Table 4.

IPA Analysis of Pathways

Functional grouping of canonical pathways assessed by IPA	Infected vehicle	Anti-Ang2 antibody	Anti-TNF antibody	Antibody combination	Pathogen-Free
Granulocyte adhesion and diapedesis	−20.9	−20.4	−11.7	0.8	0
Other leukocyte adhesion and diapedesis	−14.3	−13.8	−8.4	−2.7	0
Leukocyte extravasation signaling	−12.9	−10.5	−7.8	−3.1	0
Macrophages in arthritis	−16.4	−14.7	−9.9	−3.2	0
Macrophage NO and ROS	−13.9	−12.3	−9.6	−2.5	0
Dendritic cell maturation	−12.1	−12.1	−8.3	−4.6	0
T-cell receptor signaling	−7.5	−7.0	−5.9	−4.3	0
T and B cells in arthritis	−7.6	−7.3	−6.5	−4.0	0
B-cell activating factor signaling	−5.3	−4.9	−2.9	−0.2	0
B-cell receptor signaling	−13.4	−12.2	−10.4	−10.1	0
Acute phase response signaling	−14.8	−13.5	−10.2	−4.8	0
TNFR1 signaling	−11.6	−11.2	−10.0	−5.5	0
TNFR2 signaling	−10.8	−10.3	−7.8	0.5	0
TNFSF13 signaling	−5.6	−5.2	−3.1	−0.3	0
IL-6 signaling	−16.5	−15.7	−10.8	−1.7	0
IL-8 signaling	−12.1	−10.0	−6.4	−4.2	0
IL-10 signaling	−16.4	−16.1	−14.1	−3.9	0
IL-17 signaling	−7.6	−6.9	−6.2	−3.8	0
IL-17 signaling in airway cells	−10.4	−10.1	−8.4	−6.3	0
IL-17 signaling in fibroblasts	−10.6	−9.6	−7.3	−4.9	0
IL-17 signaling in arthritis	−8.0	−8.0	−6.6	−2.4	0
fMLP signaling in neutrophils	−8.8	−8.6	−6.7	−4.9	0
Toll-like receptor signaling	−11.1	−10.8	−8.1	−1.1	0
iNOS signaling	−13.2	−12.8	−10.9	−5.6	0
NF-κB signaling	−13.8	−12.5	−6.1	−4.0	0
PPAR signaling	−9.6	−9.1	−3.9	−0.6	0
p38 MAPK signaling	−6.7	−6.3	−4.8	0.0	0
LPS-stimulated MAPK signaling	−7.4	−6.8	−4.8	−3.2	0
Death receptor signaling	−13.2	−13.0	−10.8	−7.2	0
Apoptosis signaling	−13.1	−12.6	−10.6	−8.4	0
Glucocorticoid receptor signaling	−11.6	−10.8	−8.6	−4.5	0
Integrin signaling∗	−14.3	−8.3	−7.9	−10.0	0
Fibrosis-related signaling	−10.6	−8.2	−4.9	4.2	0
Lymphotoxin β receptor signaling∗	−6.1	−6.1	−3.8	−4.0	0
Angiopoietin signaling	−4.5	−4.2	−3.0	−1.7	0

Pathways activated by infection and suppressed by treatment. The infected vehicle column lists log10 of P values for pathways assessed by IPA for genes (condition A), where expression increased during Mycoplasma pulmonis infection for 7 days, relative to pathogen-free (scaled to 0), and the increase was suppressed by treatment. Three treatment columns show relative efficacy, calculated as log10 of P values for infected vehicle group minus the log10 of P values for the corresponding treatment. Values closer to 0 reflect smaller differences from the pathogen-free baseline.

Ang2, angiopoietin-2; fMLP, N-formyl-Met-Leu-Phe; iNOS, inducible NO synthase; IPA, Ingenuity Pathway Analysis; LPS, lipopolysaccharide; MAPK, mitogen-activated protein kinase; NO, nitric oxide; PPAR, peroxisome proliferator-activated receptor; ROS, reactive oxygen species; TNF, tumor necrosis factor; TNFR, TNF receptor; TNFSF, TNF superfamily.

^∗For all but two of these pathways, the antibody combination reduced the activity closer to the baseline than the other treatments.