genomewide characterization of host-pathogen interactions by ...

Maren Depke
Results
Gene Expression Pattern of Bone-Marrow Derived Macrophages after Interferon-gamma Treatment
Table R.3.6: IFN-γ influence on gene expression of GTPase family members in BMM of BALB/c and C57BL/6 mice.
Rosetta Resolver Annotation fold change a strain
difference
gene
Entrez
description
alias
name
Gene ID
BALB/c C57BL/6 control IFN-γ
Igtp interferon gamma induced GTPase Irgm3 16145 17.4 13.5
Iigp1 interferon inducible GTPase 1 Iigp, Irga6 60440 100.0 100.0
Irgm1 immunity-related GTPase family M member 1
Ifi1, Irgm, Iigp3, Iipg3,
LRG-47
15944 6.9 11.2
Tgtp T-cell specific GTPase Tgtp, Gtp2, Mg21, Irgb6 21822 49.0 100.0
Gbp1 guanylate binding protein 1 Mpa1, Gbp-1, Mag-1 14468 43.9 6.0 x x
Gbp2 guanylate binding protein 2 14469 17.2 31.2 x
Gbp3 guanylate binding protein 3 Gbp4 55932 21.7 15.6
Gbp4 guanylate binding protein 4 Mpa2, Mag-2, Mpa-2 17472 60.6 94.3
Gbp5 guanylate binding protein 5 Gbp5a 229898 50.7 66.8
Gbp6 guanylate binding protein 6 Gbp7 229900 9.3 7.2
Mx1 myxovirus (influenza virus) resistance 1 Mx, Mx-1 17857 10.8 6.9 x
Mx2 myxovirus (influenza virus) resistance 2 Mx-2 17858 6.1 3.5 x
Gvin1 GTPase, very large interferon inducible 1 VLIG, Iigs1, VLIG-1 74558 4.6 6.7
a Fold change values were calculated from expression intensities of IFN-γ treated BMM in comparison to control BMM from the mean
of three biological replicates. Differential expression in statistical testing with p* < 0.01 and a minimal absolute fold change of 1.5 is
indicated in bold.
BMM after IFN-γ treatment induced the expression of complement system components. Of
the classical activation pathway, the C1 subcomponents C1qa, C1qb, C1qc, C1r, and C1rb were
induced, and of the alternative pathway factor B (Cfb). Induced component C3 takes part in all
activation pathways and especially in the amplification loop of complement activation
(Table R.3.7).
Table R.3.7: IFN-γ influence on gene expression of complement components in BMM of BALB/c and C57BL/6 mice.
Rosetta Resolver Annotation fold change a strain
difference
gene
Entrez
description
alias
name
Gene ID
BALB/c C57BL/6 control IFN-γ
C1qa
complement component 1, q subcomponent, alpha
polypeptide
C1q 12259 1.3 2.3
C1qb
complement component 1, q subcomponent, beta
polypeptide
12260 2.2 2.8 x x
C1qc complement component 1, q subcomponent, C chain C1qg, Ciqc 12262 1.6 2.8 x
C1r complement component 1, r subcomponent C1ra, C1rb 50909 4.3 4.7
C1rb complement component 1, r subcomponent, b 270510 5.5 6.3
C3 complement component 3 ASP, Plp 12266 4.9 5.6
Cfb complement factor B B, Bf, Fb, H2-Bf 14962 14.1 19.5
a Fold change values were calculated from expression intensities of IFN-γ treated BMM in comparison to control BMM from the mean
of three biological replicates. Differential expression in statistical testing with p* < 0.01 and a minimal absolute fold change of 1.5 is
indicated in bold.
Other immune function related gene expression changes were conspicuous in BMM after
IFN-γ treatment. Inducible nitric oxide synthase 2 (Nos2) was increased as expected in treated
BMM. The enzyme produces NO, which acts as antimicrobial effector and as signal mediator
during immune defense processes. Another induced enzyme gene was kynureninase (Lkynurenine
hydrolase, Kynu) whose product is involved in the degradation of kynurenines, toxic
intermediates with signaling properties. Their production is amplified in inflammation settings by
the induction of indoleamine 2,3-dioxygenase (IDO), which catalyzes the first step of tryptophan
degradation in the kyurenine pathway. Interestingly, the Ido gene was not differentially
expressed in BMM after IFN-γ treatment, expression was even absent in the majority of samples.
The tryptophanyl-tRNA synthetase (Wars) was induced in IFN-γ treated BMM. Prostaglandin-
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