Chlamydia psittaci is an obligate intracellular zoonotic pathogen that causes psittacosis and severe respiratory illness in humans. Despite its clinical importance, no licensed vaccine is currently available, and antibiotic treatment may not provide long-term protection or prevent recurrent infection. To address this challenge, a computational strategy integrating structural vaccinology and immunoinformatics was used to design a multi-epitope vaccine targeting the major outer membrane porin and the virulence-associated pGP3-D protein of C. psittaci. Cytotoxic T-cell and helper T-cell epitopes were identified and screened to select antigenic candidates. The selected epitopes were joined using linker sequences together with β-defensin-3 and PADRE. The vaccine construct was evaluated using physicochemical analysis, three-dimensional structural modeling, interaction analysis with TLR2, a 500 ns molecular dynamics simulation, MM-GBSA binding free-energy analysis, immune simulation, and in silico cloning. The designed vaccine was predicted to possess favorable antigenicity, a non-allergenic profile, suitable physicochemical properties, and a global population coverage of 92.15%. Computational analyses suggested stable interaction with TLR2 and indicated structural stability of the vaccine–receptor complex during the simulation. Immune simulation predicted increased IgG levels, memory B-cell formation, activation of CD8+ T lymphocytes, and a cytokine profile consistent with Th1-type immune responses. These findings suggest that the proposed construct represents a computationally designed multi-epitope vaccine candidate that requires further evaluation through experimental studies to determine its safety, immunogenicity, and protective efficacy against C. psittaci.
Background: M1-like and M2-like macrophages are found in acute myocardial infarction, but their activation during and after ST-segment elevation myocardial infarction (STEMI) in humans is unclear. Methods: Circulating cytokines were measured in 50 patients sampled on day 1 (STEMI) and day 5 (post-STEMI), and healthy subjects (n = 22). Moreover, monocyte-derived M1-like and M2-like macrophages from the three groups were polarized and activated to analyze their phenotype and function (n = 14/group). Results: STEMI and post-STEMI patients showed elevated levels of CD80, CD86 and inflammatory cytokines such as TNF-α in M1-like macrophages, whereas the levels of CD36, CD206, and anti-inflammatory cytokines such as IL-10 were elevated in M2-like macrophages. Additionally, compared with the conditioned medium of M2-like macrophages, that of M1-like macrophages induced the expression of molecules such as CD54 and CD31 on HUVECs in STEMI and post-STEMI patients. Finally, the levels of pro- and anti-inflammatory cytokines and MMP-9 in M1-like and M2-like macrophages were similar in the plasma of STEMI and post-STEMI patients, whereas the plasma level of IL-6 was decreased in post-STEMI patients. Conclusions: M1-like and M2-like macrophages may participate simultaneously in STEMI and post-STEMI by secreting cytokines and metalloproteinases and through endothelial activation. Furthermore, these cells may contribute to the circulating cytokine microenvironment in these patients.
