Long noncoding RNA associations with an IFI27-MCEMP1 transcript pattern in Kawasaki disease.
6 affiliations
- 1Heart Center, Children's Hospital of Fudan University, Shanghai, China.
- 2School of Medicine, Stanford University, Stanford, CA, United States.
- 3OncoOmicsDx Clinical Laboratory, Rockville, MD, United States.
- 4Nippon Life Insurance Company, Osaka, Japan.
- 5Florida State University, Tallahassee, FL, United States.
- 6University of Kansas Medical Center, Kansas City, KS, United States.
Abstract
Kawasaki disease (KD) is an acute pediatric vasculitis with risk of coronary artery injury. A two-transcript IFI27-MCEMP1 score has distinguished KD from other febrile illnesses, but its relationship to long noncoding RNAs (lncRNAs) is incompletely defined. We evaluated whether peripheral blood mononuclear cell (PBMC) lncRNA expression differed between KD and febrile controls and was associated with the IFI27-MCEMP1 transcript pattern. Children younger than 8 years were prospectively enrolled at the Children's Hospital of Fudan University during 2024-2025. The newly enrolled cohort included 55 children with KD and 48 febrile controls; integration with two same-site cohorts yielded 188 children with KD and 175 febrile controls. Bulk-PBMC expression of IFI27, MCEMP1, CHROMR, MALAT1, and NEAT1 was measured by reverse transcription quantitative PCR and normalized to GAPDH. The prespecified score distinguished KD from febrile controls with areas under the receiver operating characteristic curve of 0.88 (95% CI, 0.80-0.95) in the newly enrolled cohort and 0.89 (95% CI, 0.86-0.93) in the integrated cohort. In unadjusted integrated analyses, CHROMR and MALAT1 expression was lower in KD, whereas NEAT1 did not differ significantly. CHROMR ΔCt correlated with IFI27 ΔCt (r=0.55; Holm-adjusted P<.001). After adjustment for fever duration and a CBC-derived monocyte fraction, lower CHROMR and IFI27 and higher MCEMP1 expression remained significant, whereas the MALAT1 difference was attenuated. Exact fever-day matching yielded concordant CHROMR, IFI27, and MCEMP1 group differences, but the adjusted CHROMR-IFI27 correlation was not significant in the restricted matched population. Thus, KD was associated with a bulk-PBMC transcript pattern involving CHROMR, IFI27, and MCEMP1; the MALAT1 finding was less robust. These associations motivate hypotheses about interferon-associated and myeloid-associated biology but do not establish pathway activity or causality. Multicenter studies with standardized sampling, cell-resolved profiling, and independent CHROMR assay confirmation are required.
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BibTeX
@article{liu2026long,
title = {{Long noncoding RNA associations with an IFI27-MCEMP1 transcript pattern in Kawasaki disease.}},
author = {Fang Liu and Xing Xue and Zhi Han and Bo Jin and Weiwei Li and Naoto Ozawa and Takumi Ichikawa and Ellen Ling and Xinyang Zhao and Henry Chubb and Scott R Ceresnak and Gary L Darmstadt and Doff B McElhinney and Harvey J Cohen and Seda Tierney and Xuefeng B Ling},
journal = {Frontiers in immunology},
year = {2026},
month = sep,
doi = {10.3389/fimmu.2026.1882860},
url = {https://europepmc.org/article/MED/42845816},
note = {CC BY},
}
RIS
TY - JOUR
TI - Long noncoding RNA associations with an IFI27-MCEMP1 transcript pattern in Kawasaki disease.
AU - Fang Liu
AU - Xing Xue
AU - Zhi Han
AU - Bo Jin
AU - Weiwei Li
AU - Naoto Ozawa
AU - Takumi Ichikawa
AU - Ellen Ling
AU - Xinyang Zhao
AU - Henry Chubb
AU - Scott R Ceresnak
AU - Gary L Darmstadt
AU - Doff B McElhinney
AU - Harvey J Cohen
AU - Seda Tierney
AU - Xuefeng B Ling
PY - 2026
DA - 2026/09/23
JO - Frontiers in immunology
DO - 10.3389/fimmu.2026.1882860
UR - https://europepmc.org/article/MED/42845816
AB - Kawasaki disease (KD) is an acute pediatric vasculitis with risk of coronary artery injury. A two-transcript IFI27-MCEMP1 score has distinguished KD from other febrile illnesses, but its relationship to long noncoding RNAs (lncRNAs) is incompletely defined. We evaluated whether peripheral blood mononuclear cell (PBMC) lncRNA expression differed between KD and febrile controls and was associated with the IFI27-MCEMP1 transcript pattern. Children younger than 8 years were prospectively enrolled at the Children's Hospital of Fudan University during 2024-2025. The newly enrolled cohort included 55 children with KD and 48 febrile controls; integration with two same-site cohorts yielded 188 children with KD and 175 febrile controls. Bulk-PBMC expression of IFI27, MCEMP1, CHROMR, MALAT1, and NEAT1 was measured by reverse transcription quantitative PCR and normalized to GAPDH. The prespecified score distinguished KD from febrile controls with areas under the receiver operating characteristic curve of 0.88 (95% CI, 0.80-0.95) in the newly enrolled cohort and 0.89 (95% CI, 0.86-0.93) in the integrated cohort. In unadjusted integrated analyses, CHROMR and MALAT1 expression was lower in KD, whereas NEAT1 did not differ significantly. CHROMR ΔCt correlated with IFI27 ΔCt (r=0.55; Holm-adjusted P<.001). After adjustment for fever duration and a CBC-derived monocyte fraction, lower CHROMR and IFI27 and higher MCEMP1 expression remained significant, whereas the MALAT1 difference was attenuated. Exact fever-day matching yielded concordant CHROMR, IFI27, and MCEMP1 group differences, but the adjusted CHROMR-IFI27 correlation was not significant in the restricted matched population. Thus, KD was associated with a bulk-PBMC transcript pattern involving CHROMR, IFI27, and MCEMP1; the MALAT1 finding was less robust. These associations motivate hypotheses about interferon-associated and myeloid-associated biology but do not establish pathway activity or causality. Multicenter studies with standardized sampling, cell-resolved profiling, and independent CHROMR assay confirmation are required.
SN - 1664-3224
ER -