TABLE 2 .

Activated or inactivated pathways of DE genes^a

Incubation conditions	Interaction, KEGG pathway, or disease	P valueb	Status
BL21 to medium	Cytokine-cytokine receptor interaction	9.27E–06	Activated
	Chemokine signaling pathway	4.06E–04	Activated
	Osteoclast differentiation	3.58E–03	Activated
	NF-κB signaling pathway	1.10E–02	Activated
	HTLV-I infection	1.18E–02	Activated
	Chagas disease	4.10E–02	Activated
	NOD-like receptor signaling pathway	5.48E–02	Inhibited
W3110 to medium	Cytokine-cytokine receptor interaction	4.26E–05	Activated
	Chemokine signaling pathway	1.81E–04	Activated
	NOD-like receptor signaling pathway	1.93E–04	Inhibited
	HTLV-I infection	2.67E–04	Activated
	Epstein-Barr virus infection	4.10E–04	Activated
	NF-κB signaling pathway	7.94E–04	Activated
	Osteoclast differentiation	5.47E–02	Activated

^aDE genes were input into SPIA (signaling pathway impact analysis) software to determine activated or inactivated pathways. Incubations of BL21 compared to those with medium alone resulted in the modulation of seven annotated KEGG pathways, and incubations of W3110 compared to those with medium alone also resulted in the modulation of seven annotated KEGG pathways. Common to both sets were the activation of the cytokine-cytokine receptor interaction, the chemokine signaling pathway, osteoclast differentiation, the NF-κB signaling pathway, human T-lymphotropic virus type I (HTLV-I) infection, and the inactivation of the NOD-like receptor signaling pathway.

^bP value is a Bonferroni-adjusted global P value.