Figure 1

HSP70 gene expression in children with malaria. (A) Parasitemic children (n = 72) were categorized according to “polarized” phenotypic clinical categories of non-SMA (Hb 8.0–10.9 g/dL, n = 50) and SMA (Hb <5.0 g/dL, n = 22). Global gene expression profiling was performed on total RNA isolated from WBCs using the Illumina® HumanHT-12 v4 beadchip array covering >47,000 transcripts. Panel A shows HSPA1A gene expression analysis. ^aBivariate analysis of HSPA1A gene expression between two groups was performed using unpaired t test and presented as mean (SEM). (B) HSPA1A/1B and HSP70 gene expression analysis using qRT-PCR on WBCs collected from parasitemic children (n = 73) stratified into non-SMA (Hb ≥5.0 g/dL, n = 52) and SMA (Hb <5.0 g/dL, n = 21). The cyclophilin-A gene was used as an endogenous control to normalize expression. Bivariate analysis of normalized HSPA1A/1B gene expression (arbitrary units, AU) between two groups was performed using unpaired two-tailed t test and presented as mean (SEM). (C) HSP70 gene expression in PfHz-containing monocytes and neutrophils. Bivariate analysis of normalized HSP70 (1A + IB) gene expression between PfHz-containing monocytes and neutrophils. PfHz (−) monocytes (n = 22), PfHz (+) monocytes (n = 51); PfHz(−) neutrophils (n = 65), and PfHz(+) neutrophils (n = 8). Bivariate analysis of normalized HSPA1A/1B gene expression (arbitrary units, AU) between two groups was performed using unpaired two-tailed t test and presented as mean (SEM).