**1. Introduction**

Psoriasis is a chronic autoimmune inflammatory disease characterized by skin lesions and abnormal keratinocyte proliferation. The number of cases of psoriasis vulgaris is increasing worldwide [1]. The etiology of psoriasis remains unclear, although there is evidence for genetic predisposition. The TNF receptor-associated factor 3-interacting protein 2 (*TRAF3IP2*) gene was identified in 2010 as a new susceptibility locus containing the psoriasis vulgaris disease gene in European genome-wide association studies [2]. The *TRAF3IP2* gene encodes a protein involved in IL-17 signaling, which interacts with members of the nuclear factor-kappa-B transcription factor family. Recently, an important genetic influence of the polymorphism in *TRAF3IP2* on the susceptibility to psoriasis, but not to atopic

dermatitis, was reported in a Japanese population [3,4]. Matsushima et al. [5] also reported that a genetic mutation in *Traf3ip2* mice caused an atopic dermatitis-like skin disease with hyper-IgE-emia.

The gu<sup>t</sup> microbiota observed in patients with psoriatic was less diverse when compared to that of healthy controls [6]. The gu<sup>t</sup> microbiota profile in the gu<sup>t</sup> environment has been found to significantly influence autoimmune diseases such as multiple sclerosis [7,8]. Recently, however, adults with psoriasis and/or psoriatic arthritis have learned to supplement their standard medical therapies with dietary interventions to reduce disease severity [9]. There are many reports about the relationship between immunostimulatory e ffects and dietary components of microbiota [10]. Polysaccharides are considered a dietary fiber, and work as prebiotics which are beneficial for the intestinal environment [11]. Fructo-oligosaccharides maintain intestinal barrier function, as does immunoglobulin A (IgA), in a methionine–choline-deficient mouse model of nonalcoholic steatohepatitis [12]. Secreted IgA cells in colonic tissue generate mucus that is secreted into the outermost intestinal cecal patch; the secreted mucus entraps bacteria and prevents their translocation into the tissue [13].

This study was focused on fucoidan, which is found in the cell wall matrix of brown algae. Fucoidan is a high-molecular weight (over 200,000 Daltons) sulfated polysaccharide; it consists mostly, i.e., 13% or more, of sulfated fucose and glucuronic acid [14,15]. Many reports have reported that fucoidans from various brown algae have some biological activities, such as antitumor, anticoagulant, and apoptosis induction, along with other antiallergic and immunologic activities [16–18]. Fucoidan supplementation improved fecal microbiota composition and repaired intestinal barrier function; moreover, fucoidan is an intestinal flora modulator for the potential prevention of breast cancer [19]. However, it has not been reported whether fucoidan in the diet a ffects psoriasis or changes the intestinal environment components of the intestinal environment such as mucin, IgA, and bacterial flora.

The present study demonstrated that fucoidan a ffects psoriasis symptoms; it ameliorated the effect of phenotype and altered the intestinal microbiota and the quality of secreted IgA and mucin in m-*Traf3ip2* mutant mice.
