Preliminary study of mucosal IgA in the equine small intestine: specific IgA in cases of acute grass sickness and controls.

The research investigates the role of specific IgA antibodies in combating Equine Grass Sickness (EGS), a disease believed to be caused by certain strains of the bacteria, Clostridium botulinum. The study finds higher levels of these IgA antibodies in diseased horses compared to healthy ones, suggesting that these antibodies could be crucial for the development of a successful vaccine against EGS.

Methods of Research

The research team collected tissue samples from horses suffering from Acute Grass Sickness (AGS), and from a control group of healthy horses. The sample sites included the duodenum, jejunum, and ileum regions of the gastrointestinal (GI) tract.

• In total, 25 tissue samples from AGS cases and 12 samples from control horses were collected.
• The tissue samples were extracted with a detergent named saponin in the presence of protease inhibitors, substances that prevent the breakdown of proteins.
• All samples were then analysed for total IgA antibodies and the specific IgA against neurotoxins produced by Clostridium botulinum types C and D (BoNT/C or BoNT/D).
• Samples were also tested for IgA antibodies against the surface antigens of a BoNT/C negative strain of Clostridium botulinum type C (SA) and of Clostridium tetani (TetSA), which served as a control.

Study Findings

When comparing AGS cases to control horses, the researchers found significantly higher levels of specific IgA antibodies against BoNT/C in the jejunum and ileum of horses sick with AGS. Similarly, higher specific levels against BoNT/D were found in both the duodenum and jejunum of AGS cases.

• Higher specific IgA levels against SA were detected only in the duodenum samples.
• The levels of specific IgA antibodies were nearly undetectable in control horses, suggesting that these horses had not been recently exposed to these toxins.
• For horses with AGS, higher levels of specific IgA were observed, predominantly in the jejunum and ileum.

Implications of the Research

The findings indicate that specific IgA antibodies could play a crucial role in resisting EGS disease. As such, any successful EGS vaccine should seek to invoke a mucosal response, where the production of these specific IgA antibodies is stimulated. Should this protective role of IgA be further validated, this may direct the design of future EGS vaccines.