FIGURE

Figure 5

ID
ZDB-FIG-200829-50
Publication
Bernut et al., 2020 - Deletion of cftr Leads to an Excessive Neutrophilic Response and Defective Tissue Repair in a Zebrafish Model of Sterile Inflammation
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Figure 5

TIIA-driven neutrophil apoptosis and reverse migration accelerate inflammation resolution in CF. (A)TgBAC(mpx:EGFP)i114 larvae were pretreated with 25 μM of TIIA prior to tail fin amputation procedure, then injured and immediately put back in treatments for 4 h. Neutrophil number at the wound was counted at 8 hpi (n = 21, two-tailed Bonferroni t-test). (B,C)TgBAC(mpx:EGFP)i114 larvae were injured and treated from 4 hpi with 25 μM of TIIA. (B) Neutrophil number at wound was counted at 8 hpi (n = 21, two-tailed Bonferroni t-test). (C) representative number of neutrophils remaining at wounds at 8 hpi (scale bars, 200 μm). (D) Neutrophil apoptosis quantification at 8 hpi in cftr MO treated with 25 μM of TIIA from 4 hpi and stained with TUNEL/TSA. (n = 40, Fisher t-test). (E) Reverse-migration assay in cftr MO Tg(mpx:gal4)sh267;Tg(UASkaede)i222. At 4 hpi fish were treated with 25 μM of TIIA and neutrophils at site of injury were photoconverted. The numbers of photoconverted cells that moved away from the wound were time-lapse imaged and quantified over 4 h. (F,G) Regenerative performance after TIIA treatment. (F) Regenerated fin areas are measured at 3 dpi (n = 21, two-tailed Bonferroni t-test). (G) Representative imaging of injured tail fin at 3 dpi (scale bars, 200 μm). (H) Schematic diagram showing TIIA efficiently accelerates inflammation resolution by inducing neutrophil apoptosis and reverse migration at wounds and improves tissue repair in CF animal.

Expression Data

Expression Detail
Antibody Labeling
Phenotype Data
Fish:
Condition:
Knockdown Reagent:
Observed In:
Stage: Protruding-mouth

Phenotype Detail
Acknowledgments
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