The inflammation is the protective response of the body against various harmful stimuli; however, the aberrant and inappropriate activation tends to become harmful. The acute inflammatory response tends to resolved once the offending agent is subside but this acute response becomes chronic in nature when the body is unable to successfully neutralized the noxious stimuli. This chronic inflammatory microenvironment is associated with the release of various pro-inflammatory and oncogenic mediators such as nitric oxide (NO), cytokines [IL-1β, IL-2, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)], growth factor, and chemokines. These mediators make the inflammatory microenvironment more vulnerable toward tumorigenesis. The pro-inflammatory mediators released during the chronic inflammation tends to induce several molecular signaling cascades such as nuclear factor kappa B, MAPKinase, nuclear factor erythroid 2-related factor 2, phosphoinositide-3-kinase, Janus kinases/STAT, Wnt/B-catenin, and cyclic AMP response element binding protein. The immune system and its components have a pleiotropic effect on inflammation and cancer progression. Immune components such as T cells, natural killer cells, macrophages, and neutrophils either inhibit or enhance tumor initiation depending on the type of tumor and immune cells involved. Tumor-associated macrophages and tumor-associated neutrophils are pro-tumorigenic cells highly prevalent in inflammation-mediated tumors. Similarly, presence of T regulatory (Treg) cells in an inflammatory and tumor setting suppresses the immune system, thus paving the way for oncogenesis. However, Treg cells also inhibit autoimmune inflammation. By contrast, cytotoxic T cells and T helper cells confer antitumor immunity and are associated with better prognosis in patients with cancer. Cytotoxic T cells inflict a direct cytotoxic effect on cells expressing oncogenic markers. Currently, several anti-inflammatory and antitumor therapies are under trials in which these immune cells are exploited. Adoptive cell transfer composed of tumor-infiltrating lymphocytes has been tried for the treatment of tumors after their ex vivo expansion. Mediators released by cells in a tumorigenic and inflammatory microenvironment cross talk with nearby cells, either promoting or inhibiting inflammation and cancer. Recently, several cytokine-based therapies are either being developed or are under trial to treat such types of manifestations. Monoclonal antibodies directed against TNF-α, VEGF, and IL-6 has shown promising results to ameliorate inflammation and cancer, while direct administration of IL-2 has been shown to cause tumor regression.

Oxidative stress is defined as the imbalance between reactive oxygen species (ROS) production and the endogenous antioxidant defense system, leading to cellular damage. Asthma is a common chronic inflammatory airway disease. The presence of asthma tends to increase the production of reactive oxygen species (ROS), and the antioxidant system in the lungs is insufficient to mitigate it. Therefore, asthma can lead to an exacerbation of airway hyperresponsiveness and airway inflammation. PM2.5 exposure increases ROS levels. Meanwhile, the accumulation of ROS will further enhance the oxidative stress response, resulting in DNA, protein, lipid, and other cellular and molecular damage, leading to respiratory diseases. An in‐depth study on the relationship between oxidative stress and PM2.5‐related asthma is helpful to understand the pathogenesis and progression of the disease and provides a new direction for the treatment of the disease. This paper reviews the research progress of oxidative stress in PM2.5‐induced asthma as well as highlights the therapeutic potentials of antioxidant approaches in treatment of asthma.

Lung cancer is the leading cause of cancer‐related mortality both in men and women and accounts for 18.4% of all cancer‐related deaths. Although advanced therapy methods have been developed, the prognosis of lung cancer patients remains extremely poor. Over the past few decades, clinicians and researchers have found that chemical compounds extracted from natural products may be useful for treating lung cancer. Drug formulations derived from natural compounds, such as paclitaxel, doxorubicin, and camptothecin, have been successfully used as chemotherapeutics for lung cancer. In recent years, hundreds of new natural compounds that can be used to treat lung cancer have been found through basic and sub‐clinical research. However, there has not been a corresponding increase in the number of drugs that have been used in a clinical setting. The probable reasons may include low solubility, limited absorption, unfavorable metabolism, and severe side effects. In this review, we present a summary of the natural compounds that have been proven to be effective for the treatment of lung cancer, as well as an understanding of the mechanisms underlying their pharmacological effects. We have also highlighted current controversies and have attempted to provide solutions for the clinical translation of these compounds.

Enteroviruses are a group of RNA viruses belonging to the familyPicornaviridae. They include human enterovirus groups A, B, C, and D as well as non-human enteroviruses. Enterovirus infections can lead to hand, foot, and mouth disease and herpangina, whose clinical manifestations are often mild, although some strains can result in severe neurological complications such as encephalitis, myocarditis, meningitis, and poliomyelitis. To date, research on enterovirus non-structural proteins has mainly focused on the 2A and 3C proteases and 3D polymerase. However, another non-structural protein, 2C, is the most highly conserved protein, and plays a vital role in the enterovirus life cycle. There are relatively few studies on this protein. Previous studies have demonstrated that enterovirus 2C is involved in virus uncoating, host cell membrane rearrangements, RNA replication, encapsidation, morphogenesis, ATPase, helicase, and chaperoning activities. Despite ongoing research, little is known about the pathogenesis of enterovirus 2C proteins in viral replication or in the host innate immune system. In this review, we discuss and summarize the current understanding of the structure, function, and mechanism of the enterovirus 2C proteins, focusing on the key mutations and motifs involved in viral infection, replication, and immune regulation. We also focus on recent progress in research into the role of 2C proteins in regulating the pattern recognition receptors and type I interferon signaling pathway to facilitate viral replication. Given these functions and mechanisms, the potential application of the 2C proteins as a target for anti-viral drug development is also discussed. Future studies will focus on the determination of more crystal structures of enterovirus 2C proteins, which might provide more potential targets for anti-viral drug development against enterovirus infections.