Bronchial asthma is a chronic disease characterized by pathological changes such as abnormal inflammatory reaction of the airway, abnormal changes in airway wall structure, and increased tracheal-bronchial reactivity [
1]. In recent years, according to the World Health Organization (WHO) survey, there are about 15 million people who suffer from acute attacks of bronchial asthma, affecting their quality of life and losing their ability to work every year, while about 250,000 patients worldwide die of asthma every year [
2]. In China, there are at least 30 million patients with asthma. Most patients begin to suffer from asthma before the age of 5. The proportion of children suffering from asthma before the age of 3 accounts for about 50%, especially in regions or seasons with severe fog, which poses a serious threat to asthmatic patients, and the incidence rate of asthma tends to increase by 3–5%. Therefore, further discussion on the inflammatory characteristics of asthma and early prevention and control measures are currently the focus of research and attention of respiratory disease experts all over the world [
3].
Asthma is the result of the interaction between endogenous immune system and exogenous immune system [
4]. Allergens in the environment, such as indoor dust storm (HDM), endotoxin, and virus infection, which can be combined with pathogen-related pattern recognition receptors of the bodies, and different gene expression patterns are induced by activating different signal transduction pathways, thus causing the release of various proinflammatory factors [
5]. On the one hand, various antigen-presenting cells (APC) in the body are stimulated to activate the innate immune response in the body; on the other hand, these inflammatory mediators participate in the regulation of T lymphocyte differentiation, which promote the occurrence and development of specific antigen-induced acquired immune response, and aggravate the inflammatory response of the body [
6]. Human Toll-like protein was first discovered by Medzhitov et al. in 1997. Up to now, many studies have found that at least TLR
1–10 exists in Toll receptor families. Different TLRs make different genes express after being stimulated, playing an important role in identifying self- and foreign antigens and harmful and harmless antigens [
7]. The discovery and research provided new ideas for the treatment of a variety of immune function-related disorders such as bronchial asthma and allergic bronchopulmonary aspergillosis (ABPA) and enable people to have further understanding and understanding of the interaction between the two immune systems [
8]. House dust female (HDM) is one of the major ligands of TLR4, which is ubiquitous in the air and induce acute attack of asthma. After TLR4 recognizes with HDM in the environment, it can activate intracellular transcription factor NF-kB and related protein kinases; release related cytokines, such as TNF-a, IL-8, and IL-6; and promote the metamorphosis of the body [
8]. At the same time, activated APC, such as alveolar giant cells in the airway, can further affect the transcription activity of inducible NOS and promote the production of NO, which activates the intracellular bactericidal mechanism in the body and further aggravates tissue damage. Therefore, APC has set up a bridge for the body’s immune response [
9].
Ganoderma lucidum is a valuable traditional Chinese medicine.
Ganoderma lucidum (scientific name,
Ganoderma lucidum Karst), also known as Linzhongling and Qiongzhen, is the fruiting body of
Ganoderma lucidum, a fungus of the Polyporaceae [
10]. It has effects in invigorating qi, tranquilizing mind, relieving cough and asthma, and prolonging life. It can be used for treating vertigo, insomnia, palpitation, short breath, neurasthenia, asthenia, cough, and asthma [
11]. Ganoderic acid A (GAA) is the main component of
Ganoderma lucidum, which shows a variety of pharmacological activities and has the effects of reducing blood lipid, lowering blood pressure, protecting liver, regulating liver function, etc. [
12]. However, there are few reports of GAA on OVA-induced asthma. The purpose of this paper is to explore the effect of GAA on OVA-induced asthma in mice and its mechanism.