Figure 1.
(A–F) Paraffin-embedded lung sections from uninfected dogs (controls) and dogs naturally and experimentally infected with L. infantum (BH401 strain). (A,B) Control dog: (A) Lower magnification showing pulmonary interstitial cells (alveolar wall) (asterisks), 220×. Note the regular pulmonary knob structures (black arrows). (B) Higher magnification showing interstitial cells into the interalveolar septum (asterisks), 440×. (C,D) Naturally infected dog: (C) Lower magnification showing a conspicuous thickness in the interalveolar septum (asterisks) associated with chronic interstitial pneumonitis in comparison to controls, 220×. (D) Presence of an intense chronic cell exudate into the intra-alveolar septum (asterisks); note the thickness of the pulmonary knob structures (black cross), the hypertrophy and hyperplasia of the pneumocytes (black arrows), and the hyperemia (large black arrow), 440×. (E,F) Experimentally infected dog (BH406 strain): Note immunolabeled amastigote forms of Leishmania (in brown) localized in the pulmonary interstitium (arrowheads), 440×. In (F), note the numerous macrophages loaded with immunolabeled parasites in the granuloma formation (large arrowheads), 440×. (A–D) Hematoxylin and eosin staining. (E,F) Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Alveolar duct (AD). Alveolus (Alv). Bars (A,C) = 20 µm; Bars (B,D–F) = 60 µm.
Figure 1.
(A–F) Paraffin-embedded lung sections from uninfected dogs (controls) and dogs naturally and experimentally infected with L. infantum (BH401 strain). (A,B) Control dog: (A) Lower magnification showing pulmonary interstitial cells (alveolar wall) (asterisks), 220×. Note the regular pulmonary knob structures (black arrows). (B) Higher magnification showing interstitial cells into the interalveolar septum (asterisks), 440×. (C,D) Naturally infected dog: (C) Lower magnification showing a conspicuous thickness in the interalveolar septum (asterisks) associated with chronic interstitial pneumonitis in comparison to controls, 220×. (D) Presence of an intense chronic cell exudate into the intra-alveolar septum (asterisks); note the thickness of the pulmonary knob structures (black cross), the hypertrophy and hyperplasia of the pneumocytes (black arrows), and the hyperemia (large black arrow), 440×. (E,F) Experimentally infected dog (BH406 strain): Note immunolabeled amastigote forms of Leishmania (in brown) localized in the pulmonary interstitium (arrowheads), 440×. In (F), note the numerous macrophages loaded with immunolabeled parasites in the granuloma formation (large arrowheads), 440×. (A–D) Hematoxylin and eosin staining. (E,F) Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Alveolar duct (AD). Alveolus (Alv). Bars (A,C) = 20 µm; Bars (B,D–F) = 60 µm.
Figure 2.
(A–F) Paraffin-embedded lung sections from an uninfected dog (control) and an experimentally infected dog with L. infantum (BH 401 strain). (A,C) Control dog: (A) Lower magnification showing a delicate distribution of reticular positive collagen fibers in black mainly observed in alveolar ducts (black arrows), 220×. (C) Higher magnification confirming a discrete presence of reticular collagen fibers in the intra-alveolar septa (black arrows), 440×. (B–F) Experimentally infected dog (BH401 strain). In (B), note a conspicuous chronic interstitial pneumonitis characterized by the thickening of the alveolar wall (alveolar septa) because of mononuclear cell exudate and collagen deposition (fibrosis) in comparison to the control (asterisks), 220×. (D) Higher magnification showing increased silver staining of collagen fibers in the alveolar septa (white arrowheads) and throughout the alveolar wall, mainly notable in knobs (structures of the lung parenchyma), where many of them project into the lumen of the alveolus or alveolar duct (white arrows), 440×. (E) Note a conspicuous black reticular fibers deposition in the alveolar septa as dense tangled structures described as “balls of black wool” (white arrows). Also, observe the epithelium hypertrophy and hyperplasia of the alveolar wall (white arrowheads), 440×. (F) Deep black reticular fibers’ deposition in the lung interstitium, sometimes thin (white arrows) and/or dense (arrowheads), can be observed. However, these black reticular fibers are arranged in various directions and often in a spiral or “stitch-like shape of the shortened and narrowed type” (arrowheads); 440×. Gomori’s ammoniacal silver staining. Alveolar Duct (AD). Alveolus (Alv). Bars (A,B) = 20 µm. Bars (C–F) = 60 µm.
Figure 2.
(A–F) Paraffin-embedded lung sections from an uninfected dog (control) and an experimentally infected dog with L. infantum (BH 401 strain). (A,C) Control dog: (A) Lower magnification showing a delicate distribution of reticular positive collagen fibers in black mainly observed in alveolar ducts (black arrows), 220×. (C) Higher magnification confirming a discrete presence of reticular collagen fibers in the intra-alveolar septa (black arrows), 440×. (B–F) Experimentally infected dog (BH401 strain). In (B), note a conspicuous chronic interstitial pneumonitis characterized by the thickening of the alveolar wall (alveolar septa) because of mononuclear cell exudate and collagen deposition (fibrosis) in comparison to the control (asterisks), 220×. (D) Higher magnification showing increased silver staining of collagen fibers in the alveolar septa (white arrowheads) and throughout the alveolar wall, mainly notable in knobs (structures of the lung parenchyma), where many of them project into the lumen of the alveolus or alveolar duct (white arrows), 440×. (E) Note a conspicuous black reticular fibers deposition in the alveolar septa as dense tangled structures described as “balls of black wool” (white arrows). Also, observe the epithelium hypertrophy and hyperplasia of the alveolar wall (white arrowheads), 440×. (F) Deep black reticular fibers’ deposition in the lung interstitium, sometimes thin (white arrows) and/or dense (arrowheads), can be observed. However, these black reticular fibers are arranged in various directions and often in a spiral or “stitch-like shape of the shortened and narrowed type” (arrowheads); 440×. Gomori’s ammoniacal silver staining. Alveolar Duct (AD). Alveolus (Alv). Bars (A,B) = 20 µm. Bars (C–F) = 60 µm.
Figure 3.
(A–E) Alfa actin (α-SMA) immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control) and an experimental dog infected with Leishmania infantum (BH401 strain). (A,C) Control dog: (A) Lower magnification showing restricted α-SMA-positive cell expression in cells compatible with smooth muscle fibers of alveolar duct walls (black arrows) and arteriole walls (black arrowheads), 220×. (C) Higher magnification shown in the upper right corner of the figure, α-SMA positivity only in the arteriolar wall (black arrow). Note the alveolar knobs and pulmonary structures without any positive staining (arrowheads), 440×. (B,E) Experimentally infected dog (BH401 strain): (B) Lower magnification to verify α-SMA positive cells in the alveolar hyperplastic epithelium wall and in the interstitium, just beneath the epithelium comprising the hyperplastic and hypertrophy knobs (black arrows). Note the intense chronic interstitial pneumonitis where the α-SMA positive cells are located (black asterisks), 220×. (D) Higher magnification showing the hyperplastic and hypertrophy knob structures of the alveolar ducts and alveoli (black arrowheads) and positive interstitial cells (black asterisks), 400×. (E) Note the positive α-SMA expression staining pattern just underneath the alveolar wall epithelium (knob pulmonary structures—black arrowheads), 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Alveolar duct (AD). Alveolus (Av). Terminal bronchiole (TB). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Figure 3.
(A–E) Alfa actin (α-SMA) immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control) and an experimental dog infected with Leishmania infantum (BH401 strain). (A,C) Control dog: (A) Lower magnification showing restricted α-SMA-positive cell expression in cells compatible with smooth muscle fibers of alveolar duct walls (black arrows) and arteriole walls (black arrowheads), 220×. (C) Higher magnification shown in the upper right corner of the figure, α-SMA positivity only in the arteriolar wall (black arrow). Note the alveolar knobs and pulmonary structures without any positive staining (arrowheads), 440×. (B,E) Experimentally infected dog (BH401 strain): (B) Lower magnification to verify α-SMA positive cells in the alveolar hyperplastic epithelium wall and in the interstitium, just beneath the epithelium comprising the hyperplastic and hypertrophy knobs (black arrows). Note the intense chronic interstitial pneumonitis where the α-SMA positive cells are located (black asterisks), 220×. (D) Higher magnification showing the hyperplastic and hypertrophy knob structures of the alveolar ducts and alveoli (black arrowheads) and positive interstitial cells (black asterisks), 400×. (E) Note the positive α-SMA expression staining pattern just underneath the alveolar wall epithelium (knob pulmonary structures—black arrowheads), 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Alveolar duct (AD). Alveolus (Av). Terminal bronchiole (TB). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Scheme 1.
α-SMA cell expression morphometric analysis (semiquantitative study) among dog groups: dogs naturally infected with L. infantum, experimentally infected dogs with Leishmania infantum BH 401 strain, experimentally infected dogs with Leishmania infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Scheme 1.
α-SMA cell expression morphometric analysis (semiquantitative study) among dog groups: dogs naturally infected with L. infantum, experimentally infected dogs with Leishmania infantum BH 401 strain, experimentally infected dogs with Leishmania infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Figure 4.
(A–E) Vimentin immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control) and an experimental dog infected with the Leishmania infantum BH401 strain. (A,C) Control dog: (A) Lower magnification showing restricted vimentin-positive cells in terminal bronchiole walls (interstitial tissue) (black arrowheads) and alveolar septa (lung parenchyma) (black arrows), 220×. (C) Higher magnification showing discrete vimentin positivity in the alveolar septa (black arrowheads). Note that, in the upper right corner of the figure, there is no vimentin positivity in the epithelium of the knob alveolar pulmonary structures (black arrow). (B–E) Experimentally infected dog (BH401 strain): (B) Lower magnification to verify vimentin-positive cells markedly following the chronic interstitial pneumonitis (black arrowheads). Note the hypertrophic and hyperplastic knob alveolar pulmonary structures, 440×. (D) Higher magnification showing the presence of a diffuse vimentin-positive cell exudate localized in the alveolar septa (black arrowheads). Note the hyperplastic and hypertrophy knob structures of the alveolar ducts with vimentin positivity underneath the epithelium, interstitial space (black arrowheads) 400×. (E) Note the thickness of the alveolar septa because of the inflammatory cell exudate with positive vimentin cell expression (black arrowheads). Note the granuloma formation in the pulmonary parenchyma (large black arrow), 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Terminal bronchiole (TB). Alveolar duct (AD). Alveolus (Av). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Figure 4.
(A–E) Vimentin immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control) and an experimental dog infected with the Leishmania infantum BH401 strain. (A,C) Control dog: (A) Lower magnification showing restricted vimentin-positive cells in terminal bronchiole walls (interstitial tissue) (black arrowheads) and alveolar septa (lung parenchyma) (black arrows), 220×. (C) Higher magnification showing discrete vimentin positivity in the alveolar septa (black arrowheads). Note that, in the upper right corner of the figure, there is no vimentin positivity in the epithelium of the knob alveolar pulmonary structures (black arrow). (B–E) Experimentally infected dog (BH401 strain): (B) Lower magnification to verify vimentin-positive cells markedly following the chronic interstitial pneumonitis (black arrowheads). Note the hypertrophic and hyperplastic knob alveolar pulmonary structures, 440×. (D) Higher magnification showing the presence of a diffuse vimentin-positive cell exudate localized in the alveolar septa (black arrowheads). Note the hyperplastic and hypertrophy knob structures of the alveolar ducts with vimentin positivity underneath the epithelium, interstitial space (black arrowheads) 400×. (E) Note the thickness of the alveolar septa because of the inflammatory cell exudate with positive vimentin cell expression (black arrowheads). Note the granuloma formation in the pulmonary parenchyma (large black arrow), 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Terminal bronchiole (TB). Alveolar duct (AD). Alveolus (Av). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Figure 5.
(A–E) Cytokeratin immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control dog), an experimental dog infected with the Leishmania infantum BH401 strain, and a dog naturally infected with Leishmania infantum. (A,C) Control dog: (A) Lower magnification showing discrete cytokeratin-positive cell expression in epithelial cells of the terminal bronchioles, alveolus ducts, and alveolus walls (black arrows), 220×. (C) Higher magnification showing discrete cytokeratin positivity labeling mainly in the epithelium of the arteriolar wall (black arrows), 440×. (B–E) Experimentally infected dog (BH401 strain): (B) Lower magnification to verify cytokeratin-positive cells markedly visible in the terminal bronchiole, alveolar ducts, and alveoli epithelium walls (black arrows). Additionally, observe the cytokeratin-positive cell following the intense chronic interstitial pneumonitis (black asterisks), 220×. (D,E) Higher magnification showing cytokeratin-positive cells in the pulmonary parenchyma (black asterisks). Note, in the right corner of figure (E), the presence of epithelial cytokeratin-positive cells (black arrows); 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Terminal bronchiole (TB). Alveolus duct (AD). Alveolus (Av). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Figure 5.
(A–E) Cytokeratin immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control dog), an experimental dog infected with the Leishmania infantum BH401 strain, and a dog naturally infected with Leishmania infantum. (A,C) Control dog: (A) Lower magnification showing discrete cytokeratin-positive cell expression in epithelial cells of the terminal bronchioles, alveolus ducts, and alveolus walls (black arrows), 220×. (C) Higher magnification showing discrete cytokeratin positivity labeling mainly in the epithelium of the arteriolar wall (black arrows), 440×. (B–E) Experimentally infected dog (BH401 strain): (B) Lower magnification to verify cytokeratin-positive cells markedly visible in the terminal bronchiole, alveolar ducts, and alveoli epithelium walls (black arrows). Additionally, observe the cytokeratin-positive cell following the intense chronic interstitial pneumonitis (black asterisks), 220×. (D,E) Higher magnification showing cytokeratin-positive cells in the pulmonary parenchyma (black asterisks). Note, in the right corner of figure (E), the presence of epithelial cytokeratin-positive cells (black arrows); 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Terminal bronchiole (TB). Alveolus duct (AD). Alveolus (Av). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Scheme 2.
Vimentin cell expression morphometric analysis (semiquantitative study) among dog groups: dogs naturally infected with L. infantum, experimentally infected dogs with Leishmania (L.) infantum BH 401 strain, experimentally infected dogs with Leishmania infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Scheme 2.
Vimentin cell expression morphometric analysis (semiquantitative study) among dog groups: dogs naturally infected with L. infantum, experimentally infected dogs with Leishmania (L.) infantum BH 401 strain, experimentally infected dogs with Leishmania infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Scheme 3.
Cytokeratin cell expression morphometric analysis (semiquantitative study) among the dog groups: dogs naturally infected with Leishmania infantum, experimentally infected dogs with Leishmania infantum BH 401 strain, experimentally infected dogs with Leishmania infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Scheme 3.
Cytokeratin cell expression morphometric analysis (semiquantitative study) among the dog groups: dogs naturally infected with Leishmania infantum, experimentally infected dogs with Leishmania infantum BH 401 strain, experimentally infected dogs with Leishmania infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Figure 6.
(A–E) Snail antigen homologue 1 (Snail) immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control), an experimentally infected dog with Leishmania infantum BH401 strain, and a naturally infected dog with Leishmania infantum. (A,C) Control dog: (A) Lower magnification showing a discrete Snail cell-labeling occurrence in the epithelium of the terminal bronchioles, alveolar ducts, and alveoli walls (black arrows), 220×. (C) Higher magnification showing a few Snail-positive cells (black arrows). Note the lack of inflammatory cells in the alveolar septa, 440×. (B,D) Experimentally infected dog with Leishmania infantum (BH401 strain): (B) Lower magnification showing a marked epithelium line of Snail-positive cells throughout the alveolar ducts and alveoli (black arrows). Observe an intense chronic interstitial pneumonitis characterized by the thickening of the alveolar walls with Snail-positive cells (black asterisks). (D) Higher magnification showing Snail-positive cells in the alveolar hyperplastic epithelium duct wall (black arrows), 440×. (E) Higher magnification showing Snail-positive cells in the interalveolar space following the chronic cellular exudate (black arrowheads), 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Terminal bronchiole (TB). Alveolar duct (AD). Alveolus (Av). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Figure 6.
(A–E) Snail antigen homologue 1 (Snail) immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control), an experimentally infected dog with Leishmania infantum BH401 strain, and a naturally infected dog with Leishmania infantum. (A,C) Control dog: (A) Lower magnification showing a discrete Snail cell-labeling occurrence in the epithelium of the terminal bronchioles, alveolar ducts, and alveoli walls (black arrows), 220×. (C) Higher magnification showing a few Snail-positive cells (black arrows). Note the lack of inflammatory cells in the alveolar septa, 440×. (B,D) Experimentally infected dog with Leishmania infantum (BH401 strain): (B) Lower magnification showing a marked epithelium line of Snail-positive cells throughout the alveolar ducts and alveoli (black arrows). Observe an intense chronic interstitial pneumonitis characterized by the thickening of the alveolar walls with Snail-positive cells (black asterisks). (D) Higher magnification showing Snail-positive cells in the alveolar hyperplastic epithelium duct wall (black arrows), 440×. (E) Higher magnification showing Snail-positive cells in the interalveolar space following the chronic cellular exudate (black arrowheads), 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Terminal bronchiole (TB). Alveolar duct (AD). Alveolus (Av). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Scheme 4.
Snail antigen homologue 1 (Snail) cell expression morphometric analysis (semiquantitative study) among the dog groups: dogs naturally infected with Leishmania infantum, experimentally infected dogs with Leishmania infantum BH 401 strain, experimentally infected dogs with Leishmania infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Scheme 4.
Snail antigen homologue 1 (Snail) cell expression morphometric analysis (semiquantitative study) among the dog groups: dogs naturally infected with Leishmania infantum, experimentally infected dogs with Leishmania infantum BH 401 strain, experimentally infected dogs with Leishmania infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Scheme 5.
Transforming growth factor-beta (TGF-β) cytokine expression morphometric analysis (semiquantitative study) among the dog groups: dogs naturally infected with Leishmania (L.) infantum, experimentally infected dogs with Leishmania infantum BH 401 strain, experimentally infected dogs with Leishmania (L.) infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Scheme 5.
Transforming growth factor-beta (TGF-β) cytokine expression morphometric analysis (semiquantitative study) among the dog groups: dogs naturally infected with Leishmania (L.) infantum, experimentally infected dogs with Leishmania infantum BH 401 strain, experimentally infected dogs with Leishmania (L.) infantum BH 46 strain, and uninfected dogs (controls). The “a” and “b” denote statistically significant difference (p < 0.0001).
Figure 7.
(A–E) Transforming growth factor-beta (TGF-β) cytokine immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control) and an experimentally infected dog with the Leishmania infantum BH401 strain. (A,C) Control dog: (A) Lower magnification showing a discrete TGF-β cytokine-labeling occurrence in the epithelium of the terminal bronchioles (black arrow), alveolar ducts, and alveoli walls (black arrowheads), 220×. (C) Higher magnification showing little TGF-β positivity in the interalveolar space (black arrows). Note the lack of inflammatory cells in the alveolar septa, 440×. (B,D) Experimentally infected dog (BH401 strain): (B) Lower magnification showing intense chronic pneumonitis with moderate-to-intense TGF-β positivity in the interalveolar space (black asterisks), 220×. (D) Higher magnification showing TGF-β positivity visible in the pulmonary parenchyma, 440×. (E) Higher magnification also showing the chronic cellular exudate forming two granulomas (large black arrowheads) with TGF-β positivity, 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Terminal bronchiole (TB). Alveolar duct (AD). Alveolus (Av). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Figure 7.
(A–E) Transforming growth factor-beta (TGF-β) cytokine immunohistochemical expression in paraffin-embedded lung tissue samples from an uninfected dog (control) and an experimentally infected dog with the Leishmania infantum BH401 strain. (A,C) Control dog: (A) Lower magnification showing a discrete TGF-β cytokine-labeling occurrence in the epithelium of the terminal bronchioles (black arrow), alveolar ducts, and alveoli walls (black arrowheads), 220×. (C) Higher magnification showing little TGF-β positivity in the interalveolar space (black arrows). Note the lack of inflammatory cells in the alveolar septa, 440×. (B,D) Experimentally infected dog (BH401 strain): (B) Lower magnification showing intense chronic pneumonitis with moderate-to-intense TGF-β positivity in the interalveolar space (black asterisks), 220×. (D) Higher magnification showing TGF-β positivity visible in the pulmonary parenchyma, 440×. (E) Higher magnification also showing the chronic cellular exudate forming two granulomas (large black arrowheads) with TGF-β positivity, 440×. Immunohistochemistry streptavidin–peroxidase method with counterstaining with Harris hematoxylin. Terminal bronchiole (TB). Alveolar duct (AD). Alveolus (Av). Bars (A,B) = 20 µm. Bars (C–E) = 60 µm.
Table 1.
Primary antibodies used for immunohistochemistry.
Table 1.
Primary antibodies used for immunohistochemistry.
Antigen * | Supplier | Clone | Isotipe | Specifity | Titration |
---|
α-Actin | Dako | 1A4 | mIgG2a, kappa | smooth muscle cells, myofibroblasts and myoepithelial cells | 1:100 |
Vimentin | Dako | V9 | mIgG1, kappa. | intermediate filament (IF) of the cytoskeleton of vertebrate cells | 1:50 |
E-cadherin | AbD-Serotec | 4A2c7 | Mouse/IgG1, kappa | Recombinant protein corresponding to the cytoplasmic domain of human E-cadherin | 1:30 |
Cytokeratin | Dako | AE1AE3 | IgG fraction | Pan Cytokeratin (although does not detect Cytokeratin 18) | 1:70 |
TGF-β1(v) | Santa Cruz biotechnology | sc-146 | rabbit polyclonal IgG | epitope mapping at the C-terminus of TGFβ1 | 1:50 |
Snail | Abcam | 85931 | Monoclonal, IgG | This antibody gave a positive signal against Human SNAIL | 1:100 |