Comparison of Nasal Cytokine Profiles of Human Metapneumovirus and Respiratory Syncytial Virus

Overview

Journal Asia Pac Allergy

Publisher Wolters Kluwer

Date 2017 Nov 3

PMID 29094018

Citations 8

Authors

Jin-Sung Park

Young-Ho Kim

Eunmi Kwon

Zak Callaway

Takao Fujisawa

Chang-Keun Kim

Affiliations

Soon will be listed here.

Abstract

Background: Human metapneumovirus (hMPV) and respiratory syncytial virus (RSV) share some epidemiological and clinical characteristics; however, few studies have examined the mechanisms by which these viruses induce airway inflammation.

Objective: This study was undertaken to compare cytokine profiles in hMPV and RSV patients to investigate possible differences in inflammatory pathways.

Methods: Nasopharyngeal aspirate specimens were collected from 1,008 pediatric patients hospitalized for acute lower respiratory tract infection with wheezing and 20 normal healthy controls. Patients were tested for 7 common respiratory viruses then divided into hMPV (n = 35) and RSV groups (n = 67). T helper (Th) 1 (interferon [IFN]-γ), Th2 (interleukin [IL]-4, eotaxin) and Th17 (IL-1β, IL-6) cytokine profiles were analyzed in the 3 groups.

Results: IFN-γ and IL-2 levels were significantly increased in the hMPV and RSV groups compared to the control group ( < 0.0001 and < 0.0001, respectively). IL-4 levels were significantly higher in the RSV group compared to the hMPV and control groups ( = 0.0003 and < 0.0001, respectively). Eotaxin levels showed a tendency to be higher in the RSV group compared to the hMPV group ( = 0.0580), and significantly higher compared to the control group ( < 0.0001). IL-1β levels were significantly higher in the hMPV compared to the RSV group ( < 0.0001), and IL-6 levels were significantly higher in the hMPV group compared to the control group ( < 0.0001).

Conclusion: Our results suggest that hMPV and RSV have different inflammatory mechanisms. hMPV induces airway inflammation by the Th17 pathway through release of IL-1β and IL-6, whereas RSV acts through the Th2 pathway.

Citing Articles

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