Abstract
The bovine tuberculoid granuloma is the hallmark lesion of bovine tuberculosis (bTB) due to Mycobacterium bovis infection. The pathogenesis of bTB, and thereby the process of bovine tuberculoid granuloma development, involves the recruitment, activation, and maintenance of cells under the influence of antigen, cytokines and chemokines in affected lungs and regional lymph nodes. The granuloma is key to successful control of bTB by preventing pathogen dissemination through containment by cellular and fibrotic layers. Paradoxically, however, it may also provide a niche for bacterial replication. The morphologic and cellular characteristics of granulomas have been used to gauge disease severity in bTB pathogenesis and vaccine efficacy studies. As such, it is critical to understand the complex mechanisms behind granuloma initiation, development, and maintenance.
Highlights
The T helper (TH )1/TH 2 T cell paradigm described for mice, may not transfer precisely to bovine immune responses, it can be a useful framework for understanding immune responses dominated by either cell-mediated (TH 1) or antibody-mediated (TH 2)
Later stages III/IV are associated with increased peripheral fibrosis, which eventually encapsulates the granuloma within bands of collagenous connective tissue
In humans and models of human tuberculosis fibrosis and dystrophic calcification have been described as processes associated with healing [118], healing granulomas or fibrous organizing granulomas have not been described as such in cattle, possibly due to the lack of use of chemotherapeutic agents in bovine bovine tuberculosis (bTB)
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The pathogenesis of bovine tuberculosis (bTB), and thereby the process of bovine tuberculoid granuloma development, involves the recruitment, activation, and maintenance of cells under the influence of antigen, cytokines and chemokines in affected lungs and regional lymph nodes. As part of the adaptive immune response, some macrophages and dendritic cells containing bacilli exit the alveolar spaces and enter the pulmonary interstitium where they access lymphatic or hematogenous systems and spread to local lymph nodes (tracheobronchial and mediastinal). Not surprising that the cytokine environment in developing granulomas of the lung differ from those of the associated lymph nodes, even when examined at the same time and in the same animal [24] It has been shown, in cattle experimentally infected via aerosolized M. bovis, that late-stage granulomas in the lung showed greater expression of interferon gamma (IFN-γ), transforming growth factor beta (TGF-β), interleukin (IL)-10 and IL-22 mRNA than similar-late stage granulomas in the associated tracheobronchial lymph node. Expression of IL-17A mRNA was greater in granulomas of the tracheobronchial lymph node compared to the lung [24]
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