Læknablaðið : fylgirit - 03.01.2017, Síða 33

X V I I I V Í S I N D A R Á Ð S T E F N A H Í
F Y L G I R I T 9 1
LÆKNAblaðið/Fylgirit 91 2017/103 33
lag við verndun spangar var innleitt. Niðurstöðurnar hvetja til frekari
rannsókna á upplifun ljósmæðra og kvenna á breyttu vinnulagi.
E 85 Greining alvarlegra meðfæddra hjartagalla á Íslandi 2000-2014
Hallfríður Kristinsdóttir1, Þórður Þórkelsson1, Hildur Harðardóttir2, Gylfi
Óskarsson1
1Læknadeild, Háskóli Íslands, 2 Kvennadeild, Landspítala
hallfridurkr@gmail.com
Inngangur: Nýlegar rannsóknir í nágrannalöndunum sýna að vaxandi
hlutfall (13-30%) alvarlegra meðfæddra hjartagalla greinast ekki fyrr en
eftir útskrift af fæðingarstofnun og eru börnin þá oft orðin alvarlega veik.
Sein greining hefur verið tengd verri horfum. Markmið rannsóknarinnar
er að meta hvenær alvarlegir meðfæddir hjartagallar greinast á Íslandi og
hvort sein greining þeirra sé vandamál. Niðurstöðurnar gætu haft áhrif á
skipulag nýburaskoðunar og afstöðu til nýrra greiningaraðferða.
Efniviður og aðferðir: Rannsóknin náði til allra lifandi fæddra barna
á Íslandi á tímabilinu 2000-2014, auk fóstureyðinga vegna hjartagalla.
Alvarlegur meðfæddur hjartagalli var skilgreindur sem galli sem þarfnast
inngrips eða veldur dauðsfalli á fyrsta ári lífs, eða leiðir til fóstureyðingar.
Klínískum upplýsingum var safnað úr sjúkraskrám barna og mæðra.
Niðurstöður: Á tímabilinu fundust 155 lifandi fædd börn sem greindust
með alvarlegan hjartagalla. Nýgengið var 2,33/1000 lifandi fædd börn.
Á tímabilinu voru 33 fóstureyðingar framkvæmdar vegna hjartagalla.
Algengustu hjartagallarnir voru ósæðarþrengsl (33/188), op milli slegla
(24/188) og vanþroska vinstra hjarta (21/188). 69 af 188 (36,7%) greindust
á meðgöngu. 100 börn (53,2%) greindust skömmu eftir fæðingu, fyrir
útskrift af fæðingarstofnun. 19 börn (10,1%) greindust seint, það er eftir
útskrift af fæðingarstofnun. Sá galli sem oftast greindist seint var ósæðar-
þrengsli (6/19). Ekkert barn með víxlun meginslagæða greindist á með-
göngu, en þau börn voru oft alvarlega veik við greiningu.
Ályktanir: Meðgöngugreining og skoðun nýbura fyrir útskrift af
fæðingarstofnun skilar ágætum árangri í greiningu alvarlegra meðfæddra
hjartagalla á Íslandi. Þó væri æskilegt að fækka þeim börnum sem veikjast
lífhættulega með bættri greiningu á meðgöngu og í nýburaskoðun.
E 86 Bordetella adenylate cyclase toxin manipulates innate defences
and disrupts barrier function of lung epithelial cells
Árni Ásbjarnarson1, Nikhil N. Kulkarni1, Shakir Hasan2, Radim Osicka2, Peter
Sebo2, Guðmundur H. Guðmundsson1
1Department of Life and Environmental Sciences, Biomedical Center, 2Institute of Microbiology
of the Czech Academy of Sciences
ara39@hi.is
Introduction: The adenylate cyclase toxin (CyaA) plays a key role in
virulence of Bordetella pertussis, the causative agent of whooping cough.
CyaA penetrates various host cells and subverts their immune functions
through unregulated conversion of cytosolic ATP into the signalling
molecule adenosine 3’, 5’-cyclic monophosphate (cAMP). In this study
we looked at the effect of the toxin on an in vivo like model of airway
epithelia.
Methods: We examined the effects of CyaA toxin on respiratory epitheli-
um using the air-liquid interface (ALI) differentiated human bronchial
epithelial cell line VA10. Effects were measured and analysed using
trans-epithelial resistance (TER), quantitative real time PCR, western,
ELISA and immunohistochemical staining.
Results: While a non-enzymatic CyaA AC- toxoid was unable to elevate
cAMP and had no effects, the treatment of ALI-differentiated VA10 cells
with CyaA from the basolateral side lead to enhanced mucin Muc5AC
expression and disruption of the physical barrier integrity. This was
characterized by decreased TER due to suppression of expression and
disintegration of tight junctions. At the same time expression of genes for
antimicrobial polypeptides; cathelicidin, human beta defensin-1, lactoferr-
in and lysozyme was enhanced, however expression of the human beta
defensin-2 (hBD2) gene was strongly decreased. mRNA for the pro-in-
flammatory cytokines tumor necrosis factor-α (TNFα) and interleukin-8
was downregulated, while expression of interleukin-6 and interleukin-10
genes was enhanced after 1 h and 6 h of CyaA toxin treatment, respecti-
vely.
Conclusions: CyaA toxin-catalysed synthesis of cAMP, compromised
the epithelial barrier integrity and yielded immunomodulatory cytokine
signalling of ALI-differentiated bronchial epithelial cells.
E 87 Maedi-visna virus Vif protein modulates autophagy in
macrophages
Valgerður Andrésdóttir1, Aðalbjörg Aðalbjörnsdóttir1, Stefán R. Jónsson1, Margrét
H. Ögmundsdóttir2
1Institute For Experimental Pathology, University of Iceland. 2Department of Biochemistry and
Molecular, Faculty of Medicine, University of Iceland
valand@hi.is
Introduction: Maedi-visna virus (MVV) is a lentivirus of sheep, mainly
affecting the lungs and the nervous system. Like most other lentiviruses,
MVV requires the Vif protein for efficient replication in primary macroph-
ages and in vivo. Autophagy has recently been highlighted as a cellular
mechanism important for both innate and adaptive immune response
following infection. Several viruses, including HIV, have been shown to
modulate autophagy following infection and this autophagy regulation
has been proposed to play an important role in the replication process.
Materials and methods: Macrophages were isolated from whole sheep
blood and seeded on to 8 chamber culture slides or 6 well plates. Cells
were infected with wild-type MVV or a strain lacking the vif gene. Cells
in the culture slides were fixed at days 1, 2, 3 and 4 post infection and
immunostained with antibodies against LC3 and MVV Gag and observed
by confocal microscopy. Cells in 6 well plates were harvested at days 1,
2, 3 and 4 post infection and LC3 protein levels assessed by western blot.
Coimmunoprecipitation was performed using Flag-tagged LC3 and HA-
tagged Vif.
Results: Infection of macrophages with MVV resulted in an inhibition
of autophagy three days post infection after an initial autophagy induct-
ion. Interestingly, this effect was not seen in infection with dVif MVV.
Furthermore, CoIP results showed that MVV Vif binds to the LC3 protein,
a key protein of the autophagy pathway.
Conclusion: The results imply an important role for the MVV Vif protein
in autophagy modulation following MVV infection.
E 88 LT-K63 increases cells secreting survival factors for antibody-
secreting cells in neonatal mouse bone marrow
Auður A. Aradóttir Pind1,2, Stefanía P. Bjarnarson1,2 ,Ingileif Jónsdóttir1,2,3
1Department of Immunology, Landspitali, The National University Hospital of Iceland,
Reykjavik, Iceland, 2Faculty of Medicine, University of Iceland, Reykjavik, Iceland, 3deCODE
Genetics, Reykjavik, Iceland
aaa4@hi.is