Transcriptomic data from two primary cell models stimulating human monocytes suggest inhibition of oxidative phosphorylation and mitochondrial function by N. meningitidis which is partially up-regulated by IL-10

Table 3 Gene sets enriched in human monocytes stimulated with N. meningitidis and IL-10 vs control

Name of hallmark gene set	Description^a	FDR	Number of genes in the gene set	Founder gene sets^b
Interferon gamma response	Genes up-regulated in response to IFNG	<0.001	200	82
Interferon alpha response	Genes up-regulated in response to alpha interferon proteins.	<0.001	97	82
TNF signaling via NfkB	Genes regulated by NF-kB in response to TNF	<0.001	200	120
Inflammatory response	Genes defining inflammatory response	<0.001	200	120
IL2 STAT5 signaling	Genes up-regulated by STAT5 in response to IL2 stimulation.	<0.001	200	13
IL6 JAK-STAT3 signaling	Genes up-regulated by IL6 [via STAT3, e.g., during acute phase response]	<0.001	87	24
Allograft rejection	Genes up-regulated during transplant rejection	<0.001	200	190
Complement	Genes encoding components of the complement system, which is part of the innate immune system	<0.001	200	71
KRAS signaling up	Genes up-regulated by KRAS activation	0.003	200	14
KRAS signaling down	Genes down-regulated by KRAS activation	0.007	200	16
Apoptosis	Genes mediating programmed cell death (apoptosis) by activation of caspases	0.007	161	80
Hypoxia	Genes up-regulated in response to low oxygen levels (hypoxia)	0.039	200	87

^aDescription of the gene sets were obtained from the Molecular Signatures Database
^bFounder gene sets constitute the original experiments associating the genes with specified functions or biological processes

ISSN: 1471-2172