Particulate matter (PM) has been associated with increased pulmonary and cardiovascular mortality and morbidity. Additionally, PM is known to exacerbate asthma. However, whether ambient PM exposure contributes to the onset of asthma, especially in non-atopic children and adults, is less conclusive. The current study aimed to evaluate the effects of size-fractioned PM on lung immune responses in healthy BALB/c mice. We collected PM₁₀, PM_2.5, PM₁ and PM_0.1 samples from October 2012 to August 2013 in the Taipei Basin. These PM samples were representative of urban traffic pollution. The samples were extracted and sonicated in phosphate-buffered saline (PBS). Female BALB/c mice were exposed to the samples via intratracheal instillation at three different doses: 1.75 mg/kg (35 μg/per mouse), 5 mg/kg (100 μg/per mouse), and 12.5 mg/kg (250 μg/per mouse). The mice were exposed on days 0 and 7, and PBS alone was used as a control. Following the exposures, the expression profiles of inflammatory cells and cytokines in bronchoalveolar lavage fluid (BALF) were assessed. Exposure to PM₁₀ resulted in inflammatory responses, including the recruitment of neutrophils and the induction of T helper 1 (Th1) cell-related cytokine release, such as TNF-α and IFN-γ. Furthermore, an allergic immune response, including the recruitment of eosinophils and the up-regulation of T helper 2 (Th2) cell-related cytokine release, such as IL-5 and IL-13, was also observed in the BALF of mice exposed to PM₁₀. Our study showed that exposure to PM alone caused mixed Th1/Th2 inflammatory responses in healthy mice. These findings support the hypothesis that PM may contribute to the onset of asthma.

Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disorder characterized by persistent airway inflammation and progressive airflow limitation, resulting in a significant global health burden and high mortality. This narrative review synthesizes the current evidence on the roles of leukocyte subtypes—including neutrophils, monocytes, lymphocytes, eosinophils, and basophils—in the pathogenesis and clinical management of COPD. Relevant original studies and reviews are included, providing data on leukocyte functions, associated biomarkers, and therapeutic implications. Neutrophils contribute to airway damage and remodeling by releasing proteases and reactive oxygen species, particularly in response to environmental exposure such as cigarette smoke or air pollution. Lymphocytes, especially CD8⁺ T cells, drive chronic inflammation and immune dysregulation. Monocytes differentiate into macrophages that promote airway fibrosis and persistent inflammation, further impairing lung function. Eosinophils, though classically linked to asthma, are now recognized for their role in eosinophilic COPD, where they are associated with an increased exacerbation risk and corticosteroid responsiveness. Basophils, though less studied, may influence airway inflammation through interactions with eosinophils and cytokine release. Understanding these immune cell dynamics provides insights into the heterogeneity of COPD and highlights potential targets for precision therapy. Tailored interventions based on inflammatory phenotypes may improve clinical outcomes and advance personalized treatment strategies.

Transforming growth factor-β (TGF-β) signaling plays a central role in lung tissue homeostasis, coordinating epithelial repair, immune resolution, and stromal remodeling following injury. However, persistent or dysregulated TGF-β activation is a hallmark of both idiopathic pulmonary fibrosis (IPF) and lung cancer, two devastating pulmonary diseases that are traditionally studied as distinct entities. Emerging evidence suggests that this dichotomous view may obscure shared pathogenic mechanisms driven by aberrant TGF-β signaling dynamics. In this review, we synthesize experimental, translational, and clinical findings to propose a unifying framework in which IPF and lung cancer represent endpoints along a shared TGF-β–driven pathological continuum. We highlight how the duration and intensity of TGF-β signaling determine divergent cellular outcomes across epithelial cells, fibroblasts, and immune compartments—ranging from physiological wound repair to irreversible fibrotic remodeling and the establishment of a pro-tumorigenic niche. Particular emphasis is placed on the temporal transition from acute injury responses to chronic signaling states that promote epithelial plasticity, fibroblast fixation, immune suppression, and genomic instability. By integrating fibrosis and tumorigenesis into a single pathophysiological model, this review reframes TGF-β signaling as a time-dependent disease modifier rather than a disease-specific factor. This perspective provides a conceptual basis for therapeutic strategies targeting TGF-β signaling windows to intercept disease progression before irreversible fibrosis or malignant transformation occurs.

Inflammation is a fundamental component of the immune response in host defense against pathogens and during tissue repair. Houttuynia cordata (HC), a herbaceous plant used in traditional Asian medicine, has significant anti-inflammatory and antimicrobial properties. However, the underlying mechanisms of the anti-inflammatory effects of HC are not fully understood. In this study, the immunomodulatory potential and macrophage polarization-modulating effects of HC were evaluated with a focus on cell signaling molecule expression, inflammatory cytokine production and macrophage polarization, with the aim of revealing the molecular mechanisms underlying the effects and therapeutic potential of HC. We investigated the effects of HC extract on proinflammatory cytokine production, signaling pathway activity, macrophage surface marker expression, morphology, and phagocytic activity under different treatment conditions in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Compared with LPS alone, HC treatment before LPS stimulation significantly reduced IL-1β, TNF-α, nuclear NF-κB, and pERK levels while increasing TGF-β levels. Compared with HC pretreatment, HC treatment after LPS stimulation further decreased the IL-6, TNF-α, nuclear NF-κB, and pERK levels. LPS resulted in a trend toward increased CD80 expression in macrophages. Both HC pretreatment and HC posttreatment tended to increase CD163 expression in macrophages. Our study demonstrated that HC, particularly when administered after inflammation onset, effectively reduces proinflammatory cytokine levels, modulates key signaling pathways, and polarizes macrophages toward an anti-inflammatory phenotype. These effects suggest that HC has significant therapeutic potential in treating inflammatory diseases by modulating macrophage activity.