Neutrophils, known to be mobilized and activated in high amounts through Il-17 stimulation, are a key factor for clinical manifestation and imbalance of redox systems favoring a dominant oxidative state in both severe asthma and acute lung injury (f). The aim of this study was to evaluate in mice, the effect of Secukinumab (SECU) in a model of ovalbumin-induced asthma exacerbated with LPS administration to induce ALI, compared to dexamethasone (DEXA), already known for its benefit in both asthma and ALI. Results on cytokine levels for specific Th1, Th2 and Th17 revealed an interplay of immune responses. For Th1 effector cytokines in BALF, DEXA treatment increased TNF-α levels, but TNF-α was not modified by SECU; DEXA and SECU significantly decreased IFN-γ and IL-6 levels. For typical Th2 cytokines, DEXA significantly increased Il-4, Il-5 and Il-13 levels, while SECU significantly inhibited Il-5 levels. Both SECU and DEXA significantly decreased Il-17 levels. Cytokine level changes in lung tissue homogenate were partly similar to BALF cytokines. Conclusion: in addition to DEXA, SECU possesses the ability to modulate inflammatory cytokine release and to decrease Th17 responses in ALI overlapped on exacerbated asthma in mice.

(1) Background: Recent data shed light on the association between atopic disorders (ADs) (atopic dermatitis, allergic asthma, allergic rhinitis) and spondyloarthropathies (SpAs), underpinning the critical role of T helper (Th)1-Th17/Th2-T regulatory cells disbalance. We evaluated the prevalence of AD in axial SpAs (axSpAs) and psoriatic arthritis (PsA) and explored the potential association between atopic status, disease-related parameters, and biological therapy. (2) Methods: A monocentric, retrospective study was conducted that enrolled 200 patients taking biologics. Demographics, disease, and drug-related variables, along with a screening questionnaire focused on Ads, were systematically collected. (3) Results: Overall, 51 patients (25.5%) had atopy—namely, 24.4% of axSpA and 28% of PsA, with a higher frequency of rhinitis (43%) vs. atopic dermatitis (37.2%) or asthma (21.5%). We failed to demonstrate any statistically significant difference in demographics, SpA-related parameters excepting concomitant inflammatory bowel disease, and biologic drug exposure in patients with and without atopy (p > 0.05). However, significantly more non-atopic patients need only one TNF inhibitor (54%) vs. atopic patients (28%) (p < 0.05) to control active SpA. (4) Conclusions: We successfully demonstrated that AD is associated with one out of four SpA. Irrespective of the SpA subtype, atopic patients require more frequent switching among biologics, as significantly more non-atopic patients remain on their first anti-TNF.

Background/Objectives: Atopy and spondyloarthritis (SpA) are immune-mediated diseases driven by distinct T-helper (Th) cell pathways—Th2 for atopy and Th1/Th17 for SpA. The coexistence of these divergent immune responses is increasingly recognized, particularly in the context of biological therapies that target pro-inflammatory cytokines. This study aimed to investigate Th2 cytokine profiles (IL-4, IL-5, IL-13) in atopic SpA patients receiving biological therapy to better understand how such treatment may influence immune regulation in this complex clinical setting. Methods: We conducted a prospective observational cross-sectional study on 136 SpA patients stratified by biological therapy and atopy status. Serum IL-4, IL-5, and IL-13 levels were quantified using LUMINEX immunoassays. Patients were grouped into biologically treated (BT) and Bio-Naïve (BN) cohorts and further sub-categorized by atopic phenotype (allergic rhinitis, asthma, dermatitis). Statistical comparisons of cytokine levels were made using SPSS IBM version 26 to explore associations with clinical and demographic variables. Results: IL-13 levels were significantly elevated in BT-atopic patients, particularly those with allergic rhinitis and atopic dermatitis, suggesting biological therapy may modulate Th2 responses. IL-5 remained elevated in allergic asthma cases despite treatment, indicating persistent eosinophilic activity. No significant correlation was found between cytokine levels and disease duration or therapy length. Conclusions: Biological therapy in SpA may influence Th2 cytokine expression, notably IL-13, in atopic patients. These findings underscore the importance of immune profiling in guiding personalized treatment strategies and highlight the need for further investigation into the long-term immunomodulatory effects of biologics in patients with overlapping Th1/Th2-driven diseases.

(1) Objective: The main aims of our study were to explore the drug survival and effectiveness of secukinumab in patients with axial spondyloarthritis (axSpA). (2) Methods: We underwent a retrospective analysis of consecutive axSpA treated with secukinumab as a first line of biologics or at switch in a biologic-experienced population. Efficacy data, indicating improvement in inflammation parameters (such as C-reactive protein and erythrocyte sedimentation rate) and disease activity scores (such as Ankylosing Spondylitis Disease Activity Score [ASDAS-CRP], Bath Ankylosing Spondylitis Disease Activity Index [BASDAI]), and patient-reported outcomes (pain), were assessed at 6, 12, 24, 36 and 48 months. The drug survival rate, dropout rate and discontinuation reasons (efficacy versus safety) of secukinumab were assessed in subgroup analysis (axSpA with and without exposure to biologics). (3) Results: In total, 46 patients were exposed to the IL-17A inhibitor secukinumab. The drug survival for axSpA patients 59.7% at 12 months and 31.3% at 24 months. There were no statistically significant differences in the median drug survival between biologic-naïve versus biologic-experienced subgroups. (4) Conclusions: Secukinumab has demonstrated effectiveness and safety in treating a cohort of axSpA patients in real-world settings, with a notable retention rate of the drug.

(1) Background: Although the association between psoriasis and atopic dermatitis (AD) is reported in the literature, scarce data are known about the efficacy of biologic therapy (including TNF and IL-17 inhibitors) in patients with psoriatic arthritis (PsA) and concomitant AD. (2) Objective: We aimed to explore AD in patients with PsA undergoing biologics for their active disease, focusing on prevalence and clinical and potential therapeutic implications. (3) Material and methods: We performed a retrospective analysis of 64 patients with PsA receiving various biological agents, followed-up in an academic outpatient rheumatology department up to 10 years. (4) Results: Atopic diseases were reported in about one third of cases, with a higher incidence of AD (10 cases; 52.6%) vs. atopic rhinitis (6 cases; 31.6%) and allergic asthma (3 cases; 15.8%). Three morphological patterns of AD were recognized including chronic prurigo (3 cases), a chronic lichen simplex (1 case), and eczemas (6 cases). All PsA with concomitant AD displayed a late onset of skin atopy (in their adult life) and demonstrated a specific profile (younger), from urban settings, equally distributed among genders, and requiring switching to a higher number of biologics to achieve disease control. (5) Conclusion: PsA and AD may coexist, requiring special attention when selecting the optimal biologic agent.

Background: Young-onset rheumatoid arthritis (YORA), defined by disease onset between 16–40 years, raises distinct clinical challenges related to long-term disease burden, fertility, and prolonged exposure to immunomodulatory therapy. Despite its relevance, evidence regarding treatment outcomes in this population remains limited and heterogeneous, largely due to inconsistent definitions of YORA across studies. Methods: This systematic review was conducted in accordance with the PRISMA 2020 guidelines to synthesize contemporary evidence on the efficacy and safety of biologic and targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) in younger rheumatoid arthritis populations. A structured search of PubMed and Embase was performed to identify studies published between 2020 and 2025 that evaluated advanced therapies in patients with young-onset rheumatoid arthritis or in rheumatoid arthritis cohorts reporting age-stratified outcomes for younger adults. Results: From the screened literature, 16 studies met the predefined inclusion criteria, including 6 studies explicitly defining YORA based on age at disease onset and 10 studies reporting outcomes in younger adult subgroups (<40–45 years). Across studies, younger patients demonstrated higher remission rates, greater reductions in disease activity, and superior treatment persistence compared with older-onset rheumatoid arthritis cohorts. Tumor necrosis factor inhibitors, interleukin-6 receptor antagonists, and Janus kinase inhibitors showed consistent clinical efficacy. Structural outcomes, reported in a limited number of studies, suggested low rates of radiographic progression in younger patients. Safety profiles were generally favorable, with infections and laboratory abnormalities representing the most reported adverse events and no age-specific safety signals being identified. Conclusions: Biologic and targeted therapies provide substantial clinical benefit in YORA and younger adult RA populations, with outcomes being generally superior to those observed in older-onset RA. However, heterogeneity in YORA definitions and limited long-term data highlight the need for prospective, age-at-onset-defined studies and extended pharmacovigilance to better inform lifelong treatment strategies.