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Editorial: Pathophysiological and clinical advances in asthmatic inflammation from the nasopharynx to the peripheral airway in the respiratory tract systems

Yasuhiko Koga,Y. Kamide,T. Hisada,T. Ishizuka

2023 · DOI: 10.3389/fphar.2023.1037610
Frontiers in Pharmacology · 0 Citations

TLDR

In vivo studies indicate that alternative treatment options may be promising for refractoryAsthmatic inflammatory diseases and the efficacy of the latest biologics against asthmatic inflammation.

Abstract

Asthmatic airway inflammation is associated with many diseases, ranging from the upper to the lower respiratory tract, such as eosinophilic chronic sinusitis with nasal polyps (ECRSwNP), childhood and adult asthma, eosinophilic bronchiolitis/pneumonia, and eosinophilic granulomatosis with polyangiitis (EGPA). Various biological agents have been introduced for patients refractory to oral corticosteroid-based therapy. However, the mechanism of asthma-related inflammation remains obscure, and overcoming this intractable disease remains challenging. In this Research Topic, we focused on various asthmatic inflammatory diseases to deepen the understanding of underlying complicated pathological mechanisms, and the efficacy of the latest biologics against asthmatic inflammation. An in vivo study has demonstrated the beneficial effects of classical hypoglycemic agent, metformin, in metabolic syndrome, cancer, and chronic inflammation and tissue-remodeling through AMPK-dependent or AMPK-independent mechanisms (Saisho, 2015;Wu et al., 2021). Furthermore, metformin alleviates airway inflammation in asthmatic patients with obesity (Guo et al., 2021). As shown in Figure 1, Ma et al. clarified the mechanisms of metforminmediated improvement in the airway inflammatory cell infiltration by restoring AMPKα activity using ovalbumin-sensitized asthmatic mice. Articles and reviews on this Research Topic are summarized in Figure 1; Table 1, respectively. Moreover, Iwashita et al. demonstrated that type IV collagen, an extracellular matrix protein, suppresses MUC5AC secretion by regulating integrin α2 and β1 expression in the lungs and increases Akt and ERK phosphorylation using ovalbumin-sensitized asthmatic mice. This study was consistent with a previous in vitro study (Iwashita et al., 2010). These in vivo studies indicate that alternative treatment options may be promising for refractory asthmatic inflammatory diseases. OPEN ACCESS