Urinary hyaluronidase activity in rats infected with Blastocystis hominis—evidence for invasion?

Abstract

The fact whether Blastocystis hominis can invade has always been in question. Apart from a few sporadic studies such as that done on gnotobiotic guinea pigs which showed surface invasion and mucosal inflammation of the host's intestine caused by B. hominis infection, no real documentation of invasion has been proven. Studies have shown that hyaluronidase is secreted during the penetration into the host's skin and gut by nematode parasites. Hyaluronidase activity in protozoa namely Entamoeba histolytica has also been described previously. This study attempts to determine hyaluronidase in urine samples of B. hominis-infected rats. The presence of hyaluronidase in urine provides an indirect evidence of invasion by B. hominis into colonic epithelium causing the degradation of extracellular matrix proteins namely hyaluronic acid (HA). HA is depolymerized by hyaluronidase which may be used by organisms to invade one another. In this study, the levels of urinary hyaluronidase of Sprague-Dawley rats infected with B. hominis were monitored for 30 days. Hyaluronidase levels in the infected rats were significantly higher on days 28 and 30 compared to the day before inoculation (P < 0.01 and P < 0.05, respectively). During this stage, parasitic burden in infected stools was also at a high level. Proinflammatory cytokines, interleukin-6 and interleukin-8, were also significantly higher (P < 0.05) in the serum of infected rats. The study demonstrates that since no other pathogen was present and that amoeboid forms of the parasites have been shown to exist previously, the elevated levels of hyaluronidase in this preliminary finding suggests that the organism is capable of having invasion or penetration activity in the hosts' intestine.

Pathogenic potential of Blastocystis hominis in laboratory mice

“…This may be due to the release of cysteine protease by B. hominis which lead to evasion or modulation of the immune system by degradation of host immune molecules (Puthia et al 2005), or due to the release of hyaluronidase enzyme which leads to the degradation of extracellular matrix proteins namely hyaluronic acid facilitating the invasion by B. hominis into colonic epithelium. Chandramathi et al (2010) found elevation of hyaluronidase in urine of mice infected with B. hominis provides an indirect evidence of invasion by B. hominis into colonic epithelium.…”

Stress Exacerbates Infectivity and Pathogenicity of Blastocystis hominis: In Vitro and In Vivo Evidences

“…Various reports have shown that certain subtype of this unicellular protozoan is coupled with intestinal disorders including Irritable Bowel Syndrome (IBS) [17]. Previously, we have reported on the elevation of oxidative damage and proinflammatory cytokines caused by B. hominis infection in animal model [18], [19]. We have also demonstrated that solubilized antigen from B. hominis (Blasto-Ag), at a certain concentration, could down-regulate PBMC responses while enhancing the growth of colorectal cancer cells in vitro [20].…”

A Metronidazole-Resistant Isolate of Blastocystis spp. Is Susceptible to Nitric Oxide and Downregulates Intestinal Epithelial Inducible Nitric Oxide Synthase by a Novel Parasite Survival Mechanism

“…Although reports of mucosal inflammatory changes in the human gut are inconclusive (46), Blastocystis infections do induce a host immune response (1,14,32). Recent studies have shown that the parasite causes NF-B-mediated upregulation of the proinflammatory cytokine interleukin-8 (IL-8) (32) in human T-84 colonic epithelium.…”