Raw data to "Pro-resolving lipid mediator lipoxin A4 attenuates neuro-inflammation by modulating T cell responses and modifies the spinal cord lipidome"

<p>Background: Impairments in timely resolving inflammation is now considered a key hallmark of chronic inflammation and the development of neurodegenerative diseases such as multiple sclerosis (MS). Lipoxins are among the mediators of resolution of inflammation and their role in MS is scarce.</p> <p>Results: We treated experimental autoimmune encephalomyelitis (EAE) mice, the experimental model of MS, with lipoxin A4 (LXA4) daily and intraperitoneally either mimicking a prophylactic treatment (from day 8 post immunization, namely before the acute phase) or a therapeutic treatment&nbsp; (from day 21 post immunization, namely at the peak of disease)&nbsp; and both until the end of the experiment with 100 ng/mouse of LXA4 or vehicle. When given in a prophylactic setting, LXA4 treatment significantly ameliorated EAE clinical scores (Fig.1A), counteracted the reduction in the body weight (Fig.1B) and reduced disease severity (Fig.1C) compared to EAE vehicle-treated mice. Moreover, histological examination of the spinal cord at the peak of the disease revealed a profound reduction of CD45+ inflammatory cells in LXA4-treated as compared to vehicle-treated EAE mice (Fig. 1D). However, LXA4 treatment in a therapeutic setting, slightly reduced EAE clinical scores (Fig. 1E) and did not modify body weight compared to the EAE-vehicle treaded mice (Fig.1F).</p> <p>Conclusions: These data suggest that boosting resolution of inflammation in vivo can halt clinical symptoms in experimental MS and eventually reduce or halt disease progression.</p>