In our study, an experimental model of Ag-induced arthritis (AIA) in mice was shown to mimic several aspects of the clinical-associated comorbidity periodontal disease (PD), through increased systemic reactivity to auto-Ags in a way dependent on oral microbiota. Moreover, it was shown that TNF-α might play an important role in AIA-induced PD, which was demonstrated by the use of an anti–TNF-α therapy with infliximab (the protocol was based on previous publications listed below).
Infliximab is a chimeric IgG1κ mAb, composed of human and murine regions, raised against TNF-α. Several studies demonstrate that infliximab may neutralize both human and murine TNF-α (1–18). There are many published studies in the literature supporting the effectiveness of using this Ab under different experimental conditions in murine models, including experimental colitis (1, 10), hypothalamic inflammation (2), allergic rhinitis (3), experimental Alzheimer’s disease (4), chronic hepatitis C (5), mucopolysaccharidoses (6), aneurysm (7), in vitro conditions by using macrophages (8),murine aortic transplant model (9), HSV-induced inflammation (11), Fas stimulation (12), acute asthma (13), aortic calcification during diabetes (14), and distinct mouse models of joint inflammation (15–18). In several of these studies, the use of isotype controls did not mimic the beneficial effects of infliximab in reducing TNF-α levels and signs of inflammation (4, 7, 9, 15). Under our conditions, although not mentioned in the original study, the use of isotype control Abs in further experiments was not able to prevent signs of AIA and PD. Therefore, we do believe there is enough evidence in the literature to support the use of this tool to investigate the role of TNF-α in mice.