Table 1.
Main symptoms and blood eosinophils in patients with acute schistosomiasis mansoni diagnosed at Tropical Diseases Outpatient Clinic of the University Hospital of Universidade Federal de Minas Gerais (Belo Horizonte, Brazil) from January 2014 to December 2015 and included in the study.
Fig 1.
Sera and hepatic osteopontin are upregulated in human acute schistosomiasis mansoni.
A) ELISA for osteopontin in the plasma of uninfected controls (NI, n = 21) and schistosomiasis patients with Acute (n = 3), hepatointestinal (n = 26) and hapatosplenic (n = 39) forms of disease. B) ELISA for osteopontin in the serum of uninfected controls (n = 21) and patients with acute schistosomiasis mansoni (n = 28). C) ELISA for osteopontin in the serum of uninfected controls (NI, n = 21) and patients with acute schistosomiasis mansoni (n = 28) grouped by weeks post infection. Medians are displayed; Mann-Whitney U test: #p<0.05, ##p<0.01, ###p<0.001, ####p<0.0001 vs uninfected controls; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. D) Immunohistochemistry for osteopontin in liver needle biopsy fragment of a representative subject with acute schistosomiasis mansoni (10 weeks post infection). Final magnification 100x, 200x and 400x.
Fig 2.
Sera and hepatic osteopontin are upregulated in the acute phase of murine schistosomiasis mansoni.
A) ELISA for osteopontin in the serum of uninfected (NI) mice and mice experimentally infected with S. mansoni in the acute (6,7 and 8 weeks post infection) and chronic phase (30 weeks post infection). Medians are displayed, Mann-Whitney U test: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. B) Serum osteopontin ELISA of uninfected controls and infected mice grouped by weeks post infection. Medians are displayed, Mann-Whitney U test: #p<0.05, ##p<0.01, ###p<0.001, ####p<0.0001 vs non-infected; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. C) Immunohistochemistry for osteopontin in representative liver section of uninfected mice (left), infected mice in the acute phase (middle) and infected mice in the chronic phase (right). Final magnification 200x. D) Morphometry of the immunohistochemistry for osteopontin. Means are displayed; Student’s t test: #p<0.05, ##p<0.01, ###p<0.001, ####p<0.0001 vs non-infected; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001. E) Number of osteopontin positive bile ducts per 200x power field. Means are displayed; Student’s t test: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.
Fig 3.
Soluble egg antigens induce Osteopontin expression in primary human Kupffer cells.
A) Double Immunohistochemistry for osteopontin (OPN,brown) and CD68 (macrophage marker, green) in liver needle biopsy fragment of a representative subject with acute schistosomiasis mansoni (10 weeks post infection, same case depicted in Fig 1D) demonstrating that macrophages express osteopontin in human acute schistosomiasis mansoni. The rectangle highlights the magnified area shown on the 2 pannels on the right. Final magnification 100x (left), 400x (upper right) and 600x (lower right). B) Osteopontin mRNA expression (fold change) in primary human Kupffer cells incubated with 10 μg/ml SEA or 0.0001 μg/ml LPS (lipopolysaccharide; control, same amount of endotoxin present in the SEA preparation) after 3 hours of incubation. Mean±SEM are displayed, Student’s t test: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.