3 months ( n =3 per group). l: Representative images. m, n) Number of CD31 + cells (ECs) in the lung parenchyma of Cox4i2 −/− and WT mice exposed to CS for 3 months (m, n = 4 per group). n: Representative images. o) Vascular tube formation of ECs incubated with solvent or cigarette smoke extract (CSE) in the presence or absence of primary pulmonary pericytes ( n = 4, number of tubes). Statistical analysis was performed using one-way and two-way ANOVA. Data from panels a-c, e, i, j, m and o were log-transformed prior to statistical analysis. n in figures a-g and o represents individual cell isolations per group. The data are presented as the mean ± SEM.

Article Snippet: Isolated mouse pericytes were treated with 50 ng/mL TLR4 agonist (tlrl-3pelps, InvivoGen) or left untreated for 16 hours.

Techniques: Migration, Isolation, Expressing, Cell Culture, Incubation, Solvent, Transformation Assay

Journal: bioRxiv

Article Title: Mitochondrial COX4I2 drives pericyte-dependent inflammation and emphysema

doi: 10.64898/2026.02.09.703513

Figure Lengend Snippet: Effects of S3QEL on CXCL1 levels, Cox4i2 deficiency on chemokines/cytokine levels in cell culture supernatants from pericytes and mitochondrial ROS production in pericytes a-b) MtROS production in pericytes after stimulation with the TLR4 agonist LPS-EB, as measured by MitoSOX. n =20–23 cells from three independent cell isolations per group. c, d) Protein expression of CXCL1 in cell culture supernatant from WT pericytes after stimulation with the TLR4 agonist LPS-EB following the application of MitoQ or its inactive carrier, DecylTPPLJ (c), or the mitochondrial complex III superoxide inhibitor 3 µM S3QEL (d). n =3 individual cell isolations per group. e, f) The protein level of CCL2 in the cell culture supernatant isolated from Cox4i2 −/− and WT mice (e) or from WT mice following treatment with MitoQ or its inactive carrier, DecylTPPLJ (f), and stimulation with the TLR4 agonist LPS-EB. n =3 individual cell isolations per group. g, h) Protein level of IL6 in the cell culture supernatant isolated from Cox4i2 −/− and WT mice (g) or from WT mice following treatment with MitoQ or its inactive carrier, DecylTPPLJ (h), and stimulation with the TLR4 agonist LPS-EB. n =3 individual cell isolations per group. i) Cell viability of primary pulmonary pericytes isolated from Cox4i2 −/− and WT mice and exposed to various doses of cigarette smoke extract (CSE). n =3 independent cell isolation per group. j) Mitochondrial ROS production in pericytes after exposure to 1% CSE measured by MitoSOX. n =104–132 cells from three independent cell isolations per group. k) Vascular tube formation of ECs incubated with solvent CSE in the presence or absence of primary pulmonary pericytes. n =4 isolation per group: tube length. Statistical analysis was performed using one-way or two-way ANOVA. Data from panels a, c-h and j were log-transformed prior to statistical analysis. The data are presented as the mean ± SEM.

Article Snippet: Isolated mouse pericytes were treated with 50 ng/mL TLR4 agonist (tlrl-3pelps, InvivoGen) or left untreated for 16 hours.

Techniques: Cell Culture, Expressing, Isolation, Cell Isolation, Incubation, Solvent, Transformation Assay