Piscine intestinal coccidian: Goblet cell response in juvenile Asian sea bass (Lates calcarifer) across different age groups
The parasitic protozoan, piscine intestinal coccidia, has been identified as a significant contributor to morbidity and mortality among juvenile Asian sea bass. Despite the fact that this intestinal parasite colonizes the gut and induces damage, the precise innate response of the goblet cell to piscine intestinal coccidia and the role of goblet cell in promoting protozoan infection remain elusive. This study endeavors to elucidate the goblet cell's reaction to this protozoan infection across different age groups of juvenile Asian sea bass. Intestinal samples were collected from forty-four juvenile Asian sea bass, each aged 60 and 90 days, that were infected with piscine intestinal coccidia and were obtained from marine cage farming. These samples were then processed using routine histopathological techniques, including embedding and staining. The goblet cells within the intestinal mucosa were systematically analyzed using histochemistry, Alcian blue staining. Subsequent to the analysis, goblet cells were semi-quantified and compared using statistical methods. The study findings showed a notable rise in goblet cell distribution from the anterior, mid, and posterior regions in two distinct fish groups. Specifically, the 60-day fish exhibited a significantly greater goblet cell hyperplasia compared to the 90-day fish during the infection period (p<0.05). This study examines the response of goblet cells in juvenile Asian sea bass models infected with piscine intestinal coccidia, focusing on the potential influence of age on the innate host's protective mechanisms. An interesting finding is that the 60- and 90-day-old Asian sea bass exhibited a goblet cell hyperplasia response, which is associated with coccidiosis infection.
Publication Details
- Journal
- SHILAP Revista de lepidopterología
- Published
- 2024-12-01
- Primary Topic
- Coccidia and coccidiosis research
- Type
- article
- Field-Weighted Citation Impact
- 0.00