# Pro-Inflammatory Response of Bovine Lung Explant Induced by Mycoplasma mycoides subsp. mycoides

## TL;DR

This study shows that Mycoplasma mycoides subsp. mycoides triggers a pro-inflammatory response in bovine lung tissue, involving specific cytokines and receptors.

## Contribution

The study reveals the role of TLR2 and TLR4 in the inflammatory response to Mmm in bovine lung explants.

## Key findings

- Mmm infection stimulates production of IL-1β, COX-2, 5-LOX, and iNOS in bovine lung explants.
- TLR2 and TLR4 are detected in tissue culture supernatants of Mmm-infected explants.
- mRNA expression did not show significant changes despite cytokine production.

## Abstract

Contagious bovine pleuropneumonia (CBPP) is a significant respiratory disease in cattle caused by Mycoplasma mycoides subsp. mycoides (Mmm). A better understanding of the pathogenesis of CBPP and the immune response of the host to infection will assist in the development of novel interventions to prevent disease progression. In this study, bovine lung explants (BLEs) were exposed to Mmm to investigate the upregulation and release of early inflammatory cytokines, mediators and receptors following tissue infection. Immunomodulatory molecules indicative of cell activation were investigated by immunoblotting on the BLEs and the tissue culture supernatants, and quantitative real-time PCR (RTq-PCR) was performed on the BLEs to determine the fold change in the expression of the respective mRNA. Immunoblotting indicated the production of inflammatory cytokines, mediators and receptors in Mmm-infected BLEs; however, this contrasted strongly with the mRNA expression profile, which did not show any significant fold increase. Infection of the BLEs with Mmm stimulated the production of some pro-inflammatory cytokines and mediators, including IL-1β, COX-2, 5-LOX and iNOS. Toll-like receptor proteins TLR2 and TLR4 were detected solely in the tissue culture supernatant of Mmm-infected BLEs. These receptors are considered to be involved in the recognition of Mmm by BLE tissue cells, thus triggering intracellular pathways that produce specific inflammatory cytokines and mediators, initiating the inflammatory response.