Human protozoa infection and dysplasia in ulcerative colitis: a neglected aspect in a prominent disease

Abstract

The chance of getting colorectal cancer (CRC) is higher in people with chronic ulcerative colitis (UC). The impact of parasitic infections on UC is underappreciated. The purpose of this study was to look into the effect of intestinal protozoal infections on the dysplastic changes generated by UC. The research included 152 adult patients with histologically confirmed UC and 152 healthy controls. Fecal samples were examined for the presence of parasites and fecal calprotectin (FC). The enzyme-linked immunosorbent assay measured serum anti-p53 antibodies (p53Abs) and metallothioneins (MTs). The advanced oxidation protein products (AOPPs) and reduced glutathione (GSH) levels were measured by a spectrophotometric method in all subjects. Serum C-reactive protein (CRP) and IL-6 were also measured. In addition, histopathological and immunohistochemical investigations of intestinal tissue were done. Our results exhibited significant increases in FC and CRP, IL-6, AOPPs, MTs, and p53Abs in ulcerative colitis patients with parasitic infections compared to those without parasites. In contrast, GSH levels showed a significant decrease in the same group compared with other groups. Histopathological and immunohistochemical assessments of intestinal tissue signified severe inflammation and strong expression of PD-L1 in patients with parasitic infections compared to others without parasitic infections. Our research indicated a greater frequency of intestinal protozoa in UC patients with elevated inflammatory and dysplastic biomarker levels. This suggests that these parasites may be involved in the etiology of chronic UC and the associated carcinogenetic process. This is the first report of a link between parasitic infections and dysplastic alterations in UC patients.

Keywords: AOPPs; Dysplasia; FC; MTs; PD-L1; Protozoal infections; Ulcerative colitis; p53Abs.

Fig. 1

a Blastocyst vacuolar form eosin stain (×40). b Blastocyst vacuolar form eosin stain (×100). c Blastocyst vacuolar form iodine stain (×100). d Giardia lamblia cyst form wet mount (×100). e Giardia lamblia trophozoite form wet mount (×100). f Giardia lamblia eosin–stained cyst (×40). g–h Cryptosporidium iodine and Ziehl–Neelsen stain (×100). i Entamoeba histolytica trophozoite eosin stain (×100)

Fig. 2

Photomicrograph of H&E and immunostained photomicrograph of programmed death ligand (PDLI) and P53 from colonic biopsy (×400). a GI with normal colonic mucosa. b GII with moderate inflammatory infiltrate with marked crypt distortion. c GIII with sever inflammatory infiltrate and marked mucosal ulceration. d GII with moderate dysplastic changes (nuclear hyperchromatism and stratification). e GIII with sever dysplastic changes (marked nuclear hyperchromatism and pleomorphism). f GI with negative PDL1 expression. g GII with moderate PDLI expression showing loss of membranous and cytoplasmic expression in colonic epithelium and moderate increased infiltration by the PDL1-positive cells in lamina propria. h GIII with strong PDLI expression showing loss of membranous and cytoplasmic expression in colonic epithelium and marked increased infiltration by the PDL1-positive cells in lamina propria. i GI with negative P53 expression. j GII with moderate dysplastic changes showing moderate P53 expression. k GIII with sever dysplastic changes showing strong P53 expression