In this study, we aimed to investigate the changes in the B cell subpopulations after homologous or heterologous COVID-19 boosters. Blood samples were collected after baseline (3-5 months after two doses of CoronaVac), 1 and 3 months after BNT162b2 (n=28 and n=6), and CoronaVac (n=7 and n=4) boosters. Peripheral blood mononuclear cells (PBMCs) were isolated and stained with B cell markers, the ratios of naïve (CD19+CD20+CD27-), memory (CD19+CD20+CD27+), memory B cells expressing IgG (CD19+CD20+CD27+IgG+), and effector memory B cells (CD19+CD20+CD27+CD38+) were identified with flow cytometry. Significantly higher expression of memory B cells was observed in one month with BNT162b2 (12.16% one month, 5.98% three months) and CoronaVac (14.18% one month, 9.00% three months) boosters. IgG expressing memory B cell expression was significantly higher with BNT162b2 than with CoronaVac booster in one month (22.70% and 13.95%, respectively). The ratio of effector B cells in the first month after CoronaVac booster (25.44%) was significantly higher than the BNT162b2 booster (9.90%, p=0.0263). Keywords: COVID-19, SARS-CoV-2, B cell subtypes, mRNA vaccine, inactivated vaccine

Pseudomonas aeruginosa ST235 isolates drive a distinct macrophage inflammatory program characterized by IL-1β axis dominance and suppression of canonical NF-κB-associated cytokine responses. In THP-1-derived macrophages, ST235 isolates induce robust inflammasome activation, resulting in elevated IL-1β production and altered cell death responses, while eliciting markedly lower TNFα, IL-6, IL-8, and IL-10 responses than non-ST235 isolates. In contrast, nonST235 isolates preferentially stimulate NF-κB-dependent cytokine production with weaker inflammasome activation. Mechanistically, ST235 infection suppresses NF-κB signaling and reduces caspase-1 expression, whereas caspase-8 remains unchanged, indicating that increased IL-1β production can be due to alternative inflammasome pathways or posttranscriptional modifications. Rapid macrophage death further restricts overall cytokine production, reinforcing an IL-1β-dominant inflammatory profile. ST235 isolates also selectively reprogram M2-polarized macrophages toward an M1 phenotype, as demonstrated by increased CD86 expression, while both isolate groups promote M1 polarization in unpolarized macrophages. Importantly, pyoverdine purified from ST235 isolates reproduced aspects of these responses by inducing IL-1β production and cytotoxicity more effectively than pyoverdine from non-ST235 isolates, supporting a potential contribution of ST235-derived pyoverdine to the IL-1β-dominant inflammatory phenotype. Collectively, these findings suggest that ST235 isolates modulate macrophage immune responses through suppression of NF-κB-associated responses and promotion of IL-1β-dominant inflammation, providing insights into the virulence of this high-risk clone and highlighting potential therapeutic targets. Significant statement: ST235 isolates of P. aeruginosa uniquely modulate macrophage immune responses by robustly activating inflammasome signaling, inducing IL-1β expression while suppressing other cytokines, and driving macrophage polarization toward a pro-inflammatory M1 phenotype. These findings highlight distinct pathogenic strategies of ST235 isolates that may inform targeted therapeutic interventions.