Intestinal Damage in Strongyloidiasis: The Imbalance Between Cell Death and Proliferation

Abstract

Strongyloidiasis is an endemic tropical parasitosis caused by Strongyloides stercoralis that also affects immigrants in nontropical countries. The nematode colonizes the duodenum and upper jejunum, inducing mucosal alterations. Because integrity is essential for a functional barrier, we aimed to study apoptosis and proliferation in the small bowel epithelium infected with S. stercoralis. We evaluated 23 patients and 17 controls. Apoptotic cells were detected by TUNEL and M30 immunolabelling, whereas proliferation was scored by Ki67 immunostaining and mitotic counting. Infection increased apoptotic indices in duodenum and jejunum (P < 0.001). Conversely, it decreased cell proliferation in both segments (P < 0.001). Our results showed that intestinal strongyloidiasis promotes an imbalance between cell death and proliferation. This is the first evidence of disruption of the epithelial kinetics with S. stercoralis infection, though the mechanisms remain unclear. Furthermore, our results support the idea that strongyloidiasis disturbs the mucosal integrity and can compromise the intestinal barrier.

Endoscopic and histopathological study on the duodenum of Strongyloides stercoralis hyperinfection

“…Suarez and Sanchez [19] confirmed that plasma cell infiltration, villous atrophy and severe duodenitis were the characteristics of severe strongyloidiasis. A recent study clearly demonstrated that strongyloidiasis disrupted epithelial kinetics in the human small intestine by the induction of apoptosis and inhibition of cell proliferation, thereby resulting in villous atrophy and impaired barrier function [17] . Our observations disclosed that endoscopic findings of duodenitis were more severe in the patients whose biopsies were positive for larvae than in those with negative biopsies.…”

“…However, pathognomonic findings are apparently not evident [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] . Our present study confirmed the aforementioned frequent findings.…”

“…Brasitus et al [3] 1980 1 None Brisk bleeding, deformed bulb Milder et al [4] 1981 2 ND Enlarged folds Bone et al [5] 1982 1 ND Deformed cap, obliterated second part Bhatt et al [6] 1990 1 None Mild erythema Chen et al [7] 1994 1 Corticosteroids Flattened folds, swelling mucosa, tiny ulcer Choudhry et al [8] 1995 3 DM, none Multiple serpiginous lesions, duodenal nodule Hizawa et al [9] 1996 1 HTLV-1 and corticosteroids Edema, tiny white spots Friedenberg et al [10] 1999 1 HTLV-1 Severe stenosis Overstreet et al [11] 2003 1 HIV White punctate dotting mucosa Asano et al [12] 2004 1 HTLV-1 Fine granule, coarse mucosa, disappeared folds Thompson et al [13] 2004 6 Corticosteroids, DM, HIV, none Edema, brown discoloration, erythematous spots, subepithelial hemorrhage, megaduodenum Seet et al [14] 2005 1 Anti-myeloma drugs Erythematous and granular mucosa Karmo et al [15] 2006 1 Corticosteroids Normal Ghoshal et al [16] 2006 1 Corticosteroids Multiple nodules Werneck-Silva et al [17] 2006 4 ND Erythema, erosion Csermely et al [18] 2006 1 Anti-myeloma drugs Necrotic ulcerations Suarez and Sanchez [19] 2006 11 ND Swollen folds of nodular aspect ND: Not determined.…”

“…As S. stercoralis colonizes in the duodenum where the larvae mature, endoscopic evaluation has been recognized as an important tool for diagnosing strongyloidiasis. Although there have been several reports demonstrating endoscopic findings of strongyloidiasis, most of these are case reports or small case series [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] . This study aims at investigating the relationship of endoscopic markers to clinical and histopathological findings of the duodenum in patients with S. stercoralis hyperinfection in an endemic region.…”

Hyperinfection Syndrome in Strongyloidiasis

“…Histopathological analyses of human intestines have shown that S. stercoralis eggs and adult females colonise the duodenum and upper jejunum. Studies have also demonstrated the presence of oedema, duodenal villous atrophy, and crypt hyperplasia with disrupted epithelium due to the inhibition of cell proliferation and apoptosis (Coutinho et al, 2006;Werneck-Silva et al, 2006). Surface damage, ulceration, an increase in mucus secretion and functional changes in the intestine have also been reported.…”