**1. Introduction**

Fucoidan is a complex sulfated polysaccharide that is mostly found in brown marine algae. Fucoidan exhibits a broad spectrum of biological activities, including anti-inflammatory, immunomodulatory, anti-oxidant, anti-tumor, and anti-infection effects [1–5]. Several investigators have reported a potential role of fucoidan as an anti-*Helicobacter pylori* (*H. pylori*) agen<sup>t</sup> based on its ability to disrupt the adhesion of the microbe to the gastric epithelium in vivo and in vitro [6–9]. The inhibitory effect of fucoidan derived from *Cladosiphon okamuranus* (Okinawa mozuku) on *H. pylori* was demonstrated in vitro by Shibata et al. [6]. Their study showed that the *H. pylori* binding to human gastric cell lines was inhibited more by *Cladosiphon* fucoidan than by fucoidan procured from *Fucus*. In addition, fucoidan blocked both Leb- and sulfatide-mediated attachment of *H. pylori* to gastric cells. They concluded that the inhibitory effect of *Cladosiphon* fucoidan on the binding of *H. pylori* and gastric cells might be caused by the coating with this component of the bacterial surface. However, no bacteriostatic or bactericidal activity was observed against *H. pylori* for any fucoidan preparation [9].

Fucoidan is reported to be absorbed across the intestinal tract via energy-dependent processes and pinocytosis [10–12]. In Japanese volunteers, fucoidan was detected in the majority of urine following oral administration [13]. Because the rate of fucoidan absorption through the small intestine was highly variable among the participants, various factors were suggested to influence its absorption. For example, the consumption of Okinawa mozuku (*Cladosiphon okamuranus* Tokida), a brown seaweed

containing fucoidan, is an important factor associated with fucoidan absorption. Based on a previous report by Hehemann et al. [14], we speculated that the gastrointestinal microbiota can influence the absorption of fucoidan.

*H. pylori* is a Gram-negative, spiral-shaped, microaerophilic bacterium. It colonizes the entire gastric mucosa in approximately half of the world's human population, and a poor socioeconomic condition is an important risk factor for infection [15–18]. *H. pylori* causes peptic ulcer disease and atrophic gastritis, and it is associated with primary gastric B-cell lymphoma and gastric adenocarcinoma. The host immune system cannot clear the infection, and it persists without treatment.

Many studies have focused on the modification of the gastric environment induced by *H. pylori* infection. For example, *H. pylori* infection can lead to the deficiency of vitamins, such as vitamin C, vitamin A, α-tocopherol, vitamin B12, and folic acid, as well as essential minerals [19–21]. Moreover, gastric *H. pylori* infection affects local and distant microbial populations and host responses.

Because fucoidan can bind to *H. pylori* and disrupt its attachment to the gastric epithelium [6–8], *H. pylori* infection is assumed to affect fucoidan absorption. In this study, we examined the effects of *H. pylori* infection on the absorption of fucoidan extracted from Okinawa mozuku in Japanese volunteers. Although fucoidan absorption is extremely low in humans, the fucoidan concentration after oral administration is approximately 10-fold higher in urine than in serum [22]. Therefore, urinary fucoidan concentrations were measured before and after the oral administration of mozuku fucoidan.
