Influenza virus (Influenzavirus A) and Staphylococcus aureus (S. aureus) co-infection is a critical clinical challenge, often leading to severe complications such as necrotizing pneumonia. This review elucidates the mechanisms by which influenza virus facilitates S. aureus infections through epithelial damage and immune modulation, thereby exacerbating pulmonary injury. Specifically, influenza virus infection damages respiratory epithelial cells and disrupts the integrity of the lung barrier. This process facilitates the invasion of S. aureus, which produces various virulence factors, including Panton-Valentine leukocidin (PVL) and phenol-soluble modulins (PSMs), leading to enhanced inflammation and tissue destruction. Furthermore, methicillin-resistant S. aureus (MRSA) strains are associated with higher morbidity and mortality due to their resistance to beta-lactam antibiotics and increased toxin production. Understanding the interplay between influenza virus-induced epithelial damage and S. aureus toxin-mediated immune responses is crucial for developing effective therapeutic interventions to mitigate the severity of necrotizing pneumonia. This review also explores the potential roles of adjunctive therapies, such as extracorporeal membrane oxygenation (ECMO) and novel agents like intravenous immunoglobulin (IVIG) and N-acetylcysteine (NAC), in redefining treatment paradigms for these severe infections.

Pediatric Post-COVID Condition (PPCC) represents a significant and complex long-term sequela of SARS-CoV-2 infection, affecting a subset of children and adolescents even after mild acute disease. While acute COVID-19 is generally milder in children due to a more robust innate immune response, the mechanisms driving the persistence of symptoms in PPCC remain incompletely understood and likely multifactorial. This narrative review synthesizes current epidemiological data and explores the "perfect storm" of immunological and pathophysiological alterations underpinning the condition. We examine critical hypotheses including a dysregulated immune response characterized by altered T-cell subsets, monocyte activation, and autoantibody production. We discuss the potential role of persistent SARS-CoV-2 viral reservoirs in "sanctuary sites" like the gastrointestinal tract and the reactivation of latent viruses such as Epstein-Barr virus (EBV). Furthermore, the review details downstream pathogenic pathways, including vascular endothelial inflammation (thrombo-inflammation), neuroinflammation, and metabolic dysfunctions affecting the mitochondria and tryptophan-kynurenine pathway. Finally, we address the role of microbiome dysbiosis in perpetuating systemic inflammation and the gut-lung axis dysfunction. Given the heterogeneity of clinical presentations, we conclude that PPCC is likely a syndrome of overlapping biological phenotypes. Future research must prioritize identifying these specific biological endotypes to develop targeted diagnostic and therapeutic strategies for the pediatric population.

Eosinophil-associated diseases are a group of inflammatory disorders characterized by abnormal eosinophil infiltration, which significantly impacts patients' quality of life. Interleukin-5 (IL-5), a critical cytokine that regulates eosinophil development, activation, chemotaxis, and survival, plays a central role in the pathogenesis of these diseases. This review systematically examines the molecular structure and signaling pathways of IL-5, its mechanisms of action in asthma and chronic obstructive pulmonary disease (COPD), and the development and clinical applications of monoclonal antibodies (e.g., mepolizumab, benralizumab, reslizumab) and other biologics targeting IL-5. Although IL-5-targeted therapies have yielded significant results, single-target interventions still exhibit limitations, including insufficient responses in certain patients. To address this, we explore the strategy of multi-target combination therapies, such as the synergistic inhibition of IL-5 with the IL-4/IL-13 and IL-33/ST2 pathways. We also discuss the potential of novel therapeutic approaches, including bispecific antibodies and small-molecule inhibitors. Ultimately, multi-targeted precision therapies, tailored to individual inflammatory phenotypes, are anticipated to represent a new frontier in the management of eosinophil-associated diseases.

Dysventilation is a chronic alteration of physiological ventilation patterns, characterized by a predominance of mouth or mouth-nose breathing at rest. It should not be considered a simple symptom, but rather a functional disorder in its own right, capable of disrupting facial morphogenesis and promoting neurocognitive disorders.

Dysventilation is the cause of a dysmorpho-functional spiral. The aim of this article is to determine how its multidisciplinary management, particularly through orthodontics and orofacial myofunctional therapy (OMT), can help put children back on the path to harmonious growth and offer adults better oro-cranio-facial balance.

A synthesis of published data on the morphological and functional consequences of dysventilation was performed. The conclusions of the data and recommendations concerning the organization and means of managing dysventilation and obstructive sleep apnea were reported. A clinical case is presented to illustrate the clinical management of dysventilation using the MyoSimple®, a new, patented myofunctional rehabilitation appliance featuring a specific tongue ramp.

The published data, even though of uneven methodological quality, seem to show the superiority of OMT combined with the use of a prefabricated functional appliance (PFA) compared to the implementation of OMT without PFA, particularly in the context of dysventilation management. A new approach to OMT, active and passive with PFA, which is more effective, simpler, and less time-consuming, is proposed. The MyoSimple®, a new patented prefabricated functional appliance, features a specific tongue ramp. Wearing it helps to promote tongue thrust, combined with clearing of the upper airways and promotes nasal breathing. A clinical case is presented to illustrate the clinical management of dysventilation.

Dysventilation is the cause of a dysmorpho-functional spiral. Its management must always include a phase of OMT assisted by a PFA. This simple therapeutic approach helps to achieve better orofacial functional balance in the management of dysventilation and obstructive sleep apnea and contributes to the stability of the results of orthodontic treatments.

We describe the clinical presentation, laboratory findings and complications of severe paediatric inflammatory multisystem syndrome temporally associated with severe acute respiratory syndrome coronavirus 2 (PIMS-TS), also known as multisystem inflammatory syndrome in children in a 16-year-old female diagnosed in June 2025. This case highlights the importance of prompt diagnosis of PIMS-TS in the post-coronavirus disease 2019 pandemic era to ensure timely and appropriate management.

Antioxidant peptides show significant activity and can be developed into functional foods for treating chronic diseases. Cigarette smoke components can cause damage or even apoptosis of lung cells, eventually leading to chronic lung diseases. Therefore, this study aimed to investigate the protective effects and mechanisms of Skipjack tuna peptides against in vitro cigarette smoke extract (CSE)-induced chronic obstructive pulmonary disease (COPD). The results demonstrated that tuna peptides DVGRG (S1), PHPR (S5), GRVPR (S6), and SVTEV (S7) significantly enhanced the activities of SOD, CAT, and GSH-Px by upregulating the mRNA transcription levels of Keap1 and Nrf2, consequently reducing ROS and MDA levels in CSE-induced COPD model of MLE-12 cells. Molecular docking analysis revealed that S1, S6, and S7 competitively inhibited the Keap1-Nrf2 interaction by binding to the Kelch domain of Keap1, whereas S5 operated through a non-competitive mechanism. These peptides also downregulated p65 mRNA expression and upregulated IκBα mRNA expression, leading to a significant reduction in inflammatory cytokines of IL-1β, IL-6, and TNF-α, thereby alleviating inflammatory responses. Furthermore, these peptides significantly inhibited CSE-induced apoptosis by restoring mitochondrial membrane potential and upregulating the Bcl-2/Bax ratio. Additionally, S1, S5, S6, and S7 promoted MLE-12 cell migration in a concentration-dependent manner, suggesting a role in lung epithelial repair and regeneration. In conclusion, tuna peptides S1, S5, S6, and S7 exert antioxidant, anti-inflammatory, anti-apoptotic, and cell migration-promoting effects through the regulation of the Keap1/Nrf2 and NF-κB signaling pathways, as well as Bcl-2/Bax apoptotic balance, providing a promising strategy for mitigating CSE-induced lung injury.

The MiT/TFE family transcription factors play a critical role in lysosomal biogenesis, autophagy, mitochondrial turnover and lipid catabolism by regulating the Coordinated Lysosomal Expression and Regulation (CLEAR)gene network. The dysregulation of MiT/TFE activity has been implicated in the onset and progression of cancer and neurodegeneration, but its functions in association with pulmonary diseases remain poorly understood. In this review, we systematically summarize the findings from human pulmonary diseases and associated genetic disorders, such as asthma, cancer, Birt-Hogg-Dube (BHD) syndrome, and lung injury models that implicate MiT/TFE dysregulation in pathogenic progression. We also discussed MiT/TFE regulation and signaling through pathways involving mTORC1, AMPK, and lysosomal stress in different cellular contexts. Finally, we discussed significant mechanistic gaps, such as the absence of in vivo models targeting the combined activity of TFEB and TFE3 in disease progression and prevention. In conclusion, these insights seek to offer a comprehensive framework for understanding MiT/TFE signaling in human lung diseases and could present a promising opportunity for directing future mechanistic and translational research.

Eosinophilic chronic rhinosinusitis with nasal polyps (ECRSwNP) features extensive eosinophil infiltration, yet the molecular mechanisms driving this process are not fully elucidated. IL-29 and TLR4 are known inflammatory modulators, but their dose-dependent interplay in ECRSwNP remains uncharted. This study aimed to explore how IL-29 activates TLR4 signalling to promote eosinophil infiltration in ECRSwNP.

Thirty patients with ECRSwNP and 30 controls post-nasal septum correction were recruited. Eosinophil infiltration was assessed via haematoxylin-eosin staining, while IL-29 and TLR4 expression and correlation were analysed using qPCR and immunohistochemistry. In vitro, eosinophils were stimulated with IL-29 (10-100 ng/mL) ± TLR4 inhibitor TAK-242, with migration measured by Transwell assay, cytokine secretion by ELISA, and NF-κB/MAPK signalling by western blot.

Patients with ECRSwNP exhibited significantly elevated eosinophil infiltration and IL-29/TLR4 expression (p < 0.05), with a robust correlation (r = 0.6018, p < 0.0001). IL-29 dose-dependently enhanced eosinophil migration and cytokine production, and the effects were reversed by TLR4 blockade, accompanied by decreased NF-κB and MAPK phosphorylation, indicating TLR4-mediated regulation.

Dose-dependent IL-29 activation of TLR4 signalling drives eosinophil infiltration in ECRSwNP, offering novel mechanistic insights and potential therapeutic targets for this condition.

Influenza viruses are significant causes of acute respiratory infections, often leading to severe health issues and mortality. These viruses undergo continuous mutations and genetic reassortments, resulting in annual epidemics and potential pandemics. The A(H3N2) strains exhibit high genetic and antigenic variability, that influence vaccine efficacy. This study aimed to assess the prevalence of influenza viruses, including A(H3N2) strains, in Kazakhstan during 2020-2025. The study used nasopharyngeal swab and serum samples obtained from patients. The presence of influenza virus antigens in nasopharyngeal swabs was analyzed using real-time polymerase chain reaction. The level of specific antibodies in the blood serum was determined using the hemagglutination inhibition reaction and enzyme-linked immunosorbent assay methods. Influenza A/H1N1, A/H3N2 and B viruses were diagnosed using real-time PCR. Antibodies to A/H1N1pdm09, A/H3N2 and B were detected in serological studies. Our studies revealed a trend toward seasonal patterns in influenza A viruses circulation. Therefore, it was established that the A/H3N2 strains dominated in Kazakhstan during the 2021-2022 and 2023-2024 epidemic seasons. The 2023-2024 strains belong to the specific genetic clade J.2 or 3C.2a1b.2a.2a.3a.1. These studies confirmed the role of influenza viruses in the etiology of respiratory infections and emphasized the need to continue monitoring their spread in Kazakhstan.

The coronavirus disease 19 pandemic disrupted pediatric respiratory infections through non-pharmaceutical interventions and altered contact patterns. Long-term comparisons across the pandemic timeline in children remain limited. In this study, we analyzed 15,657 respiratory specimens from patients ≤ 18 years at Dankook University Hospital (2007-2023) using multiplex polymerase chain reaction assays targeting 15 viruses. Age-stratified positivity rates were compared across pandemic phases. Children ≤ 6 years comprised 88.61% of the study population. Human rhinovirus showed the highest detection rate (24.06%), followed by adenovirus (12.33%), respiratory syncytial virus-subtypes A and B (RSV-A: 11.13%; RSV-B: 8.65%), human parainfluenza virus-type 3 (HPIV-3; 6.21%), human metapneumovirus (HMPV; 5.33%), and enterovirus (2018-2023; EV; 10.96%). Monthly distributions differed (p < 0.001). RSV peaked in late autumn and winter; influenza and seasonal coronaviruses in winter and spring; HMPV, HPIV-3, EV, and human bocavirus in summer and fall. Positivity declined during the pandemic, rebounding in 2023, most prominently among children aged 1-6 years (84.91%). HPIV-3 and EV increased (p < 0.001). RSV-A predominated pre-pandemic, whereas RSV-B showed a non-significant relative increase post-pandemic; no subtype differences occurred during the pandemic. Findings demonstrate pathogen-specific shifts in predominance and seasonality and support ongoing surveillance and pediatric care planning.