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Effects of inflammatory stimuli on responses of macrophages to Mycoplasma bovis infection
Monica Baquero1, Ksenia Vulikh1, Cassidy Wong1
1Department of Pathobiology, University of Guelph, Guelph, Ontario, Canada.
Abstract:
Inflammation in the respiratory tract is thought to worsen the disease response to Mycoplasma bovis infection. This study investigated the cells involved in this response with a focus on proteases and cytokines as harmful effector mechanisms. By immunohistochemistry, Mac387-positive macrophages were the main cell type comprising the foci of caseous necrosis in cattle with M. bovis pneumonia. Thus, the study evaluated how priming of different types of macrophages with bacterial lysate (or pro-inflammatory cytokines induced by the bacterial lysate) affected their responses to M. bovis infection. Inducible responses were detected in monocyte-derived macrophages (M1-MDMs and M2-MDMs), whereas pulmonary alveolar macrophages (PAMs) were minimally affected by priming or infection. M. bovis-infected MDMs secreted MMP-12 and SPLA2, and priming with pro-inflammatory cytokines increased the secretion of cathepsin B in response to M. bovis infection. Of these, there were higher concentrations of cathepsin B and SPLA2 in lungs with M. bovis pneumonia compared to healthy lungs, and these are potential mechanisms for macrophage-induced lung damage in M. bovis infection. Priming of MDMs with either bacterial lysate or with pro-inflammatory cytokines caused an enhanced response to M. bovis infection with respect to IL-8 and IL-1β secretion. The findings of this study suggest proteases, lipases and cytokines derived from monocyte-derived macrophages as possible mediators by which prior inflammation in the respiratory tract worsen disease outcomes from M. bovis infection.
Insights
Prior respiratory inflammation worsens Mycoplasma bovis infection outcomes. Monocyte-derived macrophages release proteases and cytokines, contributing to lung damage and disease severity.
Area of Science:
- Veterinary Immunology
- Bovine Respiratory Disease
- Pathogen-Host Interactions
Background:
- Respiratory tract inflammation exacerbates Mycoplasma bovis infection.
- Macrophages are key cellular players in bovine pneumonia.
- Proteases and cytokines are implicated as harmful effector mechanisms.
Purpose of the Study:
- Investigate macrophage responses to Mycoplasma bovis infection.
- Determine the role of proteases and cytokines in M. bovis-induced lung damage.
- Evaluate the effect of priming on macrophage responses.
Main Methods:
- Immunohistochemistry to identify macrophages in M. bovis pneumonia lesions.
- Priming of monocyte-derived macrophages (MDMs) and pulmonary alveolar macrophages (PAMs) with bacterial lysate or cytokines.
- Assessing protease (MMP-12, SPLA2, cathepsin B) and cytokine (IL-8, IL-1β) secretion post-infection.
Main Results:
- Mac387-positive macrophages were prevalent in M. bovis pneumonia lesions.
- MDMs, but not PAMs, showed inducible responses to priming and M. bovis infection.
- M. bovis-infected MDMs secreted MMP-12 and SPLA2; cathepsin B increased with cytokine priming.
- Elevated cathepsin B and SPLA2 levels were found in infected lungs.
- Priming enhanced IL-8 and IL-1β secretion from MDMs upon M. bovis infection.
Conclusions:
- Monocyte-derived macrophages release proteases (cathepsin B, MMP-12, SPLA2) and cytokines (IL-8, IL-1β) that mediate lung damage in M. bovis infection.
- Prior inflammation primes MDMs, enhancing their detrimental response to M. bovis.
- These macrophage-derived factors are potential mediators linking respiratory inflammation to worsened M. bovis disease outcomes.
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