Virus infections and sudden death in infancy: the role of interferon-
Respiratory infections have been implicated in Sudden Infant Death Syndrome (SIDS). As interferon- (IFN-) is a major response to virus infection, we examined: 1 ) single nucleotide polymorphism (SNP), IFNG T+874A, in SIDS infants, their parents and ethnic groups with different incidences of SIDS;...
Main Authors: | , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Frontiers Media S.A.
2015-03-01
|
Series: | Frontiers in Immunology |
Subjects: | |
Online Access: | http://journal.frontiersin.org/Journal/10.3389/fimmu.2015.00107/full |
id |
doaj-5f987fcba6944013b01d439a5ef99ee6 |
---|---|
record_format |
Article |
spelling |
doaj-5f987fcba6944013b01d439a5ef99ee62020-11-25T00:30:00ZengFrontiers Media S.A.Frontiers in Immunology1664-32242015-03-01610.3389/fimmu.2015.00107128520Virus infections and sudden death in infancy: the role of interferon-Sophia eMoscovis0Sophia eMoscovis1Ann eGordon2Osama eAlmadani3Maree eGleeson4Maree eGleeson5Rodney J. Scott6Rodney J. Scott7Rodney J. Scott8Sharron eHall9Sharron eHall10Sharron eHall11Christine eBurns12Christine eBurns13Christine eBurns14Caroline eBlackwell15Caroline eBlackwell16University of NewcastleHunter Medical Research InstituteUniversity of EdinburghUniversity of EdinburghUniversity of NewcastleHunter Medical Research InstituteUniversity of NewcastleHunter Medical Research InstituteHunter Area Pathology ServiceUniversity of NewcastleHunter Medical Research InstituteHunter Area Pathology ServiceUniversity of NewcastleHunter Medical Research InstituteHunter Area Pathology ServiceUniversity of NewcastleHunter Medical Research InstituteRespiratory infections have been implicated in Sudden Infant Death Syndrome (SIDS). As interferon- (IFN-) is a major response to virus infection, we examined: 1 ) single nucleotide polymorphism (SNP), IFNG T+874A, in SIDS infants, their parents and ethnic groups with different incidences of SIDS; 2) model systems with a monocytic cell line (THP-1) and human peripheral blood monocytes (PBMC) for effects of levels of IFN- on inflammatory responses to bacterial antigens identified in SIDS; 3) interactions between genetic and environmental factors on IFN- responses. IFNG T+874A genotypes were determined for: SIDS infants from three countries; families who had a SIDS death; populations with high (Indigenous Australian), medium (Caucasian) and low (Bangladeshi) SIDS incidences. The effect of IFN- on cytokine responses to endotoxin was examined in model systems with THP-1 cells and human PBMC to endotoxin. The IFN-γ responses to endotoxin and toxic shock syndrome toxin (TSST-1) were assessed in relation to genotype, gender and reported smoking. There was a marginal association with IFNG T+874A genotype and SIDS (P =0.06). Indigenous Australians had significantly higher proportions of the IFNG T+874A SNP (TT) associated with high responses of IFN-. THP-1 cells showed a dose dependent effect of IFN- on cytokine responses to endotoxin. For PBMC, IFN- enhanced interleukin (IL)-1β, IL-6 and tumor necrosis factor- (TNF-) responses but reduced IL-8 and IL-10. Active smoking had a suppressive effect on baseline levels of IFN-. There was no effect of gender or genotype on IFN- responses to bacterial antigens tested;; however, significant differences were observed between genotypes in relation to smoking. The results indicate virus infections contribute to dysregulation of cytokine responses to bacterial antigens and studies on physiological effects of genetic factors must include controls for recent or concurrent infection and exposure to cigarette smoke.http://journal.frontiersin.org/Journal/10.3389/fimmu.2015.00107/fullCytokinescigarette smokeethnicitysudden infant death syndromeIFN- |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Sophia eMoscovis Sophia eMoscovis Ann eGordon Osama eAlmadani Maree eGleeson Maree eGleeson Rodney J. Scott Rodney J. Scott Rodney J. Scott Sharron eHall Sharron eHall Sharron eHall Christine eBurns Christine eBurns Christine eBurns Caroline eBlackwell Caroline eBlackwell |
spellingShingle |
Sophia eMoscovis Sophia eMoscovis Ann eGordon Osama eAlmadani Maree eGleeson Maree eGleeson Rodney J. Scott Rodney J. Scott Rodney J. Scott Sharron eHall Sharron eHall Sharron eHall Christine eBurns Christine eBurns Christine eBurns Caroline eBlackwell Caroline eBlackwell Virus infections and sudden death in infancy: the role of interferon- Frontiers in Immunology Cytokines cigarette smoke ethnicity sudden infant death syndrome IFN- |
author_facet |
Sophia eMoscovis Sophia eMoscovis Ann eGordon Osama eAlmadani Maree eGleeson Maree eGleeson Rodney J. Scott Rodney J. Scott Rodney J. Scott Sharron eHall Sharron eHall Sharron eHall Christine eBurns Christine eBurns Christine eBurns Caroline eBlackwell Caroline eBlackwell |
author_sort |
Sophia eMoscovis |
title |
Virus infections and sudden death in infancy: the role of interferon- |
title_short |
Virus infections and sudden death in infancy: the role of interferon- |
title_full |
Virus infections and sudden death in infancy: the role of interferon- |
title_fullStr |
Virus infections and sudden death in infancy: the role of interferon- |
title_full_unstemmed |
Virus infections and sudden death in infancy: the role of interferon- |
title_sort |
virus infections and sudden death in infancy: the role of interferon- |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Immunology |
issn |
1664-3224 |
publishDate |
2015-03-01 |
description |
Respiratory infections have been implicated in Sudden Infant Death Syndrome (SIDS). As interferon- (IFN-) is a major response to virus infection, we examined: 1 ) single nucleotide polymorphism (SNP), IFNG T+874A, in SIDS infants, their parents and ethnic groups with different incidences of SIDS; 2) model systems with a monocytic cell line (THP-1) and human peripheral blood monocytes (PBMC) for effects of levels of IFN- on inflammatory responses to bacterial antigens identified in SIDS; 3) interactions between genetic and environmental factors on IFN- responses. IFNG T+874A genotypes were determined for: SIDS infants from three countries; families who had a SIDS death; populations with high (Indigenous Australian), medium (Caucasian) and low (Bangladeshi) SIDS incidences. The effect of IFN- on cytokine responses to endotoxin was examined in model systems with THP-1 cells and human PBMC to endotoxin. The IFN-γ responses to endotoxin and toxic shock syndrome toxin (TSST-1) were assessed in relation to genotype, gender and reported smoking. There was a marginal association with IFNG T+874A genotype and SIDS (P =0.06). Indigenous Australians had significantly higher proportions of the IFNG T+874A SNP (TT) associated with high responses of IFN-. THP-1 cells showed a dose dependent effect of IFN- on cytokine responses to endotoxin. For PBMC, IFN- enhanced interleukin (IL)-1β, IL-6 and tumor necrosis factor- (TNF-) responses but reduced IL-8 and IL-10. Active smoking had a suppressive effect on baseline levels of IFN-. There was no effect of gender or genotype on IFN- responses to bacterial antigens tested;; however, significant differences were observed between genotypes in relation to smoking. The results indicate virus infections contribute to dysregulation of cytokine responses to bacterial antigens and studies on physiological effects of genetic factors must include controls for recent or concurrent infection and exposure to cigarette smoke. |
topic |
Cytokines cigarette smoke ethnicity sudden infant death syndrome IFN- |
url |
http://journal.frontiersin.org/Journal/10.3389/fimmu.2015.00107/full |
work_keys_str_mv |
AT sophiaemoscovis virusinfectionsandsuddendeathininfancytheroleofinterferon AT sophiaemoscovis virusinfectionsandsuddendeathininfancytheroleofinterferon AT annegordon virusinfectionsandsuddendeathininfancytheroleofinterferon AT osamaealmadani virusinfectionsandsuddendeathininfancytheroleofinterferon AT mareeegleeson virusinfectionsandsuddendeathininfancytheroleofinterferon AT mareeegleeson virusinfectionsandsuddendeathininfancytheroleofinterferon AT rodneyjscott virusinfectionsandsuddendeathininfancytheroleofinterferon AT rodneyjscott virusinfectionsandsuddendeathininfancytheroleofinterferon AT rodneyjscott virusinfectionsandsuddendeathininfancytheroleofinterferon AT sharronehall virusinfectionsandsuddendeathininfancytheroleofinterferon AT sharronehall virusinfectionsandsuddendeathininfancytheroleofinterferon AT sharronehall virusinfectionsandsuddendeathininfancytheroleofinterferon AT christineeburns virusinfectionsandsuddendeathininfancytheroleofinterferon AT christineeburns virusinfectionsandsuddendeathininfancytheroleofinterferon AT christineeburns virusinfectionsandsuddendeathininfancytheroleofinterferon AT carolineeblackwell virusinfectionsandsuddendeathininfancytheroleofinterferon AT carolineeblackwell virusinfectionsandsuddendeathininfancytheroleofinterferon |
_version_ |
1725328493857734656 |