Stereotypic immune response in Mycobacterium avium ssp. paratuberculosis infection among different Swiss caprine genotypes.

Abstract

Paratuberculosis is an infection with Mycobacterium avium ssp. paratuberculosis (MAP) causing chronic enteritis in domestic and wild ruminants worldwide. In goats, the infection is caused by C (cattle)-type and S (sheep)-type strains. In this study, the correlation between different MAP strains and histomorphological lesions in the small and large intestines, as well as the mesenteric lymph nodes, in Swiss goats (Caprae aegagrus hircus) was investigated. Ten Swiss caprine MAP isolates were characterized using polymerase chain reaction (PCR) and enzymatic restriction-based single nucleotide polymorphism (SNP) analysis. In addition, mycobacterial interspersed repetitive units and variable-number tandem repeats (MIRU-VNTR) profiling was performed, and the correlation with histologic lesions, scored as previously described for goats, was analyzed. Furthermore, immunohistochemical expression of CD3, CD79a, Iba1, cleaved caspase 3, and interleukin (IL)-17 was evaluated, and a morphometric analysis was conducted to quantify the different inflammatory cells. Diffuse multibacillary lesions were found in C-type/L'Institut national de recherche pour l'agriculture, l'alimentation et l'environnement (INRAE) Nouzilly MIRU-VNTR (INMV)1 (2/10) and S-type/INMV220 (1/10) animals. Diffuse lymphocytic lesions occurred in C-type/INMV1 (2/10) animals, while diffuse mixed lesions were observed in S-type/INMV218 (3/10) and S-type/INMV220 (2/10) animals. No significant differences in intestinal histological lesion scores were detected between S- and C-type INMV strains. Morphometrical analysis revealed similar inflammatory and apoptotic cell numbers in the intestinal mucosa of C- and S-type animals; however, S-type animals exhibited significantly more Iba1- and cleaved caspase 3-positive cells in mesenteric lymph nodes. Lesions in mesenteric lymph nodes might indicate a differentially regulated course in MAP pathogenesis.