Journal: Journal of Innate Immunity

Article Title: IL-1 Mediates Tissue-Specific Inflammation and Severe Respiratory Failure in COVID-19

doi: 10.1159/000524560

Figure Lengend Snippet: Calprotectin is increased in patients with ARDS due to COVID-19. a , b Concentrations of calprotectin (S100A8/A9) and HMGB1 were measured in the plasma from HVs, from patients with COVID-19 who did not develop ARDS during follow-up on the day of hospital admission, and from patients with ARDS by COVID-19 on the first day of ARDS. Comparison by the Mann-Whitney U test; * p < 0.05; ** p < 0.01; *** p < 0.001; ****; p < 0.0001. c , d suPAR was measured in 40 patients screened for participation in the SAVE trial (3). None of the patients with suPAR less than 6 ng/mL developed ARDS, whereas 6 patients (30%) with suPAR 6 ng/mL or more developed ARDS. c Concentrations of calprotectin in 20 patients with suPAR less than 6 ng/mL and in 20 patients with suPAR 6 ng/mL or more. Comparison by the Mann-Whitney U test; * p < 0.05. d Correlation of levels of suPAR with plasma calprotectin on day of admission Spearman rank correlation coefficients ( r s ), interpolation lines, and p values are provided. ns, nonsignificant.

Article Snippet: In separate experiments, mice were receiving 1 h before each day of i.v. treatment with plasma from patients with ARDS from COVID-19 i.p. either N/S 0.9% or 1.5 mg/kg of MRP8/14 (S100A8/A9) Chicken Polyclonal Antibody (Origene, Rockville, MD, USA).

Techniques: MANN-WHITNEY

Journal: Journal of Innate Immunity

Article Title: IL-1 Mediates Tissue-Specific Inflammation and Severe Respiratory Failure in COVID-19

doi: 10.1159/000524560

Figure Lengend Snippet: Murine IL-1α and S100A8/A9 drive the hyperinflammation caused by SARS-CoV-2. In a COVID-19-like infection model, C57Bl6 mice were challenged i.v. with plasma of patients with ARDS due to COVID-19 for 3 consecutive days. In separate experiments, on each day of plasma challenge, mice were treated with Flo1-2a anti-murine IL-1α antibody or XB2001 human IL-1α antibody or murine isotype control for Flo1-2a or pre-treated with anti-S100A8/A9. Mice were sacrificed on day 4. a–c TNFα in the lung, ileum, and colon and modulation by blockade of human or murine IL-1α. d , e IL-6 in the lung, ileum, and colon and modulation by blockade of human or murine IL-1α. f IFNγ in the lung, ileum, and colon and modulation by blockade of human or murine IL-1α. g–i MPO activity in the lung, ileum, and colon and modulation by blockade of human or murine IL-1α. j TNFα in the lung and modulation by blockade of S100A8/A9. k IFNγ in the lung and modulation by blockade of S100A8/A9. l IL-6 in the lung and modulation by blockade of S100A8/A9. m MPO activity in the lung and modulation by blockade of S100A8/A9. Comparison by the Mann-Whitney U test; * p < 0.05; ** p < 0.01; *** p < 0.001. ns, nonsignificant.

Article Snippet: In separate experiments, mice were receiving 1 h before each day of i.v. treatment with plasma from patients with ARDS from COVID-19 i.p. either N/S 0.9% or 1.5 mg/kg of MRP8/14 (S100A8/A9) Chicken Polyclonal Antibody (Origene, Rockville, MD, USA).

Techniques: Infection, Activity Assay, MANN-WHITNEY

Journal: Cancers

Article Title: Influence of Malignant Pleural Fluid from Lung Adenocarcinoma Patients on Neutrophil Response

doi: 10.3390/cancers14102529

Figure Lengend Snippet: Phenotype of neutrophils present in pleural effusions from HF and LAC.

Article Snippet: Panel C included anti-CD14-APC, -CD15-PE-Cy7 (BD Bioscience, San Jose, CA, USA, clone HI98), -S100A8/9-FITC (OriGene Technologies Inc, Rockville, MD, clone BM4025F) and -HLA-DR-APC-H7 (BD Biosciences, clone G46-6).

Techniques: Expressing