Rheumatic Heart Disease: An In-Depth Review of Prevention, Pathophysiology, and Treatment Options

Received: 02-Oct-2025, Manuscript No. JDAR-25-171573; , Pre QC No. JDAR-25-171573 (PQ); , QC No. JDAR-25-171573; , Manuscript No. JDAR-25-171573 (R); , DOI: 10.4303/JDAR/236467

Introduction

COPD is a common lung disorder characterized by persistent airway inflammation and a gradual decline in respiratory function. It affects approximately 400 million people worldwide, and its prevalence is steadily increasing, causing significant economic and social impact. The mechanisms underlying the disease’s development remain poorly understood. Potential contributing factors include smoking, genetic predisposition, and various local and environmental factors [1].

Imbalances in the intestinal microbiome significantly influence the progression of COPD. The intestinal microbiome includes both beneficial and harmful microorganisms that inhabit the tissues and lining of the intestine, forming a complex microbial ecosystem. Ecological microbial imbalance of the gut microbial community can influence the organism’s immunological harmony and connected with disturbances in various structures, including adiposity, insulin resistance, arterial hardening, and hepatic steatosis [2,3]. Alterations in the gut microbial community can influence the lung environment, as microbial populations are present throughout both the upper and lower airways. Pulmonary conditions frequently occur alongside digestive symptoms, and individuals with gastrointestinal issues may also show signs in the breathing apparatus. For instance, people with respiratory flu infection often experience digestive symptoms in addition to pulmonary ones, at the same time those diagnosed with chronic intestinal inflammation exhibit shifts in gut flora, with nearly half of chronic intestinal inflammation individuals showing reduced lung activity. This two-way interaction between the digestive and respiratory systems is known as the digestive-respiratory pathway [4].

The connection between the digestive tract and pulmonary system has an important meaning in conditions affecting breathing. Progressive respiratory disease frequently overlaps with persistent digestive disorders, with individuals suffering from progressive respiratory disease being 2-3 times more likely to develop chronic intestinal inflammation than those without respiratory issues [5]. Likewise, individuals with chronic intestinal inflammation may face an elevated risk of progressive respiratory disease in contrast to physically fit people. Among chronic intestinal inflammation types, those with chronic intestinal inflammation affecting Gastrointestinal (GI) tract and affecting large intestine and rectum have relative risks of 2.72 and 1.83, correspondingly, for developing progressive respiratory disease [6].

This digestive-respiratory link can impact progressive respiratory disease advancement through immune cell movement, impairment of mucosal defenses, alterations of immune signaling molecules in both digestive and respiratory environments, and other mechanisms [7,8]. Earlier studies examined alterations in intestinal microorganisms in relation to progressive respiratory disease, but findings have been somewhat fragmented, leaving a discrepancy between the digestive-respiratory pathway theory and practical progressive respiratory disease care. Consequently, consolidating research on the digestive-respiratory pathway and its link to progressive respiratory disease could enhance strategies for disease outcome control [9]. This analysis explores the underlying mechanisms connecting the digestive-respiratory pathway to progressive respiratory disease and emphasizes last therapeutic innovations that target this pathway, aiming to assess its potential in preventing and managing progressive respiratory disease [10].

The digestive-respiratory theory

Recent research has increasingly indicated a connection between respiratory and gastrointestinal systems, commonly referred to as the gastro-pulmonary concept. This concept proposes that, due to their shared origin in the endoderm during embryonic development, the lungs and digestive tract are interrelated, facilitating a “shared epithelial reply.” In this mechanism, the epithelial lining of the intestines can modulate immune activity in the lungs, and the reverse may also occur, impacting the progression of conditions in either system [11].

The communication between these anatomical components involves the movement of microorganisms from one to the other and the transfer of metabolic products, primarily from the gut’s microbial community to the respiratory system. Among the most recognized metabolic intermediates carried through this gastro-pulmonary connection are short-chain lipids, which play a critical role in both localized and whole-body immune functions, as well as in maintaining tissue balance [12]. The precise pathway of acids’ activity within the pulmonary system remains unclear. According to Dang and other scientists, short-chain lipids may not exert straightforward effects in the pulmonary organs, as they do not collect there, nor are pulmonary-resident bacteria capable of producing them in large quantities [13]. Instead, short-chain lipids are synthesized by intestinal tract microbes, enter the bloodstream, and subsequently activate immune cells in other areas of the body, which then move to the pulmonary system. Additionally, short-chain lipids stimulate hematopoietic cells in the medullary tissue, which later move to the respiratory organs, influencing immune activity there [14,15].

Host-microbial mutualism in the intestinal-respiratory connection

The gut and respiratory microbial community: RHD is understood as the result of a The gut microbial community has developed a mutualistic relationship with the human body, significantly impacting health by facilitating food breakdown, producing essential vitamins, blocking the entry of harmful organisms, and supporting immune system regulation [16,17]. This ecosystem, found throughout the digestive system, in healthy humans consists of approximately 150 unique bacterial species, primarily from groups such as Bacteroidetes, Firmicutes, Proteobacteria, Actinobacteria, and Verrucomicrobia. Fungi are also a key component of this indigenous flora, although fungal diversity in well-functioning systems is limited to a few species, with species such as Saccharomyces cerevisiae, Malassezia restricta, and Candida albicans being particularly common [18,19]. Fungi outnumber bacteria by size, ranging from 100 to 1000 times, although fungi are less common. However, they can complement the bacterial role in supporting immunity and protecting mucous membranes both under normal conditions and when the intestinal microbial community is imbalanced. Furthermore, bacterial organisms can influence fungal behavior [20].

Although both the respiratory and intestinal organs develop from the same embryonic tissue in the early upper gastrointestinal tract, their microbial communities differ significantly in structure, spectrum, and role. The microbial environment of the lungs consists primarily of transient microbes originating from the upper respiratory tract, such as the nostrils, nasal cavities, nasal air spaces, and pharyngeal regions (upper pharynx and midpharynx) [21]. Although Bacteroidetes and Firmicutes dominate both ecosystems, their bacterial communities differ markedly in their taxonomic rank. In lung tissue, common genera include Streptococcus spp., Veillonella spp., and Prevotella, while in the intestinal environment, Bacteroides, Faecalibacterium, and Bifidobacterium are more typical. In cases of disease or microbial imbalance, other microorganisms, such as viruses or fungal species, may also be detected in the lung organs [22].

The respiratory microbial community in progressive respiratory disease

The lung microbial community significantly influences the onset and progression of progressive respiratory disease. This condition is associated with an imbalance in the respiratory microbial community, characterized by the proliferation of harmful bacteria, which leads to a rapid deterioration in respiratory function [23,24]. Studies of the respiratory microbial community in participants with progressive respiratory disease revealed a decrease in microbial diversity compared to healthy individuals, as well as an increase in the presence of various bacterial genera belonging to different taxonomic groups (Hemophilus spp., Afipia, Brevundimonas, Curvibacter, Moraxella, Neisseria, and Undibacterium spp. from the phylum Proteobacteria, Corynebacterium spp. from the phylum Actinobacteria, Capnocytophaga spp. from the phylum Bacteroidetes, and Leptolyngbya spp. from the phylum Cyanobacteria). Moreover, the severity of progressive respiratory disease correlates with a decrease in the diversity of lung microbial communities and an increase in the number of harmful microorganisms. Pathogens such as Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis have been identified in mucus cultures from the tracheobronchial tree of individuals with persistent progressive respiratory disease [25,26]. In contrast, patients with exacerbations of progressive respiratory disease exhibit an imbalance in the lung microbial community, characterized by an increased proportion of Moraxella spp. from the phylum Proteobacteria along with a decreased presence of Firmicutes. Importantly, an increased ratio of Proteobacteria to Firmicutes indicates that the deterioration may be associated with a disruption in the bacterial community, while deterioration in leukocytes indicates a decrease in this ratio. Disruption of the resident lung microbial community during unexpected worsening of progressive respiratory disease leads to the expansion of pathogens such as Acinetobacter spp and Klebsiella spp, suggesting that the beneficial lung microbial community plays a protective role against colonization by harmful microorganisms [27]. Decreased microbial diversity in individuals with progressive respiratory disease was found to be inversely correlated with interleukin-8, suggesting that lower species diversity may be associated with pathogen-immobilizing traps that clear microorganisms by penetrating the surface barrier. Furthermore, mannose-associated protein was found to impair cellular uptake of Haemophilus influenzae [28,29]. A 2018 study by Dicker and others found that patients with progressive respiratory disease who lack mannose-associated protein have a more diverse lung microbial community and experience fewer episodes of deterioration [30]. Furthermore, viral agents such as rhinoviruses and influenza virus are detected in approximately 10%-15% of mucus samples from patients with persistently progressive respiratory disease, compared to 30%-60% in patients with advanced disease. The airway fungal community also shows a higher proportion of Candida, Aspergillus, Candid, Phialosimplex, Penicillium, Cladosporium, and Eutypella species in COPD patients. Therefore, diseases caused by pathogenic bacteria, viruses, and pathogenic fungi may contribute to worsening respiratory conditions and the development of an extensive inflammatory response [31,32].

Gut-lung microbiome interactions in progressive respiratory diseases

Studies examining pulmonary-gut interactions in respiratory diseases such as chronic respiratory diseases, progressive respiratory diseases, cystic fibrosis, and respiratory infections suggest that these diseases may be prevented or ameliorated by modifying the gut microbiome [33]. The gut and lung microbiomes appear to interact to influence mucosal immunity. For example, mice with a compromised gut microbiome due to drug treatment exhibit increased vulnerability to infections that cause air sac inflammation, with their immune cells exhibiting altered gene expression that leads to decreased phagocytosis and impaired bacterial clearance [34,35]. Conversely, respiratory infections caused by bacteria and viruses in the respiratory system of mice have been found to disrupt the gut microbiome. In a mouse model of life-threatening widespread inflammation, it was shown that an imbalance in the gut microbial community affects the microbial composition of the lungs by altering the levels of inflammatory molecules in the bloodstream and promoting the migration of gut microbes into the airways [36,37].

Medical observations have emerged for chronic obstructive pulmonary disease. A pioneering investigation linking heightened digestive tract permeability to acute flareups in chronic lung disease proposed a potential role for gut bacterial communities in worsening. Maintaining the structural soundness of the epithelial tissue is essential for blocking the infiltration of dangerous agents (such as microbes and their byproducts) into the bloodstream [38,39]. When intestinal lining stability is compromised, this can lead to a more permeable lining tissue obstacle, promoting the movement of bacteria into systemic circulation and triggering widespread inflammation. Alterations in the gut bacterial population associated with chronic obstructive pulmonary disease have also been documented [40]. For example, a recent analysis using comprehensive fecal metagenomic and metabolic profiling found distinct differences in the bacterial and metabolic makeup of the intestines in those with chronic obstructive pulmonary disease compared to healthy subjects, including an increase in certain «Streptococcus parasanguinis B» species in the disease group. A previous investigation into acute disease episodes revealed an elevated presence of both “Streptococcus parasanguinis B» and “Streptococcus salivarius” in fecal samples, with only “Streptococcus parasanguinis B” showing an increase in respiratory samples [41]. In addition, research examining intestinal and pulmonary microbial communities from 15 individuals undergoing a 14-day regimen of medications for bacterial infections and reducing inflammation for acute flare-ups found differences in specific classification rank between the two various forms of specimens, although no notable change was seen in the multiplicity of primary microbial groups [42]. Collectively, these investigations point to a potential interaction between intestinal and pulmonary ecosystems, which may be key in the development of chronic obstructive pulmonary disease; however, the pathways through which this interaction influences microbial communities are still unclear.

Molecular mechanisms through intestinal-respiratory postconnection in progressive respiratory disease

Impact of pyrin domain-containing 3 inflammasome response in progressive respiratory disease: The multiprotein complex within immune cells, specifically the protein known as Nucleotide-Binding Domain (NOD)-like Receptor (NLR) family pyrin domain-containing 3 (NLRP3), becomes active in response to a variety of signals and plays a vital role in inborn immune defenses [43,44]. The activation of NLRP3 initiates inflammatory immune cell attraction and modulates the immune response in organs such as the digestive system and lungs. In many cases, bacterial infections within the gut are managed by the intestinal immune response. Nevertheless, certain pathogens that evade this response have been observed to enter the bloodstream, reaching the lungs and triggering inflammation [45,46]. Both the gut and lung microbial communities can impact NLRP3 role. Additionally, multiprotein complexes may also become promoted due to interactions between microbial molecules and proteins recognizing pathogens, with variations in multiprotein complex responses observed in different stages of COPD intensity [47]. The activation of NLRP3 further leads to protease activity and the release of inflammatory signaling molecules like immune mediator IL-1β and immune cytokine IL-18. This cascade has been associated with the onset of respiratory tract inflammation in COPD. In single-nuclear lymphocytes and monocytes and bronchial biopsy samples, the mRNA grades of NLRP3, protease, Pyrin domain-containing protein ASC, immune cytokine IL-18, and immune mediator IL-1β were higher in COPD exacerbation than in smokers. However, these mRNA grades were reduced in COPD individuals in a balanced condition, indicating a link between the NLRP3 multiprotein complex and COPD exacerbation [48,49].

Several placebo-controlled studies have indicated that focusing on multiprotein complex-associated targets (such as proinflammatory IL-1 proteins) did not yield benefits for individuals with COPD in intermediate to advanced levels [50,51]. For example, a study administering monthly injected into the vein doses of an inflammation blocker targeting IL-1β, over 45 weeks showed no analytically significant improvement in initial-second lung capacity or full exhaled air volume between the experimental and comparison groups. Additionally, the use of inflammation-targeting antibody for IL-1R1, demonstrated no enhancement in respiratory capacity or overall life condition in patients experiencing the worsening of COPD over a 52-week period [52]. Similarly, studies of cytokine-targeting antibody for IL-18, and inflammation-targeting P2X7 blocker, produced comparable outcomes. Nevertheless, a few mentioned trials did not fully evaluate the effects of these therapies on disease mechanisms due to insufficient outcomes. Therefore, larger, rigorously designed researches are needed to determine the impact of these multiprotein complex-targeting agents [53,54].

The inflammatory proteasome is a definite form of the proteasome essential for breaking down proteins within immune cells. It serves as a crucial regulator of immune cell development, inflammatory response, and autoimmune processes [55]. The last research has shown that proteasome levels are elevated in mononuclear cells from the blood of patients with advanced progressive respiratory disease compared to matched control subjects. Notably, proteasome stimulation was noticeable in blood immune cells of young men who smoke s and patients with serious progressive respiratory disease [56]. The equivalent investigation revealed that blocking immunoproteasome activity decreased inflammatory cytokine production in immune cells derived from progressive respiratory disease patients, suggesting that aiming the proteolytic complex in immune cells might offer a therapeutic approach for advanced progressive respiratory disease [57].

Molecular gene-regulatory changes in progressive respiratory disease

Gene-regulatory changes have been recognized as contributors to shifts in gut microbial populations and to the evolution of progressive respiratory disease. Nonetheless, the precise influence of these gene- modifying changes on the control of gut and respiratory tract microbial community in progressive respiratory disease is still mostly undefined [58]. Primarily, DNA methyl group addition is extensively studied in the context of gene-regulatory abnormalities in individuals who smoke, with or without progressive respiratory disease. DNA Methyltransferases (DNMTs) are enzymes responsible for adding a methyl group (CH₃) to DNA to influence gene activity. These enzymes are particularly responsive to nourishment accessibility and can be influenced by endogenous compounds generated by gut bacteria [59]. Methyl group DNA addition patterns are linked to gene activity signature in respiratory tract tissue from progressive respiratory disease patients. However, whether this type of modification impacts the microbial community associated with progressive respiratory disease in the gut and respiratory tract requires additional investigation.

Secondly, individuals with COPD exhibit reduced levels of Histone-modifying enzyme HDAC2 in contrast to those who don’t smoke, potentially contributing to heightened phlogistic process [60]. Other histone deacetylases, including HDAC family member 5, HDAC family member 8, and Sirtuin enzyme 1 also show weakened activity in progressive respiratory disease. It has been established that the gut microbial community can influence HDAC activity by producing short-chain fatty acids. Consequently, aiming the multi-enzyme complexes involving histone deacetylases could present a therapeutic approach for progressive respiratory disease [61].

Thirdly, increasing evidence suggests that the gut microbial flora plays an important role in controlling post-transcriptional regulators, which can in turn inhibit or reduce the risk of progressive respiratory disease evolution. Profiling analyses have shown that about 140 post-transcriptional regulators are altered in progressive respiratory disease patients compared to fit individuals, while around 70 post-connection transcriptional regulators have changed expression pattern in progressive respiratory disease relative to smoking people [62]. Diagnostic findings indicate that the goals of post-transcriptional regulators are concentrated in genes linked to cytokine synthesis. Nevertheless, profiles of post-transcriptional regulators have not yet been contrasted between the respiratory system and gastrointestinal tract in progressive respiratory disease cases. Forthcoming research is needed to clarify the immunomodulatory effects of post-transcriptional regulators within the intestinal-respiratory connection [63,64].

Metabolic products from the intestinal microbiome, such as low-molecular-weight fatty acids, folate nutrients, vitamin B7, and trimethylamine compounds, can influence gene-regulatory alterations. Elevated levels of circulating trimethylamine compounds have been linked to higher death rate in individuals with progressive respiratory disease, regardless of disease advancement [65,66]. However, the precise mechanisms through which gene-regulatory changes control trimethylamine compounds concentrations remain uncertain. Although various approaches have been developed to reduce trimethylamine compounds concentrations in the treatment of atherosclerosis, they come with implicit adverse effects. It remains to be determined whether these strategies aimed at trimethylamine compounds reduction could be applicable to progressive respiratory disease and warrant further investigation [67,68]. Additionally, there is research identifying a range of metabolic products, including those derived from fatty molecules, protein-building blocks, and foreign compounds, that are linked to progressive respiratory disease. These metabolic products may serve as implicit biological indicators for determining progressive respiratory disease in upcoming research [69].

Therapeutic methods

Healthy diet: Dietary choices significantly influence the composition of the gut microbial community, making diet an obvious therapeutic option. Long-term studies involving over 120,000 people aged 12 to 16 years have shown that maintaining a healthy diet reduces the progression of respiratory diseases by 33% [70]. Research shows that increasing fiber intake from sources such as grains, fruits, and vegetables is, conversely, associated with the progression of respiratory diseases, while consuming fiber-rich foods helps control the progression of respiratory diseases, primarily by increasing levels of volatile fatty acids in the intestine [71].

Jang and other researchers reported that a fiber-rich diet is strongly associated with reduced inflammation in both specific areas and overall, as well as with reduced alveolar damage and cell death. Switching to a high-fiber diet has been shown to alter the composition of the microbial community in the gastrointestinal tract and lungs, primarily by reducing the proportion of gram-positive and gram-negative bacteria and stimulating fiber breakdown in the gastrointestinal tract, which leads to increased levels of volatile fatty acids in the bloodstream [72,73]. Increasing the concentration of volatile fatty acids and increasing the number of beneficial microorganisms in the intestine through fiber consumption may be one way to alleviate the symptoms of progressive respiratory disease.

A study of the full spectrum of metabolites in a biological sample showed that the linoleic acid pathway has a pronounced effect on alveolar damage in people consuming a diet rich in fiber and pectin, which potentially slows the progression of COPD. Furthermore, a gut-targeted diet including whey peptides has been shown to reduce lung inflammation and minimize elastase-induced alveolar damage in mice by increasing gastrointestinal volatile fatty acid levels [74,75]. Thus, dietary interventions, particularly those that include lipid-rich regimens that influence the innate immune system and reduce whole-body inflammation, may provide significant protective benefits by helping prevent the development of progressive respiratory diseases, respiratory-related mortality, and smoking-related cancers. These approaches may also serve as a promising non-pharmacological strategy for treating or slowing progressive respiratory diseases [76,77].

Essential fatty acids, such as omega-3 oils, provide a variety of health benefits. Higher intake of these fats is associated with a lower risk of developing progressive respiratory diseases and may influence the diversity and composition of the gut microbiota, as well as modulate inflammatory agents, including endotoxins and interleukin-17 [78]. Moreover, a diet rich in these fatty acids can regulate volatile fatty acid levels and significantly contribute to maintaining intestinal immune function and microbial balance, improving physical performance and life outcomes in people with progressive respiratory diseases.

Furthermore, vitamin D is crucial for maintaining intestinal balance by preventing the overgrowth of harmful bacteria, reducing inflammation, and maintaining barrier integrity [79]. Vitamin D deficiency leads to shifts in the composition of the gut microbiome, favoring Gram-negative bacteria and decreasing the number of Gram-positive bacteria. In people with progressive respiratory disease, vitamin D promotes immune cell activation and the development of the pulmonary microbial community, and higher vitamin D intake is positively correlated with improved lung function. Dietary choice is a manageable condition for people with progressive respiratory disease, and a diet rich in fiber, balanced lipids, and adequate calciferol is beneficial for those suffering from this disease [80].

Healthy microbiota strains and bacterial phages

Certain subtypes of microorganisms that beneficially influence immune system activity and/or infectious pathogens are classified as probiotics. Oral administration of Bifidobacterium longum has been shown to improve immune function and viability in mice infected with Klebsiella pneumoniae [81,82]. Supplementation with the probiotic species Bifidobacterium breve and Lactobacillus rhamnosus suppressed airway inflammation and lung injury in mice with progressive respiratory disease.

The commensal bacteria Parabacteroides goldsteinii isolated from mice with progressive respiratory disease have been shown to reduce intestinal inflammation, enhance mitochondrial and ribosome function in the colon, normalize altered amino acid metabolism in the host bloodstream, suppress lung inflammation, and correct the symptoms of progressive respiratory disease [83,84]. Furthermore, P. goldsteinii endotoxins have anti-inflammatory properties and can significantly alleviate progressive respiratory disease by blocking the Toll receptor 4 immune response. This study suggests that favorable microbial subtypes and their bioactive components have the potential to serve as possible treatment modalities for the inhibition or therapy of progressive respiratory disease [85,86].

However, the clinical implementation of probiotics, microbial community transplantation, or bacteria-derived products to correct microbiome imbalances or restore a healthy microbial environment remains at the experimental stage. These mechanisms need to be tested in large-scale, randomized clinical trials before they can be widely implemented [87]. Frequent antibiotic use in people with sudden worsening of progressive respiratory disease disrupts a wide range of microbes, including non-target species, which may lead to the development of bacterial resistance.

In contrast, bacteriophages natural or engineered viruses that specifically target bacterial cells are attracting attention due to their potential therapeutic role. Several studies have reported the successful use of bacterial viruses to treat antibiotic-resistant infections. However, optimal administration approaches, dosages, and duration of treatment still require further research [88,89].

Stool microbiota transplant

Stool microbiota transfer has demonstrated global impact in humans, including enhanced nuclear transcription factor pathway activation and endotoxins-mediated response of Nuclear factor kappa B in lung tissue of murine models with lung damage, as well as increased levels of inflammatory factors pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) in the pulmonary system [90,91]. However, fecal transplant has been shown to block nuclear factor kappa B activation and reduce the secretion of immune response cytokines in the lungs. In a mouse model of alveolar damage induced by nicotine intake, the stool transplantation group exhibited relatively intact alveoli, while levels of inflammatory cytokine IL-6 and immune regulator IFN-γ were significantly lower in the bronchoalveolar lavage fluid and serum of stool microbiota transfer-treated mice [92,93].

Additionally, protein-coding RNA expressions of other key inflammatory mediators, including pro-inflammatory cytokine IL-1β and enzymes MMP-9 and MMP-12, were diminished in the stool microbiota-treated group. These findings suggest that gut microbial community transplantation can facilitate lung tissue damage and influence the inflammatory responses associated with alveolar breakdown triggered by nicotine intake, implying that intestinal flora transfer may help mitigate both site-specific and systemic manifestations of alveolar breakdown [94].

Bacteroidaceae and Lachnospiraceae, bacteria capable of converting fibers into volatile fatty acids, increased at the family level following stool microbiota transfer and regimen of lipid saturated interventions in ivestigation of microbial community. Both stool microbiota transfer and lipid saturated regime reduce progression of lung tissue degeneration by modulating site-specific and general inflammation and changing gut microbial composition [95]. This suggests that it may be possible to mediate therapeutically to slow progressive respiratory disease advancement. However, stool microbiota transfer has not yet been investigated in individuals with progressive respiratory disease, and additional clinical trials are necessary to evaluate the potency of this strategy in individuals with progressive respiratory disease.

Classical eastern healing practices

Caoshi silkworm blend have demonstrated positive impact on the symptoms of individuals with steady progressive respiratory disease. The mechanisms behind these effects may stem from the variations between those with steady COPD and healthy individuals. Cure with Qibai lung health capsules has been shown to alter the gut and lung microbiota, improving microbial diversity in progressive respiratory disease-affected animals, potentially enhancing lung function and promoting a restored the two subsets balance of T cells involved in immune homeostasis [96].

Xuanbai Chengqi Decoction has been found to alleviate lung inflammation by reshaping the intestinal microbiome and correcting the disruption between the two subsets of T cells in a murine model with progressive respiratory disease. Seabuckthorn Wuwei Pulvis supports pulmonary activity and reduces inflammation by modulating the intestinal microbial community, boosting volatile fatty acids production, and reinforcing intestinal barrier integrity in murine models with endotoxins-and nicotine intake progressive respiratory disease [97].

A mixed approach of traditional Chinese medicine and Western medicine has shown to enhance pulmonary system activity, lower C-reactive protein and acute-phase protein SAA, and reduce damage to the pulmonary and intestinal lining, while also mitigating systemic inflammatory responses in rats with sudden worsenings of COPD. Additional studies are needed to clarify the approaches by which these traditional medicines exert their effects [98].

Conclusion

Funding

This research was funded by Russian Science Foundation, grant number 25-15-00064.

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