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 2 Gene sets enriched in human monocytes stimulated with N. meningitidis vs control

Name of hallmark gene set	Description^a	FDR	Number of genes in the gene set	Founder gene sets^b
Interferon alpha response	Genes up-regulated in response to alpha interferon proteins	<0.001	97	82
Interferon gamma response	Genes up-regulated in response to IFNG	<0.001	200	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
Allograft rejection	Genes up-regulated during transplant rejection	<0.001	200	190
IL6 JAK-STAT3 signalling	Genes up-regulated by IL6 [via STAT3, e.g., during acute phase response]	<0.001	87	24
IL2 STAT5 signaling	Genes up-regulated by STAT5 in response to IL2 stimulation	<0.001	200	13
KRAS signaling down	Genes down-regulated by KRAS activation	<0.001	200	16
KRAS signaling up	Genes up-regulated by KRAS activation	<0.001	200	14
Apoptosis	Genes mediating programmed cell death (apoptosis) by activation of caspases	<0.001	161	80
Complement	Genes encoding components of the complement system, which is part of the innate immune system	0.001	200	71
Epithelial mesenchymal transition	Genes defining epithelial-mesenchymal transition, as in wound healing, fibrosis and metastasis	0.001	200	106
Coagulation	Genes encoding components of blood coagulation system; also up-regulated in platelets	0.015	138	71
Estrogen response late	Genes defining late response to estrogen	0.007	200	59
Hypoxia	Genes up-regulated in response to low oxygen levels (hypoxia)	0.015	200	87

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