Respiratory diseases, such as asthma and chronic obstructive pulmonary disease (COPD), are critical areas of medical research, as millions of people are affected worldwide. In fact, more than 9 million deaths worldwide were associated with respiratory diseases in 2016, equivalent to 15% of global deaths, and the prevalence is increasing every year as the population ages. Due to inadequate treatment options, the treatments for many respiratory diseases are limited to relieving symptoms rather than curing the disease. Therefore, new therapeutic strategies for respiratory diseases are urgently needed. Poly (lactic-co-glycolic acid) micro/nanoparticles (PLGA M/NPs) have good biocompatibility, biodegradability and unique physical and chemical properties, making them one of the most popular and effective drug delivery polymers. In this review, we summarized the synthesis and modification methods of PLGA M/NPs and their applications in the treatment of respiratory diseases (asthma, COPD, cystic fibrosis (CF), etc.) and also discussed the research progress and current research status of PLGA M/NPs in respiratory diseases. It was concluded that PLGA M/NPs are the promising drug delivery vehicles for the treatment of respiratory diseases due to their advantages of low toxicity, high bioavailability, high drug loading capacity, plasticity and modifiability. And at the end, we presented an outlook on future research directions, aiming to provide some new ideas for future research directions and hopefully to promote their widespread application in clinical treatment.

Asthma is a chronic airway inflammatory disease with complex mechanisms, and these patients often encounter difficulties in their treatment course due to the heterogeneity of the disease. Currently, clinical treatments for asthma are mainly based on glucocorticoid-based combination drug therapy; however, glucocorticoid resistance and multiple side effects, as well as the occurrence of poor drug delivery, require the development of more promising treatments. Nanotechnology is an emerging technology that has been extensively researched in the medical field. Several studies have shown that drug delivery systems could significantly improve the targeting, reduce toxicity and improve the bioavailability of drugs. The use of multiple nanoparticle delivery strategies could improve the therapeutic efficacy of drugs compared to traditional delivery methods. Herein, the authors presented the mechanisms of asthma development and current therapeutic methods. Furthermore, the design and synthesis of different types of nanomaterials and micromaterials for asthma therapy are reviewed, including polymetric nanomaterials, solid lipid nanomaterials, cell membranes-based nanomaterials, and metal nanomaterials. Finally, the challenges and future perspectives of these nanomaterials are discussed to provide guidance for further research directions and hopefully promote the clinical application of nanotherapeutics in asthma treatment.

Cells are the smallest units that make up living organisms, which constantly undergo the processes of proliferation, differentiation, senescence and death. Dead cells need to be removed in time to maintain the homeostasis of the organism and keep it healthy. This process is called efferocytosis. If the process fails, this may cause different types of diseases. More and more evidence suggests that a faulty efferocytosis process is closely related to the pathological processes of respiratory diseases. In this review, we will first introduce the process and the related mechanisms of efferocytosis of the macrophage. Secondly, we will propose some methods that can regulate the function of efferocytosis at different stages of the process. Next, we will discuss the role of efferocytosis in different lung diseases and the related treatment approaches. Finally, we will summarize the drugs that have been applied in clinical practice that can act upon efferocytosis, in order to provide new ideas for the treatment of lung diseases.

One of the common illnesses that affect women’s physical and mental health is urinary tract infection (UTI). The disappointing results of empirical anti-infective treatment and the lengthy time required for urine bacterial culture are two issues. Antibiotic misuse is common, especially in females who experience recurrent UTI (rUTI). This leads to a higher prevalence of antibiotic resistance in the microorganisms that cause the infection. Antibiotic therapy will face major challenges in the future, prompting clinicians to update their practices. New testing techniques are making the potential association between the urogenital microbiota and UTIs increasingly apparent. Monitoring changes in female urinary tract (UT) microbiota, as well as metabolites, may be useful in exploring newer preventive treatments for UTIs. This review focuses on advances in urogenital microbiology and organismal metabolites relevant to the identification and handling of UTIs in an attempt to provide novel methods for the identification and management of infections of the UT. Particular attention is paid to the microbiota and metabolites in the patient’s urine in relation to their role in supporting host health.

Recently, extreme weather has been regarded as a risk factor for exacerbating allergic airway inflammation (AAI), but its underlying mechanism remains unclear. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has been implicated in various lung diseases. This study investigated whether cold exposure aggravated OVA-induced AAI by promoting ferroptosis. A murine AA model was established using OVA sensitization and challenge. Mice were exposed to cold temperatures (10 °C or 4 °C) for 4 h daily. Ferroptosis was assessed by measuring ferroptosis-related markers (GPX4, ACSL4, FTL), iron deposition (Alcian Blue-Periodic Acid-Schiff Staining), lipid peroxidation (MDA), antioxidant levels (GSH), and mitochondrial ultrastructure (TEM). The ferroptosis inhibitor ferrostatin-1 (Fer-1) was administered to evaluate its protective effects. Airway inflammation, lung function, and histopathology were also analyzed. Cold exposure significantly worsened AA symptoms, including increased Th2 cytokine levels (IL-4, IL-5, IL-13, IL-33), impaired lung function, and enhanced airway remodeling and mucus production. These effects were more pronounced at 4 °C. Cold exposure also induced ferroptosis, as evidenced by decreased GPX4 and FTL, increased ACSL4, elevated iron and MDA levels, reduced GSH, and mitochondrial damage. Treatment with Fer-1 mitigated these changes, alleviating inflammation, improving lung function, and reducing histological damage. Cold exposure exacerbated AAI by inducing ferroptosis in lung tissues. Inhibition of ferroptosis with Fer-1 attenuated these aggravation effects, suggesting ferroptosis as a potential mechanistic link between cold exposure and AAI severity. Targeting ferroptosis might offer a novel therapeutic strategy for mitigating AAI under cold conditions.