Abstract
Footrot is a common inflammatory bacterial disease affecting the health and welfare of sheep worldwide. The pathogenesis of footrot is complex and multifactorial. The primary causal pathogen is the anaerobic bacterium Dichelobacter nodosus, with Fusobacterium necrophorum also shown to play a key role in disease. Since immune-mediated pathology is implicated, the aim of this research was to investigate the role of the host response in interdigital dermatitis (ID) and footrot. We compared the expression of Toll-like receptors (TLRs) and pro-inflammatory cytokines and the histological appearance of clinically normal in comparison to ID and footrot affected tissues. Severe ID and footrot were characterised by significantly increased transcript levels of pro-inflammatory cytokines TNFα and IL1β and the pattern recognition receptors TLR2 and TLR4 in the interdigital skin. This was reflected in the histopathological appearance, with ID and footrot presenting progressive chronic-active pododermatitis with a mixed lymphocytic and neutrophilic infiltration, gradually increasing from a mild form in clinically normal feet, to moderate in ID and to a focally severe form with frequent areas of purulence in footrot. Stimulation with F. necrophorum and/or D. nodosus extracts demonstrated that dermal fibroblasts, the resident cell type of the dermis, also contribute to the inflammatory response to footrot bacteria by increased expression of TNFα, IL1β and TLR2. Overall, ID and footrot lead to a local inflammatory response given that expression levels of TLRs and IL1β were dependent on the disease state of the foot not the animal.
Highlights
Footrot is a bacterial infection of the interdigital skin of the sheep foot resulting in lameness, and is the greatest welfare and economic concern for sheep farmers and veterinary surgeons in the UK (Goddard et al, 2006)
Since bacteria were observed in the dermis in tissue sections from feet with footrot, we investigated TLR1, TLR2, TLR4, TLR6, IL-1ˇ and TNFexpression in ovine dermal fibroblasts, a resident dermal cell type, in response to LPS and heat-killed extracts of D. nodosus and F. necrophorum (Fig. 3)
Enhanced expression of TLR2 and TLR4 in response to infection has been observed in another ovine infectious disease, Johne’s disease, caused by Mycobacterium avium subspecies paratuberculosis (MAP) (Taylor et al, 2008)
Summary
Footrot is a bacterial infection of the interdigital skin of the sheep foot resulting in lameness, and is the greatest welfare and economic concern for sheep farmers and veterinary surgeons in the UK (Goddard et al, 2006). Davenport et al / Veterinary Immunology and Immunopathology 161 (2014) 90–98 is required to initiate disease Bacterial replication in this damaged skin leads to interdigital dermatitis (ID) where the superficial epidermal layers are inflamed, damaged and slough off irregularly. A second bacterium, Fusobacterium necrophorum, may play a role in the pathogenesis of footrot It either facilitates disease development by increasing the damage to the interdigital skin and promoting ID that subsequently permits replication of D. nodosus (Egerton et al, 1969; Roberts and Egerton, 1969) or F. necrophorum is secondary to D. nodosus but may exacerbate the severity and persistence of footrot (Beveridge, 1941; Kennan et al, 2010, 2011; Witcomb et al, 2014)
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