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Effects of and its serine protease inhibitors on autophagy of host small intestinal cells. | LitMetric

Effects of and its serine protease inhibitors on autophagy of host small intestinal cells.

Infect Immun

Heilongjiang Provincial Key Laboratory of Zoonosis, College of Veterinary Medicine, Northeast Agricultural University, Harbin, Heilongjiang, China.

Published: November 2023

AI Article Synopsis

  • In eukaryotes, autophagy acts as a defense mechanism against pathogens through self-degradation, and this study investigates its role in small intestinal cells during trichinellosis.
  • The research employed various techniques, such as electron microscopy and Western blotting, revealing that parasites induce the formation of autophagosomes and alter the expression of autophagy-related genes and proteins in the host's small intestine.
  • Additionally, serine protease inhibitors (SPIs) were found to enhance autophagy through specific pathways, with a particular advantage shown by AdSPI, highlighting their potential role in understanding intestinal dysfunction post-infection.

Article Abstract

In eukaryotes, autophagy is induced as an innate defense mechanism against pathogenic microorganisms by self-degradation. Although trichinellosis is a foodborne zoonotic disease, there are few reports on the interplay between survival strategies and autophagy-mediated host defense. Therefore, this study focused on the association between and autophagy of host small intestinal cells. In this study, the autophagy-related indexes of host small intestinal cells after infection were detected using transmission electron microscopy, hematoxylin and eosin staining, immunohistochemistry, quantitative real-time polymerase chain reaction, and Western blotting. The results showed that autophagosomes and autolysosomes were formed in small intestinal cells, intestinal villi appeared edema, epithelial compactness was decreased, microtubule-associated protein 1A/1B-light chain 3B (LC3B) was expressed in lamina propria stromal cells of small intestine, and the expression of autophagy-related genes and proteins was changed significantly, indicating that induced autophagy of host small intestinal cells. Then, the effect of on autophagy-related pathways was explored by Western blotting. The results showed that the expression of autophagy-related pathway proteins was changed, indicating that regulated autophagy by affecting autophagy-related pathways. Finally, the roles of serine protease inhibitors (SPIs), such as Kazal-type SPI (KaSPI) and Serpin-type SPI (AdSPI), were further discussed and experiments. The results revealed that SPIs induced autophagy by influencing autophagy-related pathways, and AdSPI has more advantages. Overall, our results indicated that induced autophagy of host small intestinal cells, and its SPIs play an important role in enhancing autophagy flux by affecting autophagy-related pathways. These findings lay a foundation for further exploring the pathogenesis of intestinal dysfunction of host after infection, and also provide some experimental and theoretical basis for the prevention and treatment of trichinellosis

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10652968PMC
http://dx.doi.org/10.1128/iai.00103-23DOI Listing

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