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. 2021 Jun 19;52(1):90.
doi: 10.1186/s13567-021-00958-2.

Lawsonia intracellularis infected enterocytes lack sucrase-isomaltase which contributes to reduced pig digestive capacity

Emma T Helm  1 , Eric R Burrough  2 , Fernando L Leite  3 , Nicholas K Gabler  4
Affiliations

Lawsonia intracellularis infected enterocytes lack sucrase-isomaltase which contributes to reduced pig digestive capacity

Emma T Helm et al. Vet Res. .

Abstract

Lawsonia intracellularis is endemic to swine herds worldwide, however much is still unknown regarding its impact on intestinal function. Thus, this study aimed to characterize the impact of L. intracellularis on digestive function, and how vaccination mitigates these impacts. Thirty-six L. intracellularis negative barrows were assigned to treatment groups (n = 12/trt): (1) nonvaccinated, L. intracellularis negative (NC); (2) nonvaccinated, L intracellularis challenged (PC); and (3) L. intracellularis challenged, vaccinated (Enterisol® Ileitis, Boehringer Ingelheim) 7 weeks pre-challenge (VAC). On days post-inoculation (dpi) 0 PC and VAC pigs were inoculated with L. intracellularis. From dpi 19-21 fecal samples were collected for apparent total tract digestibility (ATTD) and at dpi 21, pigs were euthanized for sample collection. Post-inoculation, ADG was reduced in PC pigs compared with NC (41%, P < 0.001) and VAC (25%, P < 0.001) pigs. Ileal gross lesion severity was greater in PC pigs compared with NC (P = 0.003) and VAC (P = 0.018) pigs. Dry matter, organic matter, nitrogen, and energy ATTD were reduced in PC pigs compared with NC pigs (P ≤ 0.001 for all). RNAscope in situ hybridization revealed abolition of sucrase-isomaltase transcript in the ileum of PC pigs compared with NC and VAC pigs (P < 0.01). Conversely, abundance of stem cell signaling markers Wnt3, Hes1, and p27Kip1 were increased in PC pigs compared with NC pigs (P ≤ 0.085). Taken together, these data demonstrate that reduced digestibility during L. intracellularis challenge is partially driven by abolition of digestive machinery in lesioned tissue. Further, vaccination mitigated several of these effects, likely from lower bacterial burden and reduced disease severity.

Keywords: Cell proliferation; Digestibility; Intestinal integrity; Lawsonia intracellularis; Notch signaling; Vaccine; Wnt signaling.

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Conflict of interest statement

FLL is an employee of Boehringer Ingelheim Animal Health, a partial funder of this study. As one of the authors, FLL had influence over the study design. However, there was no point at which conclusions or interpretations put forward, that were suggested by FLL, without full agreement of the other authors.

Figures

Figure 1
Figure 1
Fecal shedding and antibody response. A Fecal shedding and B antibody response in non-infected pigs (NC), non-vaccinated, Lawsonia intracellularis inoculated pigs (PC), and vaccinated, Lawsonia intracellularis inoculated pigs (VAC). PC and VAC pigs were inoculated at days post-inoculation 0 and serum and fecal swabs were collected weekly for 3 weeks. Data represents 12 pigs/treatment.
Figure 2
Figure 2
Ileal lesion severity at days post-inoculation 21. Panels A and B represent macroscopic lesions in non-infected pigs (NC, black), non-vaccinated Lawsonia intracellularis inoculated pigs (PC, white), and vaccinated Lawsonia intracellularis inoculated pigs (VAC, blue), while panels C through F describe microscopic lesion severity. A Frequency of macroscopic lesion severity score. B Average lesion length (cm) of lesion, if any. C Inflammation score wherein 0  =  none/minimal, 1  =  mild, 2  =  moderate, and 3  =  severe. D Proliferation of crypts, wherein 0  =  none/minimal, 1  =  mild, 2  =  moderate, and 3  =  severe. E Lesion distribution score, wherein 0  =  none, 1  =  focal, 2  =  multifocal, and 3  =  diffuse. F L. intracellularis immunohistochemistry (IHC) scoring, where 0  =  no antigen stain, 1  =  1–25% of crypts, 2  =  26–50% of crypts, 3  =  51–75% of crypts, 4  =   > 75% of crypts positive for antigen.
Figure 3
Figure 3
Ileal and colonic mitochondrial reactive oxygen species (ROS) production. ROS production was quantified in mitochondria isolated from non-infected pigs (NC), non-vaccinated Lawsonia intracellularis inoculated pigs (PC), and vaccinated Lawsonia intracellularis inoculated pigs (VAC) at days post-inoculation 21.
Figure 4
Figure 4
RNA chromogenic in-situ hybridization dual probe for sucrase-isomaltase (brown) and Hes1 (red). Transcripts were quantified in the ileum of non-infected pigs (NC), non-vaccinated Lawsonia intracellularis inoculated pigs (PC), and vaccinated Lawsonia intracellularis inoculated pigs (VAC) at days post-inoculation 21. Representative images of dual stain in A NC, B PC, and C VAC pigs. Sucrase-isomaltase transcript was found throughout the intestinal epithelium, particularly concentrated in the mid-villus region and villus tips. Near complete abolition of this transcript was observed in affected crypts in pigs challenged with L. intracellularis. The abundance of transcription factor Hes1 was also evaluated by RNA in-situ hybridization. D Example of Hes1 staining in the crypts. Hes1 transcript appeared sporadically throughout the crypt-villus axis in all treatment groups. However, due to the overwhelming sucrase-isomaltase staining, this transcript was unable to be quantified. E Quantification of sucrase isomaltase stain in the crypt, mid-villus, and villus tip.
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