Pathoimmunological analyses of fatal E11 infection in premature infants

Wei Luo; Lixia Wang; Zhengrong Chen; Ming Liu; Yixue Zhao; Yucan Wu; Bing Huang; Ping Wang

doi:10.3389/fcimb.2024.1391824

Pathoimmunological analyses of fatal E11 infection in premature infants

Front Cell Infect Microbiol. 2024 Jul 9:14:1391824. doi: 10.3389/fcimb.2024.1391824. eCollection 2024.

Authors

Wei Luo^#¹, Lixia Wang^#², Zhengrong Chen³, Ming Liu⁴, Yixue Zhao¹, Yucan Wu¹, Bing Huang⁵, Ping Wang¹

Affiliations

¹ Department of Neonatology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
² College of Pediatrics, Guangzhou Medical University, Guangzhou, China.
³ Department of Pathology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
⁴ Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
⁵ Department of Gastroenterology, Guangdong Provincial Key Laboratory of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

^# Contributed equally.

Abstract

E11 causes acute fulminant hepatitis in newborns. We investigated the pathological changes of different tissues from premature male twins who died due to E11 infection. The E11 expression level was higher in the liver than in other tissues. IP10 was upregulated in liver tissue in the patient group, and might be regulated by IFNAR and IRF7, whereas IFNα was regulated by IFNAR or IRF5.

Keywords: E11; IFNα; IP10; acute fulminant hepatitis; premature male twins.

MeSH terms

Chemokine CXCL10
Fatal Outcome
Humans
Infant, Newborn
Infant, Premature*
Interferon-alpha
Liver* / pathology
Male

Substances

Chemokine CXCL10
Interferon-alpha
CXCL10 protein, human