Background: Despite all the available treatments, psoriasis remains incurable; therefore, finding personalized therapies is a continuous challenge. Psoriasis is linked to a gut microbiota imbalance, highlighting the importance of the gut–skin axis and its inflammatory mediators. Restoring this imbalance can open new perspectives in psoriasis therapy. We investigated the effect of purified IgY raised against pathological human bacteria antibiotic-resistant in induced murine psoriatic dermatitis (PSO). Methods: To evaluate the immune portrayal in an imiquimod experimental model, before and after IgY treatment, xMAP array and flow cytometry were used. Results: There were significant changes in IL-1α,β, IL-5, IL-6, IL-9, IL-10, IL-12 (p70), IL-13, IL-15, IL-17a, IFN-γ, TNF-α, IP-10/CXCL10, MCP-1/CCL2, MIP-1α/CCL3, MIP-1β/CCL4, MIG/CXCL9, and KC/CXCL1 serum levels. T (CD3ε⁺), B (CD19⁺) and NK (NK1.1⁺) cells were also quantified. In our model, TNF-α, IL-6, and IL-1β cytokines and CXCL1 chemokine have extremely high circulatory levels in the PSO group. Upon experimental therapy, the cytokine serum values were not different between IgY-treated groups and spontaneously remitted PSO. Conclusions: Using the murine model of psoriatic dermatitis, we show that the orally purified IgY treatment can lead to an improvement in skin lesion healing along with the normalization of cellular and humoral immune parameters.

Biofilms are structured communities of microorganisms embedded in a self-produced extracellular polymeric substance (EPS) matrix, whose development significantly enhances microbial resistance to antibiotics, disinfectants, and host immune defenses, posing major challenges in clinical, industrial, and environmental settings. Compared with planktonic cells, biofilm-associated microorganisms can exhibit up to 10- to 1000-fold increased tolerance to antimicrobial agents, contributing to the persistence of biofilm-associated infections (BAIs). These infections remain difficult to eradicate due to reduced penetration, altered metabolic states, and the presence of dormant or persister cells. Anti-biofilm strategies can be broadly classified into physical approaches (e.g., ultrasound, mechanical stress, and light-based approaches) that target biofilm structure; chemical and enzymatic methods (e.g., EPS-degrading enzymes) that destabilize the matrix; and biological and molecular strategies (e.g., quorum-sensing (QS) inhibitors, anti-virulence agents, bacteriophages, phage-derived antimicrobial molecules, antimicrobial peptides, and natural bioactive compounds) that modulate biofilm development and integrity by targeting regulatory pathways and matrix stability through distinct mechanisms of action. Natural compounds, including lactoferrin, lactoferrin-derived peptides, and probiotic and postbiotic fractions of lactic acid bacteria (LAB), as well as plant-derived metabolites, have shown promising anti-biofilm effects, with efficacy often enhanced through complementary or potentially synergistic interactions. However, despite these advancements, clinical translation remains limited. For example, BAIs account for approximately 80% of chronic infections, with high recurrence rates and therapeutic failure reported in device-associated infections and chronic wounds. These limitations highlight the need for clinically translatable, multimodal approaches that integrate structural biofilm disruption, antimicrobial targeting, and host response modulation to design more effective and sustainable anti-biofilm strategies.

Lactoferrin (Lf) is an iron-chelating glycoprotein present in the whey protein fraction in the milk of the majority of mammals. Since identifying bovine Lf (bLf) 85 years ago, the interest in this molecule has grown significantly. Thus, apart from its iron-binding and related antioxidant mechanisms, Lf was described as implicated in protecting the human organism by its immune-promoting, antimicrobial, and anti-carcinogenic mechanisms. Since the intrauterine period and throughout life, Lf ensures a balance between innate and adaptative immunity and can inhibit the growth of pathogenic microorganisms and tumor metastasis. This paper summarizes the aforementioned mechanisms of this multivalent molecule involved in innate immunity.

Background: SARS-CoV-2 immunity is understudied in cancer patients. Here, we monitored natural/vaccine-induced SARS-CoV-2 immunity in patients with head and neck cancer (HNC) stratified as vaccinated (mRNA/adenovirus-based vaccines), convalescent, and hybrid immunity. Methods: Plasma/PBMC samples were collected from 49 patients with HNC and 14 non-oncologic controls recruited between August 2021 and March 2022. Longitudinal follow-up was performed on 25 HNC patients. Plasma antibodies (Abs) against Spike (S1/S2), receptor-binding domain (RBD), and nucleocapsid (NC) of IgG/IgA isotypes and 25 cytokines/chemokines were quantified using MILLIPLEX^® technology. The frequency, phenotype, and isotype of circulating SARS-CoV-2-specific B-cells were studied by flow cytometry using RBD tetramers (Tet⁺⁺). The proliferation of B-cells and CD4+ and CD8+ T-cells in response to Spike/NC peptides was monitored by a carboxyfluorescein succinimidyl ester (CFSE) assay. Results: Plasma SARS-CoV-2 S1/S2/RBD IgG/IgA Abs were detected in all HNC participants at enrollment median time since immunization (TSI) 117 days at levels similar to controls and were significantly higher in convalescent/hybrid versus vaccinated. NC IgG/IgA Abs were only detected after infection. The frequency of Tet++ B-cells, enriched in the CD27+ memory phenotype and IgG/IgA isotype, positively correlated with plasma levels of RBD IgG/IgA Abs and Spike-specific CD4+ T-cell proliferation, regardless of the immunization status and TSI. Spike/NC-specific B-cell proliferation reached the highest levels in convalescent HNC and was positively correlated with NC IgG Abs, but not with the frequency of Tet++ B-cells. Finally, Tet++ B-cell frequencies remained stable between the two subsequent visits (median TSI: 117 versus 341 days), indicating their ability to persist for a relatively long time. Conclusions: This study monitored SARS-CoV-2 humoral/cellular immunity in an HNC cohort relative to non-oncologic participants and demonstrates that SARS-CoV-2-specific B-cells persist beyond 11 months post-immunization. These findings have implications for the management of HNC in the context of SARS-CoV-2 infection and other viral infections.

Multidrug resistance (MDR) is a major global health challenge, necessitating alternative or adjuvant strategies such as lactoferrin (Lf) and probiotics. Opportunistic bacteria are key drivers of healthcare-associated infections (HAIs) due to their ability to form biofilms and cause persistent infections. Lf, a glycoprotein present in mammalian milk and secretions, exhibits antimicrobial properties as part of innate immunity. Similarly, probiotics—primarily lactic acid bacteria (LAB)—influence pathogen growth and adhesion. This study evaluated the antimicrobial and anti-biofilm effects of purified bovine Lf (bLf) versus commercial Lf, alone and combined with LAB-derived supernatants, against several opportunistic strains. Using qualitative and quantitative methods, we assessed the antimicrobial, anti-adherence, and immunomodulatory activities of bLf (Sigma-Aldrich), commercial Lf (Jarrow Formulas), and LAB supernatants. High-purity bLf demonstrated superior antimicrobial and antibiofilm effects compared to supplement-derived Lf. Furthermore, commercial Lf, combined with LAB metabolites, effectively inhibited biofilm formation, reduced inflammation, and prevented bacterial adhesion to eukaryotic cells. These findings support the potential use of lactoferrin, alone or in synergy with probiotics, as adjuvants or prophylactic agents, particularly for immunocompromised patients, to limit bacterial adherence and prevent chronic infections.

Background: To fill the knowledge gap regarding the antiviral immunity in oncologic patients, we performed a comparative study on natural/vaccine-induced SARS-CoV-2 immunity in head and neck cancer (HNC) in Romania. Methods: Blood was collected from HNC (n=49) and controls (n=14), stratified as vaccinated (RNA/adenovirus-based vaccines), convalescent, and hybrid immunity. Plasma IgG/IgA antibodies (Abs) against Spike (S1/S2), receptor binding domain (RBD), and nucleocapsid (NC), and cytokines were quantified using the MILLIPLEX; technology. The frequency/phenotype/isotype of RBD-specific B-cells were studied by flow cytometry using tetramers (Tet++). Cell proliferation in response to Spike/NC peptides was monitored by carboxyfluorescein succinimidyl ester (CFSE) assay. A longitudinal follow-up was performed on n=25 HNC. Findings: Levels of S1/S2/RBD-specific IgG/IgA Abs were similarly high in HNC and controls, but significantly increased in convalescent/hybrid versus vaccinated HNC. NC-specific IgG/IgA Abs were only detected in convalescent/hybrid immunity groups. The frequency of Tet++ B-cells in HNC was similar to controls, irrespective of the immunization status, and correlated positively with RBD IgG/IgA Abs and negatively with the time since immunization (TSI). Compared to total B-cells, Tet++ were enriched in CD27+ memory phenotype and IgG/IgA isotype. A linear regression model identified Spike S2 IgG and NC IgA Abs as strong positive predictors of Tet++ frequencies, while IL-6 was a marginally significant negative predictor. Tet++ frequency remained stable at median TSI of 341 versus 117 days, despite a decline in memory phenotype. Interpretation: HNC participants mount efficient and durable SARS-CoV-2 humoral immunity, with RBD-specific IgG/IgA Abs and Tet++ B-cells representing the major immunization outcomes.