Field, E. | Search bioRxiv

bioRxiv2024

Tree diversity reduces pathogen damage in temperate forests: a systematic review and meta-analysis

Diversifying planted forests to reduce the risks associated with large scale disturbances, such as pathogens, is a major aim of sustainable forest management. Previous meta-analyses have shown that insect pest damage is lower in mixed forest stands compared to monocultures, but the same has not been shown for pathogens. Here, we provide the first systematic review and meta-analysis specifically testing the effects of tree species diversity on pathogen damage. Relevant studies were retrieved using bibliographic databases and internet searches, as well as previously unpublished data sets contributed by stakeholders. We found that more diverse forest stands overall had significantly lower pathogen damage, and that this result was most pronounced in temperate forests for which the most studies were available. Although in some cases tree diversity had a strong effect, this was not universal and was influenced neither by pathogen specialism, nor by the presence of alternative hosts in stands. Instead, we found that tree neighbour identity rather than species richness emerged as a crucial variable impacting pathogen damage in mixed stands. Neighbour identity effects reported in studies were far-ranging, including impacts on the microclimate of stands. Future work should focus on mechanistic explanations that could underpin neighbour identity effects in mixed forests. We suggest the use of the disease triangle as a tool for considering the multiple factors that can influence pathogen damage in mixed forest stands.

ecology↗

bioRxiv2023

Innate Immune Signaling in Hearts and Buccal Mucosa Cells of Patients with Arrhythmogenic Cardiomyopathy

STRUCTURED ABSTRACTO_ST_ABSObjectivesC_ST_ABSWe sought to determine if persistent innate immune signaling via NF{kappa}B occurs in cardiac myocytes in patients with arrhythmogenic cardiomyopathy and if this is associated with myocardial infiltration of pro-inflammatory cells expressing CCR2. We also determined if buccal mucosa cells from young subjects with inherited disease alleles exhibit NF{kappa}B signaling. BackgroundNF{kappa}B signaling in cardiac myocytes causes disease in a mouse model of arrhythmogenic cardiomyopathy by mobilizing CCR2-expressing macrophages which promote myocardial injury and arrhythmias. Buccal mucosa cells exhibit pathologic features similar to those seen in cardiac myocytes in patients with arrhythmogenic cardiomyopathy. MethodsWe analyzed myocardium from arrhythmogenic cardiomyopathy patients who died suddenly or required cardiac transplantation. We also analyzed buccal mucosa cells from young subjects with inherited disease alleles. The presence of immunoreactive signal for RelA/p65 in nuclei of cardiac myocytes and buccal cells was used as a reliable indicator of active NF{kappa}B signaling. We also counted myocardial CCR2-expressing cells. ResultsNF{kappa}B signaling was seen in cardiac myocytes in 34 of 36 cases of arrhythmogenic cardiomyopathy but in none of 19 age-matched controls. Cells expressing CCR2 were increased in patient hearts in numbers directly correlated with the number of cardiac myocytes showing NF{kappa}B signaling. NF{kappa}B signaling also occurred in buccal cells in young subjects with active disease. ConclusionsPatients with clinically active arrhythmogenic cardiomyopathy exhibit persistent innate immune responses in cardiac myocytes and buccal mucosa cells reflecting an inflammatory process that fails to resolve. Such individuals may benefit from anti-inflammatory therapy. CONDENSED ABSTRACTNF{kappa}B signaling in cardiac myocytes causes arrhythmias and myocardial injury in a mouse model of arrhythmogenic cardiomyopathy by mobilizing pro-inflammatory CCR2-expressing macrophages to the heart. Based on these new mechanistic insights, we analyzed hearts of arrhythmogenic cardiomyopathy patients who died suddenly or required cardiac transplantation. We observed active NF{kappa}B signaling in cardiac myocytes associated with marked infiltration of CCR2-expressing cells. We also observed NF{kappa}B signaling in buccal mucosa cells obtained from young subjects with active disease. Thus, anti-inflammatory therapy may be effective in arrhythmogenic cardiomyopathy. Screening buccal cells may be a reliable way to identify patients most likely to benefit. HIGHLIGHTS- Inflammation likely contributes to the pathogenesis of arrhythmogenic cardiomyopathy but the responsible mechanisms and the roles of specific classes of immune cells remain undefined. - NF{kappa}B signaling in cardiac myocytes is sufficient to cause disease in a mouse model of arrhythmogenic cardiomyopathy by mobilizing injurious myeloid cells expressing CCR2 to the heart. - Here, we provide evidence of persistent NF{kappa}B signaling in cardiac myocytes and increased CCR2-expressing cells in hearts of patients with arrhythmogenic cardiomyopathy. We observed a close correlation between the number of cardiac myocytes with active NF{kappa}B signaling and the number of CCR2-expressing cells in patient hearts. - We also provide evidence of active NF{kappa}B signaling in buccal mucosa cells associated with initial onset of disease and/or disease progression in young subjects with arrhythmogenic cardiomyopathy alleles.

pathology↗