Nasopharyngeal prostaglandin E2 in infant bronchiolitis

Kim Griggs; Kevin Forsyth; Dani Dixon

doi:10.3109/01902148.2011.622427

Nasopharyngeal prostaglandin E2 in infant bronchiolitis

Kim Griggs, Kevin Forsyth, Dani Dixon

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

The mechanism by which severe bronchiolitis can result in the development of recurrent childhood wheeze is unclear. However, mucosal inflammation and immune activation may play a major role. Prostaglandin (PG) E2 has been highlighted as a possible therapeutic target for both the treatment of bronchiolitis and the prevention of subsequent airway hyperresponsiveness. The aim of this pilot study was to examine PGE2 in the airways of infants hospitalised with bronchiolitis. Nasopharyngeal aspirates (NPA) were collected from 18 infants within 12 hours of admission and assayed by enzyme immunoassays for PGE2, interleukin (IL)-10, and IL-12, as well as cyclooxygenase (COX) 1 and 2 activity. NPA PGE2 concentration correlated with length of illness preadmission, but was not related to disease severity, causal virus, or IL-10. NPA COX 1 and 2 activity and IL-12 were all below the level of detection. Neither NPA PGE2 nor disease severity was related to development of recurrent wheeze over 3 years following bronchiolitis. These data suggest that nasopharygeal PGE2 at hospital admission may be neither directly causal or diagnostic of severity of infant bronchiolitis, or prognostic of development of recurrent wheeze. However, large-cohort temporal examinations are required to adequately define this mediator as a therapeutic target for bronchiolitis.

Original language	English
Pages (from-to)	600-605
Number of pages	6
Journal	Experimental Lung Research
Volume	37
Issue number	10
DOIs	https://doi.org/10.3109/01902148.2011.622427
Publication status	Published - Dec 2011

Bibliographical note

Funding Information:
Funding for this study was provided by the Financial Markets Fund for Children, the Channel 7 Children’s Research Foundation, and the Flinders Medical Centre Foundation. The authors gratefully acknowledge the infants and parents who participated in the study. The authors also thank Dr. Victoria Atkinson for performing the RDAI scoring and Ms. Malgosia Krupa for technical assistance. Address correspondence to Dani-Louise Dixon, Intensive and Critical Care Unit, Flinders Medical Centre, Bedford Park, South Australia 5042, Australia. E-mail: [email protected]

Copyright:
Copyright 2011 Elsevier B.V., All rights reserved.

Keywords

Asthma
Cytokines
Nasopharygeal aspirate
Pulmonary inflammation
Respiratory syncytial virus

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.3109/01902148.2011.622427

Cite this

@article{bb3f9913d2c64d0ea83af0814d4e116d,

title = "Nasopharyngeal prostaglandin E2 in infant bronchiolitis",

abstract = "The mechanism by which severe bronchiolitis can result in the development of recurrent childhood wheeze is unclear. However, mucosal inflammation and immune activation may play a major role. Prostaglandin (PG) E2 has been highlighted as a possible therapeutic target for both the treatment of bronchiolitis and the prevention of subsequent airway hyperresponsiveness. The aim of this pilot study was to examine PGE2 in the airways of infants hospitalised with bronchiolitis. Nasopharyngeal aspirates (NPA) were collected from 18 infants within 12 hours of admission and assayed by enzyme immunoassays for PGE2, interleukin (IL)-10, and IL-12, as well as cyclooxygenase (COX) 1 and 2 activity. NPA PGE2 concentration correlated with length of illness preadmission, but was not related to disease severity, causal virus, or IL-10. NPA COX 1 and 2 activity and IL-12 were all below the level of detection. Neither NPA PGE2 nor disease severity was related to development of recurrent wheeze over 3 years following bronchiolitis. These data suggest that nasopharygeal PGE2 at hospital admission may be neither directly causal or diagnostic of severity of infant bronchiolitis, or prognostic of development of recurrent wheeze. However, large-cohort temporal examinations are required to adequately define this mediator as a therapeutic target for bronchiolitis.",

keywords = "Asthma, Cytokines, Nasopharygeal aspirate, Pulmonary inflammation, Respiratory syncytial virus",

author = "Kim Griggs and Kevin Forsyth and Dani Dixon",

note = "Funding Information: Funding for this study was provided by the Financial Markets Fund for Children, the Channel 7 Children{\textquoteright}s Research Foundation, and the Flinders Medical Centre Foundation. The authors gratefully acknowledge the infants and parents who participated in the study. The authors also thank Dr. Victoria Atkinson for performing the RDAI scoring and Ms. Malgosia Krupa for technical assistance. Address correspondence to Dani-Louise Dixon, Intensive and Critical Care Unit, Flinders Medical Centre, Bedford Park, South Australia 5042, Australia. E-mail: [email protected] Copyright: Copyright 2011 Elsevier B.V., All rights reserved.",

year = "2011",

month = dec,

doi = "10.3109/01902148.2011.622427",

language = "English",

volume = "37",

pages = "600--605",

journal = "Experimental Lung Research",

issn = "0190-2148",

publisher = "Informa Healthcare",

number = "10",

}

TY - JOUR

T1 - Nasopharyngeal prostaglandin E2 in infant bronchiolitis

AU - Griggs, Kim

AU - Forsyth, Kevin

AU - Dixon, Dani

N1 - Funding Information: Funding for this study was provided by the Financial Markets Fund for Children, the Channel 7 Children’s Research Foundation, and the Flinders Medical Centre Foundation. The authors gratefully acknowledge the infants and parents who participated in the study. The authors also thank Dr. Victoria Atkinson for performing the RDAI scoring and Ms. Malgosia Krupa for technical assistance. Address correspondence to Dani-Louise Dixon, Intensive and Critical Care Unit, Flinders Medical Centre, Bedford Park, South Australia 5042, Australia. E-mail: [email protected] Copyright: Copyright 2011 Elsevier B.V., All rights reserved.

PY - 2011/12

Y1 - 2011/12

N2 - The mechanism by which severe bronchiolitis can result in the development of recurrent childhood wheeze is unclear. However, mucosal inflammation and immune activation may play a major role. Prostaglandin (PG) E2 has been highlighted as a possible therapeutic target for both the treatment of bronchiolitis and the prevention of subsequent airway hyperresponsiveness. The aim of this pilot study was to examine PGE2 in the airways of infants hospitalised with bronchiolitis. Nasopharyngeal aspirates (NPA) were collected from 18 infants within 12 hours of admission and assayed by enzyme immunoassays for PGE2, interleukin (IL)-10, and IL-12, as well as cyclooxygenase (COX) 1 and 2 activity. NPA PGE2 concentration correlated with length of illness preadmission, but was not related to disease severity, causal virus, or IL-10. NPA COX 1 and 2 activity and IL-12 were all below the level of detection. Neither NPA PGE2 nor disease severity was related to development of recurrent wheeze over 3 years following bronchiolitis. These data suggest that nasopharygeal PGE2 at hospital admission may be neither directly causal or diagnostic of severity of infant bronchiolitis, or prognostic of development of recurrent wheeze. However, large-cohort temporal examinations are required to adequately define this mediator as a therapeutic target for bronchiolitis.

AB - The mechanism by which severe bronchiolitis can result in the development of recurrent childhood wheeze is unclear. However, mucosal inflammation and immune activation may play a major role. Prostaglandin (PG) E2 has been highlighted as a possible therapeutic target for both the treatment of bronchiolitis and the prevention of subsequent airway hyperresponsiveness. The aim of this pilot study was to examine PGE2 in the airways of infants hospitalised with bronchiolitis. Nasopharyngeal aspirates (NPA) were collected from 18 infants within 12 hours of admission and assayed by enzyme immunoassays for PGE2, interleukin (IL)-10, and IL-12, as well as cyclooxygenase (COX) 1 and 2 activity. NPA PGE2 concentration correlated with length of illness preadmission, but was not related to disease severity, causal virus, or IL-10. NPA COX 1 and 2 activity and IL-12 were all below the level of detection. Neither NPA PGE2 nor disease severity was related to development of recurrent wheeze over 3 years following bronchiolitis. These data suggest that nasopharygeal PGE2 at hospital admission may be neither directly causal or diagnostic of severity of infant bronchiolitis, or prognostic of development of recurrent wheeze. However, large-cohort temporal examinations are required to adequately define this mediator as a therapeutic target for bronchiolitis.

KW - Asthma

KW - Cytokines

KW - Nasopharygeal aspirate

KW - Pulmonary inflammation

KW - Respiratory syncytial virus

UR - http://www.scopus.com/inward/record.url?scp=81355161124&partnerID=8YFLogxK

U2 - 10.3109/01902148.2011.622427

DO - 10.3109/01902148.2011.622427

M3 - Article

SN - 0190-2148

VL - 37

SP - 600

EP - 605

JO - Experimental Lung Research

JF - Experimental Lung Research

IS - 10

ER -

Nasopharyngeal prostaglandin E2 in infant bronchiolitis

Abstract

Bibliographical note

Keywords

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this