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Figure 4

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ZDB-IMAGE-221018-114
Source
Figures for Charlie-Silva et al., 2022
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Figure Caption

Figure 4

The inflammatory condition caused by λ-CGN extends along the entire boundaries of the peritoneal cavity. (A, B) Mesentery. (A-left) Basal condition showing the absence of reactive leukocytes in the mesenteric conjunction between the adipose cells and the pancreatic tissue. (A-right) In the mesentery of the 3.5% λ-CGN-induced swollen fish, extensive leukocyte infiltrates are observed after 4h. Note the vast leukocyte (yellow arrowheads) infiltrating the area and into the adjacent musculature. (B) Graphical representation of the leukocyte infiltrate counts per optical field (n = 10) in the λ-CGN treated fish. (C, D) Intestine. (C-left) Basal condition showing the unaltered physiological architecture of the intestine where epithelial cells, goblet cells and intestinal folds are clearly defined (gray arrows). (C-right) In the fish treated with 3.5% λ-CGN, obvious histopathological alterations and a strong reduction of fish intestinal loops and major structural components due to fluid accumulation (edema) are clearly observed (purple arrowheads). (D) Percentage quantification of the intestinal epithelia detachment (Left) and Goblet cells (Right) recorded in 10 fields per slide (n = 15 slides per condition) between the control and the λ-CGN-treated fish. Sections stained with hematoxylin-eosin. Objectives 40X; projective 2X. Staining: regular H&E-Harris. Scale bar 80μm at 40X. Results were analyzed using an unpaired t-test (p < 0.05) respective to the control value.Error bars indicate SD.

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