Inhalation exposure to noxious environments, workplaces, and behaviors is a major cause of chronic respiratory disorders, which rank among the most prevalent non-communicable diseases globally. Pathophysiological processes are common to various pulmonary
diseases, including lung inflammation, damage, and repair. Normally, innate immunity serves as the host's first line of defense against microbial infections and in reaction to the destruction or loss of host cells. When dysregulated, innate immunity becomes a crucial
element of several respiratory disorders. Even so, different diseases exhibit varied inflammatory responses. For instance, asthma is often accompanied by eosinophilic inflammation, whereas COPD and ARDS share neutrophilic inflammation. Numerous stressors can result in lung damage, such as trauma, bacterial and viral infections, toxic
inhalations, auto-immune responses, and microbial dysbiosis. Chronic inflammation processes lead to conditions like asthma, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis.

Although therapies for lung disease can be useful in treating
symptoms, they are not curative. Chronic inflammation also contributes to the progression of lung cancer by providing essential chemicals to the tumor microenvironment through
extracellular vesicles. It causes lung tissue damage by increasing the rate of cell division, causing mutations and damage to DNA. Lung cancer risk may be increased by inflammation, which may also stimulate anti-apoptotic signaling. The COVID-19 pandemic
has emphasized the severe consequences associated with the dysfunction of these mechanisms, yet understanding of the underlying biological pathways is limited. Proteins, lipids, carbohydrates, and nucleic acids can be impacted by oxidative and nitrosative stress in cells. Thus, distinct lung pathophysiology has been linked to distinct molecular mechanisms that prevent oxidative-mediated tissue damage. Research on oxidative stress can help identify new therapy targets and shed light on the etiology of lung disease. To produce a state-of-the-art product that summarizes our current understanding and knowledge gaps in this field and suggests future approaches, novel targets, and next- generation experimental models, we are proposing a Research Topic with the title 'Immunomodulators and oxidative signaling as potential therapeutic targets for lung diseases.'

Potential topics include, but are not limited to, the following:

• Lung diseases include asthma, COPD, acute lung injury, pulmonary fibrosis, and lung cancer.
• Molecular pathways associated with oxidative stress induced lung inflammation, and it signature of the immune response.
• Alterations in the transcriptomic and proteomic profiles associated with pulmonary arterial hypertension.
• Cellular and molecular targets for immunomodulation in lung diseases.
• Identification and validation of novel biomarkers for diagnosis and monitoring of asthma and COPD.
• Preventive and therapeutic approaches through modulating oxidative signals in airway, alveolar epithelial cell damage and inflammatory cell accumulation.
• Targeted drug delivery, immunomodulation, and inflammation in lungs via nanoparticles and nanomaterials.
• Use of dietary supplements and nutraceuticals for the amelioration of lung inflammation.
• Utilization of natural products to reduce the thrombosis mediated in lung inflammatory disorder.
• We encourage the exploration of preclinical, pathophysiological, biochemical, and pharmacological studies.

We are pleased to invite all researchers and research teams that are interested in the field of Immunomodulation and oxidative signaling as potential therapeutic targets for lung diseases to this Topic with their manuscript(s). Full original research papers, short communications, and reviews regarding this topic are all welcome.

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Frontiers in Medical Technology

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