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This study was conducted to investigate the percentages of Th22 and Th17 cells in the peripheral blood of septic patients with and without acute lung injury (ALI) and their clinical significance. A total of 479 patients were divided into non-ALI and ALI groups. The percentages of Th22 and Th17 cells and the levels of interleukin 22 (IL-22), 6 (IL-6), and 17 (IL-17) were determined. Receiver operating characteristic curve analysis was performed to assess the diagnostic value of Th22 and Th17 cells to predict sepsis-induced ALI. The lung injury prediction score (LIPS), IL-6, IL-17, and IL-22 levels and the percentages of Th17 and Th22 cells were significantly higher in the ALI group (P

Background: Acute lung injury (ALI) is one of the major complications of severe sepsis. This study was conducted to investigate the levels of Th22 and Th17 cells in the peripheral blood septic patients with ALI and their clinical significance. Results: A total of 479 septic patients admitted between January 2013 to January 2018 were divided into non-ALI (n = 377) and ALI groups (n = 102) based on the presence or absence of ALI. The levels of Th22 and Th17 cells, interleukin 22 (IL-22), 6 (IL-6) and 17 (IL-17) were determined. Receiver operating characteristic curve (ROC) analysis was performed to assess the early diagnostic value of Th22 and Th17 cells to predict sepsis-induced ALI. The lung injury prediction score (LIPS), IL-6, IL-17, IL-22, and levels of Th17 and Th-22 cells were 9.13, 14.02 ng/L, 13.06 ng/L, 22.90 ng/L, 8.80% and 7.40%, respectively, in the ALI patients and were significantly higher in the ALI group than in non-ALI group (P < 0.05). Pearson correlation analysis showed that LIPS, IL-17, IL-22, Th17 cells and Th22 cells were significant factors affecting sepsis-induced ALI (P < 0.05). The correlation analysis showed that the levels of Th22 cells in the peripheral blood of septic patients with ALI were positively correlated with LIPS, IL-22 and the levels of Th17 cells (P < 0.05), and the levels of Th17 cells were positively correlated with LIPS and IL-17 (P < 0.01). Multivariate logistic regression analysis showed that the LIPS (OR = 1.130), IL-17 (OR = 1.982), IL-22 (OR =2.612) and levels of Th17 (OR = 2.211) and Th22 (OR =3.230) cells were independent risk factor for ALI. The area under the curve of Th22 cells was 0.844 with a cutoff value of 6.81% to predict ALI. The sensitivity and specificity for early diagnosis of sepsis-induced ALI by Th22 cells were 78.72% and 89.13% respectively, which were better but statistically similar as compared with Th17 cells (P > 0.05). Conclusions: The levels of Th22 and Th17 cells in peripheral blood are significantly increased in septic patients with induced ALI, and may be used for early diagnose of sepsis-induced ALI.

Recurrent, de novo, meiotic non-allelic homologous recombination events between low copy repeats, termed LCR22s, leads to the 22q11.2 deletion syndrome (22q11.2DS; velo-cardio-facial syndrome/DiGeorge syndrome). Although most 22q11.2DS patients have a similar sized 3 million base pair (Mb), LCR22A-D deletion, some have nested LCR22A-B or LCR22A-C deletions. Our goal is to identify additional recurrent 22q11.2 deletions associated with 22q11.2DS, serving as recombination hotspots for meiotic chromosomal rearrangements. Here, using data from Affymetrix 6.0 microarrays on 1,680 22q11.2DS subjects, we identified what appeared to be a nested proximal 22q11.2 deletion in 38 (2.3%) of them. Using molecular and haplotype analyses from 14 subjects and their parent(s) with available DNA, we found essentially three types of scenarios to explain this observation. In eight, the proximal breakpoints occurred in a small sized 12 kb LCR distal to LCR22A, referred to LCR22A+, resulting in LCR22A+-B or LCR22A+-D deletions. Six of these eight subjects had a nested 22q11.2 deletion that occurred during meiosis in a parent carrying a benign 0.2 Mb duplication of the LCR22A-LCR22A+ region with a breakpoint in LCR22A+. Another six had a typical de novo LCR22A-D deletion on one allele and inherited the LCR22A-A+ duplication from the other parent thus appearing on microarrays to have a nested deletion. LCR22A+ maps to an evolutionary breakpoint between mice and humans and appears to serve as a local hotspot for chromosome rearrangements on 22q11.2. ispartof: Human Molecular Genetics vol:27 issue:7 pages:1150-1163 ispartof: location:England status: published