Activation of MyD88-Dependent TLR Signaling Modulates Immune Response of the Mouse Heart during Pasteurella multocida Infection.

Pasteurella multocida (P. multocida) is an important zoonotic pathogen. In addition to lung lesions, necropsies have revealed macroscopic lesions in the heart in clinical cases. However, most previous studies focused on lung lesions while ignoring heart lesions. Therefore, to investigate the immune response of the P. multocida-infected heart, two murine infection models were established by using P. multocida serotype A (Pm HN02) and D (Pm HN01) strains. Histopathological examination revealed heterogeneous inflammatory responses, including immune cell infiltration in the epicardial and myocardial areas of the heart. Transcriptome sequencing was performed on infected cardiac tissues. To explore the traits of immune responses, we performed the functional enrichment analysis of differentially expressed genes, gene set enrichment analysis and gene set variation analysis. The results showed that the innate immune pathways were significantly regulated in both groups, including the NOD-like receptor signaling pathway, the complement and coagulation cascade and cytokine-cytokine receptor interaction. The Toll-like receptor signaling pathway was only significantly activated in the Pm HN02 group. For the Pm HN02 group, immunohistochemistry analysis further verified the significant upregulation of the hub component MyD88 at the protein level. In conclusion, this study reveals critical pathways for host heart recognition and defense against P. multocida serotypes A and D. Moreover, MyD88 was upregulated by P. multocida serotype A in the heart, providing a theoretical basis for future prevention, diagnosis and treatment research.

Human influenza A virus causes myocardial and cardiac-specific conduction system infections associated with early inflammation and premature death.

AIMS: Human influenza A virus (hIAV) infection is associated with important cardiovascular complications, although cardiac infection pathophysiology is poorly understood. We aimed to study the ability of hIAV of different pathogenicity to infect the mouse heart, and establish the relationship between the infective capacity and the associated in vivo, cellular and molecular alterations. METHODS AND RESULTS: We evaluated lung and heart viral titres in mice infected with either one of several hIAV strains inoculated intranasally. 3D reconstructions of infected cardiac tissue were used to identify viral proteins inside mouse cardiomyocytes, Purkinje cells, and cardiac vessels. Viral replication was measured in mouse cultured cardiomyocytes. Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were used to confirm infection and study underlying molecular alterations associated with the in vivo electrophysiological phenotype. Pathogenic and attenuated hIAV strains infected and replicated in cardiomyocytes, Purkinje cells, and hiPSC-CMs. The infection was also present in cardiac endothelial cells. Remarkably, lung viral titres did not statistically correlate with viral titres in the mouse heart. The highly pathogenic human recombinant virus PAmut showed faster replication, higher level of inflammatory cytokines in cardiac tissue and higher viral titres in cardiac HL-1 mouse cells and hiPSC-CMs compared with PB2mut-attenuated virus. Correspondingly, cardiac conduction alterations were especially pronounced in PAmut-infected mice, associated with high mortality rates, compared with PB2mut-infected animals. Consistently, connexin43 and NaV1.5 expression decreased acutely in hiPSC-CMs infected with PAmut virus. YEM1L protease also decreased more rapidly and to lower levels in PAmut-infected hiPSC-CMs compared with PB2mut-infected cells, consistent with mitochondrial dysfunction. Human IAV infection did not increase myocardial fibrosis at 4-day post-infection, although PAmut-infected mice showed an early increase in mRNAs expression of lysyl oxidase. CONCLUSION: Human IAV can infect the heart and cardiac-specific conduction system, which may contribute to cardiac complications and premature death.

Heart Infection Prognosis Analysis by Two-dimensional Spot Tracking Imaging.

Cardiovascular death is one of the leading causes worldwide; an accurate identification followed by diagnosing the cardiovascular disease increases the chance of a better recovery. Among different demonstrated strategies, imaging on cardiac infections yields a visible result and highly reliable compared to other analytical methods. Two-dimensional spot tracking imaging is the emerging new technology that has been used to study the function and structure of the heart and test the deformation and movement of the myocardium. Particularly, it helps to capture the images of each segment in different directions of myocardial strain values, such as valves of radial strain, longitudinal strain, and circumferential strain. In this overview, we discussed the imaging of infections in the heart by using the two-dimensional spot tracking.

Endocarditis infecciosa actinomicótica de la válvula mitral: caso de autopsia y revisión de la literatura / Actinomycotic infective endocarditis of the mitral valve: anatomoclinical case and review of literature

La infección actinomicótica del corazón es una enfermedad poco común, especialmente cuando el compromiso endocárdico valvular es primario. Sólo unos pocos casos han sido publicados. Comunicamos un caso de endocarditis primaria por Actinomyces sp de la válvula mitral, diagnosticada en la necropsia de un hombre de 34 años con antecedentes de valvulopatía reumática crónica, que falleció con una endocarditis infecciosa.

Actinomycotic infections of the heart is an uncommon disease, especially if the infection affects the valvular endocardium as primary focus. Just a few cases have been reported previously. We report a case of primary endocarditis of the mitral valve caused by Actinomyces sp diagnosed at necropsy in a 34 year-old man with history of chronic rheumatic disease presenting as a usual case of infective endocarditis.