Gut-lung Axis Research Articles

Mechanisms underlying Th2-dominant pneumonia caused by plastic pollution derivatives (PPD): A molecular toxicology investigation that encompasses gut microbiomics and lung metabolomics

An investigation was conducted by researchers on how dibutyl phthalate (DBP) and polystyrene microplastics (PS-MP) influence the development of pneumonia using a mouse model. For a duration of five weeks, the mice were subjected to exposure of DBP (30mg/kg/day) and PS-MP (0.1mg/day). The findings indicated notable pathological alterations in airway tissues, increased oxidative stress levels, and intensified inflammation, thereby establishing a connection between plastic pollution and pneumonia. Further examination indicated the involvement of ferroptosis and oxidative stress in the progression of the disease. Administration of deferoxamine (DFO) (100mg/kg) resulted in symptom relief and reduced pathological alterations, as validated by metabolomic investigations. Increased levels of reactive oxygen species (ROS) triggered a Th2-mediated eosinophilic inflammatory response, marked by elevated IL-4 and reduced IFN-γ via the NFκB pathway. Moreover, analyses of the gut microbiome and metabolomics demonstrated that PPD modifies microbial populations and pulmonary metabolism, linking its effects on pneumonia through the gut-lung axis. This research highlights the health hazards associated with plastic pollution and proposes a framework for tackling these issues.

Alteration of the Gut–Lung Axis After Severe COVID-19 Infection and Modulation Through Probiotics: A Randomized, Controlled Pilot Study

Background: The gut–lung axis could be a potential therapeutic target for improving post-acute COVID-19 symptoms, and probiotics have been proposed as possible modulators. Aim: We conducted a pilot study to understand alterations in the gut–lung axis and to explore the effects of a probiotic in post-acute COVID-19 disease. Methods: We included patients after severe COVID-19 disease (sCOV, n = 21) in a randomized, placebo-controlled trial to test the effect of a probiotic (Pro-Vi 5, Institute Allergosan, Graz, Austria) in a six-month intervention and used patients after mild disease (mCOV, n = 10) as controls, to compare the intestinal microbiome, metabolome, and patient-reported outcomes and biomarkers along the gut–lung axis at baseline and throughout probiotic intervention. Results: Compared to mCOV patients, sCOV patients showed lower microbial richness, which was significantly improved by probiotic intervention. A reorganization of Ruminococcaceae and Lachnospiraceae taxa was observed in sCOV patients but remained unaffected by the intervention. Serum metabolome showed a dysregulation of lipoproteins in accordance with higher BMI and comorbidities in sCOV patients. HDL and LDL fractions/components were temporarily decreased in the probiotic group. Stool metabolome was altered at baseline in sCOV patients and an increase in L-DOPA after 3 months and butyrate after 6 months of intervention could be observed. Probiotics partially improved reduced quality of life and modulated altered immune responses in sCOV patients. Increased intestinal permeability at baseline remained unaffected. Conclusion: The study provides evidence of long-term alterations of the gut–lung axis after severe COVID-19 infection and suggests that probiotics can modulate the biomarkers of the gut–lung axis.

Integrative metabolomic and microbiomic profiling: Unveiling the therapeutic mechanisms of Yangyinqingfei Decoction in acute lung injury

Acute lung injury (ALI) is a severe inflammatory condition characterized by disruption of the alveolar-capillary barrier, leading to impaired gas exchange and respiratory failure. The gut-lung axis has emerged as a crucial player in the pathogenesis of ALI, highlighting the potential therapeutic value of modulating gut microbiota and associated metabolic pathways. This study aimed to investigate the mechanisms underlying the protective effects of Yangyinqingfei Decoction (YYQFD) in treating ALI from the perspective of the gut-lung axis using an integrative multi-omics approach. Eight key gut microbiota genera were identified and associated with YYQFD treatment, including Lachnospiraceae, Prevotellaceae_NK3B31_group, Lachnospiraceae_NK4A136_group, and unclassified_Eubacterium_coprostanoligenes_group, etc. Metabolomic analysis revealed significant regulation of purine metabolism and pyrimidine metabolism pathways by YYQFD, involving metabolites such as xanthine, inosine, hypoxanthine, guanine, deoxyadenosine, thymine, and thymidine. Correlation analysis demonstrated significant associations between specific gut microbiota and metabolites, suggesting their potential as diagnostic or therapeutic targets. Furthermore, the mediation analysis revealed that YYQFD might regulate deoxyadenosine and L-isoleucine levels via the unclassified_Eubacterium_Coprostanoligenes_group and unclassified_Clostridia_vadinBB60_group, contributing to its therapeutic effects in ALI. This finding highlights the importance of the gut-lung axis in the therapeutic mechanisms of YYQFD and provides insights for future research and development of targeted interventions.

Investigating disturbances of the core material system in the lung-gut axis of COPD based on the transcriptomics-metabolomics-microbiomics integration strategy

Investigating disturbances of the core material system in the lung-gut axis of COPD based on the transcriptomics-metabolomics-microbiomics integration strategy

Integrated multi-omics analysis of the microbial profile characteristics associated with pulmonary arterial hypertension in congenital heart disease.

Dysregulation of immune and inflammatory cells around blood vessels and metabolic dysfunction are key mechanisms in the development of pulmonary arterial hypertension (PAH). The homeostasis of the human microbiome plays a crucial role in regulating immune responses and the progression of diseases. For pulmonary arterial hypertension associated with congenital heart disease involving body-lung shunt (PAH-CHD), the potential impact of the microbiome on the "gut-lung axis" remains underexplored. This study recruited 15 healthy individuals and 15 patients with pulmonary arterial hypertension due to congenital heart disease from Fuwai Yunnan Hospital, Chinese Academy of Medical Sciences, and Kunming Children's Hospital. We performed differential analyses of metabolites and microbiota from both the gut and lower respiratory tract for these two groups. The goal was to investigate the "gut-lung axis" microbiome and metabolome profiles in children with PAH-CHD and to analyze the interrelationships between these profiles. Ultimately, we aim to propose the potential value of these profiles in aiding diagnosis. The results indicated that the gut and pulmonary microbiota of children with PAH-CHD are characterized by an increased abundance of beneficial symbionts, which are closely linked to changes in the metabolome. Metabolite functional enrichment analysis revealed energy metabolism reprogramming in the PAH-CHD group, with active metabolic pathways associated with bile acid secretion and carnitine homeostasis. Moreover, the differential expression of metabolites was correlated with right heart function and growth development.IMPORTANCEPrevious studies have primarily focused on the relationship between the gut microbiome and PAH. However, the impact of microbial homeostasis on the progression of PAH-CHD from the perspective of the gut-lung axis has not been adequately elucidated. Our study utilizes an integrated multi-omics approach to report on the differential characteristics of gut and lung microbiota between children with PAH-CHD and reference subjects. We found that microbiota influence the pathological changes and disease manifestations of PAH-CHD through their metabolic activity. Additionally, alterations in metabolites impact the microbial ecological structure. Our findings suggest that modulating the microbiome composition may have positive implications for maintaining and regulating the immune environment and pathological progression of PAH-CHD.

Gut–lung axis in birds

Gut–lung axis in birds

The gut microbiota modulates airway inflammation in allergic asthma through the gut-lung axis related immune modulation: A review.

The human gut microbiota is a vast and complex microbial community. According to statistics, the number of bacteria residing in the human intestinal tract is approximately 10 times that of total human cells, with over 1,000 different species. The interaction between the gut microbiota and various organ tissues plays a crucial role in the pathogenesis of local and systemic diseases, exerting a significant influence on disease progression. The relationship between the gut microbiota and intestinal diseases, along with its connection to the pulmonary immune environment and the development of lung diseases, is commonly referred to as the "gut-lung axis." The incidence of bronchial asthma is rising globally. With ongoing research on gut microbiota, it is widely believed that intestinal microorganisms and their metabolic products directly or indirectly participate in the occurrence and development of asthma. Based on the gut-lung axis, this review examines recent research suggesting that the intestinal microbiota can influence the occurrence and progression of allergic asthma through the modulation of cytokine immune balance and mucosal integrity. Though the precise immune pathways or microbial species influencing asthma through the gut-lung axis are still under exploration, summarizing the immune modulation through the gut-lung axis in allergic asthma may provide insights for the clinical management of the condition.

Genetic evidence of bidirectional mendelian randomization study on the causality between gut microbiome and respiratory diseases contributes to gut-lung axis

Observational studies and clinical trials have suggested the relationship between the gut microbiome and respiratory diseases, but the causality between them remains unclear. Firstly, we selected eight respiratory diseases Genome-wide association study (GWAS) datasets mainly from the FinnGen collaboration as outcomes. The exposure was based on GWAS statistics about the gut microbiome, sourced from the MiBioGen consortium, including gut microbial taxa. The causal link between the gut microbiome and respiratory illnesses was then estimated using a Two-sample Mendelian randomization (MR) analysis, including the inverse-variance weighted (IVW), weighted median, MR-Egger, simple mode, and weighted mode. To ensure reliability, F-statistics and sensitivity tests were conducted. Furthermore, we performed a reverse MR analysis of the pre-Mendelian positive findings to possible reverse causality. For the 196 gut microbe taxa, the IVW analysis suggested 88 potential associations with eight clinically prevalent respiratory diseases. Among them, 30 causal associations were found in more than one MR method. Multiple statistical corrections have confirmed three causal associations: genus Holdemanella was a risk factor for chronic obstructive pulmonary disease (COPD) (P = 1.3 × 10−4, OR = 1.18), family FamilyXIII was a protective factor for COPD (P = 1.3 × 10−3, OR = 0.75), and genus Oxalobacter was a risk factor for asthma (P = 2.1 × 10−4, OR = 1.09). Our MR analysis results indicate that there would be a causal relationship between the gut microbiome and respiratory diseases, contributing to the gut-lung axis. This finding offers new insights into the gut microbiome’s roles in respiratory diseases’ clinical prevention, pathogenesis, and improvement of clinical symptoms. Further randomized controlled trials are necessary to clarify the protective effect of probiotics and fecal microbial transplantation on respiratory health.

Diet-microbiome interactions influence lung function in chronic obstructive pulmonary disease

Chronic Obstructive Pulmonary Disease (COPD) affects 30 million Americans. Previous epidemiologic work has shown that diet can impact pulmonary function in those with and without COPD. Diet is also a major driver of gut microbiome composition and function. Importantly, the gut microbiome has also been associated with lung health (i.e., the gut-lung axis) in both preclinical and clinical studies. Despite this growing body of evidence, many questions remain regarding the gut-lung axis. Specifically, how the microbiome impacts the relationship between diet factors and spirometry or stage of disease in people with COPD is little understood. We hypothesize that there are taxonomic differences in the gut microbiome among the different stages of COPD and that diet microbiome interactions influence pulmonary function. This study aimed to identify how the GI microbiota correlated with the severity of respiratory disease in COPD patients and how the microbiome may mediate the relationship between diet, including fiber and omega-3 fatty acids, and lung function outcomes.

Air-Pollution-Mediated Microbial Dysbiosis in Health and Disease: Lung-Gut Axis and Beyond.

Growing evidence suggests physiological and pathological functions of lung and gut microbiomes in various pathologies. Epidemiological and experimental data associate air pollution exposure with host microbial dysbiosis in the lungs and gut. Air pollution through increased reactive oxygen species generation, the disruption of epithelial barrier integrity, and systemic inflammation modulates microbial imbalance. Microbiome balance is crucial in regulating inflammation and metabolic pathways to maintain health. Microbiome dysbiosis is proposed as a potential mechanism for the air-pollution-induced modulation of pulmonary and systemic disorders. Microbiome-based therapeutic approaches are increasingly gaining attention and could have added value in promoting lung health. This review summarizes and discusses air-pollution-mediated microbiome alterations in the lungs and gut in humans and mice and elaborates on their role in health and disease. We discuss and summarize the current literature, highlight important mechanisms that lead to microbial dysbiosis, and elaborate on pathways that potentially link lung and lung microbiomes in the context of environmental exposures. Finally, we discuss the lung-liver-gut axis and its potential pathophysiological implications in air-pollution-mediated pathologies through microbial dysbiosis.

Intestinal microbiome dysbiosis increases Mycobacteria pulmonary colonization in mice by regulating the Nos2-associated pathways

Increasing researches reveal gut microbiota was associated with the development of tuberculosis (TB). How to prevent or reduce Mycobacterium tuberculosis colonization in the lungs is a key measure to prevent TB. However, the data on gut microbiota preventing Mycobacterium colonization in the lungs were scarce. Here, we established the clindamycin-inducing intestinal microbiome dysbiosis and fecal microbial transplantation models in mice to identify gut microbiota’s effect on Mycobacterium’s colonization in the mouse lungs and explore its potential mechanisms. The results showed that clindamycin treatment altered the diversity and composition of the intestinal bacterial and fungal microbiome, weakened the trans-kingdom network interactions between bacteria and fungi, and induced gut microbiome dysbiosis in the mice. Gut microbiota dysbiosis increases intestinal permeability and enhances the susceptibility of Mycobacterium colonization in the lungs of mice. The potential mechanisms were gut microbiota dysbiosis altered the lung transcriptome and increased Nos2 expression through the ‘gut–lung axis’. Nos2 high expression disrupts the intracellular antimicrobial and anti-inflammatory environment by increasing the concentration of nitric oxide, decreasing the levels of reactive oxygen species and Defb1 in the cells, and promoting Mycobacteria colonization in the lungs of mice. The present study raises a potential strategy for reducing the risks of Mycobacteria infections and transmission by regulating the gut microbiome balance.

Exposure to toluene diisocyanate induces dysbiosis of gut-lung homeostasis: Involvement of gut microbiota

Toluene diisocyanate (TDI) is a major industrial compound that induces occupational asthma with steroid-resistant properties. Recent studies suggest that the gastrointestinal tract may be an effective target for the treatment of respiratory diseases. However, the alterations of the gut-lung axis in TDI-induced asthma remain unexplored. Therefore, in this study, a model of stable occupational asthma caused by TDI exposure was established to detect the alteration of the gut-lung axis. Exposure to TDI resulted in dysbiosis of the gut microbiome, with significant decreases in Barnesiella_intestinihominis, Faecalicoccus_pleomorphus, Lactobacillus_apodemi, and Lactobacillus_intestinalis, but increases in Alistipes_shahii and Odoribacter_laneus. The largest change in abundance was in Barnesiella_intestinihominis, which decreased from 12.14 per cent to 6.18 per cent. The histopathological abnormalities, including shorter length of intestinal villi, thinner thickness of muscularis, reduced number of goblet cells and inflammatory cell infiltration, were found in TDI-treated mice compared to control mice. In addition, increased permeability (evidenced by significantly reduced levels of ZO-1, Occludin and Claudin-1) and activation of TLR4/NF-κB signaling were observed in the intestine of these TDI-exposed mice. Concurrently, exposure to TDI resulted in airway hyperresponsiveness, overt cytokine production (e.g., IL-4, IL-5, IL-13, IL-25, and IL-33), and elevated IgE level within the respiratory tract. The expression of tight junction proteins is reduced and TLR4/NF-κB signaling is activated in the lung following TDI treatment. In addition, correlation analyses showed that changes in the gut microbiota were correlated with TDI exposure-induced airway inflammation. In conclusion, the present study suggests that the immune gut-lung axis may be involved in the development of TDI-induced asthma, which may have implications for potential interventions against steroid-resistant asthma.

The Influence of the Gut Microbiota on Host Health: A Focus on the Gut–Lung Axis and Therapeutic Approaches

The human gut microbiota is a complex ecosystem harboring thousands of microbial strains that play a crucial role in maintaining the overall well-being of its host. The composition of the gut microbiota varies with age from infancy to adulthood and is influenced by dietary habits, environment, and genetic disposition. Recent advances in culture-independent techniques and nucleic acid sequencing have improved our understanding of the diversity of the gut microbiota. The microbial species present in the gut release short-chain fatty acids (SCFAs), which have anti-inflammatory properties. The gut microbiota also plays a substantial role in modulating the host′s immune system, promoting immune tolerance, and maintaining homeostasis. The impact of the gut microbiota on the health of the host is quite evident, as gut dysbiosis has been linked to various diseases, including metabolic disorders, autoimmune diseases, allergies, and inflammatory bowel diseases. The gut microbiota has bidirectional communication with the respiratory system, creating the gut–lung axis, which has been associated with different respiratory diseases. Therapeutic approaches targeting the gut microbiota, such as probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation (FMT), aim to restore microbial balance and promote the growth of beneficial strains in the gut. Nonetheless, gaining knowledge of the complex interactions between the gut microbiota and the host is necessary to develop personalized medicine approaches and microbiota-based therapies for various conditions. This review summarizes studies related to the gut–lung axis with particular emphasis on the role of the microbiota. Future research directions are also discussed.

Modulatory effects of traditional Chinese medicines on gut microbiota and the microbiota-gut-x axis.

The gut microbiota offers numerous benefits to the human body, including the promotion of nutrient absorption, participation in metabolic processes, and enhancement of immune function. Recent studies have introduced the concept of the gut-organ axis, which encompasses interactions such as the gut-brain axis, gut-liver axis, and gut-lung axis. This concept underscores the complex interplay between gut microbiota and various organs and tissues, including the brain, heart, lungs, liver, kidneys, muscles, and bones. Growing evidence indicates that gut microbiota can influence the onset and progression of multi-organ system diseases through their effects on the gut-organ axis. Traditional Chinese medicine has demonstrated significant efficacy in regulating the gastrointestinal system, leveraging its unique advantages. Considerable advancements have been made in understanding the role of gut microbiota and the gut-organ axis within the mechanisms of action of traditional Chinese medicine. This review aims to elucidate the roles of gut microbiota and the gut-organ axis in human health, explore the potential connections between traditional Chinese medicine and gut microbiota, and examine the therapeutic effects of traditional Chinese medicine on the microbiota-gut-organ axis. Furthermore, the review addresses the limitations and challenges present in current research while proposing potential directions for future investigations in this area.

Association of the gut microbiome and different phenotypes of COPD and asthma: a bidirectional Mendelian randomization study.

Mounting evidence has revealed the association between gut microbiota and both chronic obstructive pulmonary disease (COPD) and asthma; however, the causal association between gut microbiota and specific disease phenotypes remains to be determined. This study employed bidirectional two-sample Mendelian randomization (MR) analyses to investigate the potential causal relationship between gut microbiota and these conditions. The research utilized genome-wide association study (GWAS) data from the MiBioGen consortium for gut microbiota and the integrative epidemiology unit (IEU) Open GWAS for these conditions. Four MR analysis methods were employed: the inverse variance weighted (IVW) test, MR-Egger, weighted median, and weighted mode methods. The IVW method results are considered the primary findings. Sensitivity analyses, including heterogeneity tests, horizontal pleiotropy analysis, and leave-one-out analysis, were used to enhance robustness. Our MR study identified eight gut microbiota taxa potentially associated with the risk of different types of COPD and asthma. These include two taxa for early-onset COPD: Streptococcaceae [odds ratio (OR) = 1.315, 95% confidence interval (CI) = 1.071-1.616, P = 0.009] and Holdemanella (OR = 1.199, 95% CI = 1.063-1.352, P = 0.003); three for later-onset COPD: Acidaminococcaceae (OR = 1.312, 95% CI = 1.098-1.567, P = 0.003), Holdemania (OR = 1.165, 95% CI = 1.039-1.305, P = 0.009), and Marvinbryantia (OR = 0.814, 95% CI = 0.697-0.951, P = 0.009); one for allergic asthma: Butyricimonas (OR = 0.794, 95% CI = 0.693-0.908, P = 0.001); and two for non-allergic asthma: Clostridia (OR = 1.255, 95% CI = 1.043-1.511, P = 0.016) and Clostridiales (OR = 1.256, 95% CI = 1.048-1.506, P = 0.014).IMPORTANCEIndividuals with diverse phenotypes of chronic obstructive pulmonary disease (COPD) and asthma exhibit different responses to the conventional "one treatment fits all" approach. Recent research has revealed the significant role of the gut-lung axis in both COPD and asthma. However, the specific impact of gut microbiota on different subtypes of these conditions remains poorly understood. Our study has identified eight gut microbiota that may be associated with the risk of different types of COPD and asthma. These findings provide evidence suggesting a potential causal relationship between gut microbiota and various phenotypes of COPD and asthma. This offers a new perspective on the origins of different disease phenotypes and points toward future exploration of phenotype-specific and personalized therapies.

A-239 Cxcl10 induced gut dysbiosis exacerbates acute lung injury and secondary infection in influenza by inhibiting il22

Abstract Background Secondary infections are the most cause of severe pulmonary injury and death in influenza. CXCL10, known as interferon γ-induced protein 10(IP-10), is highly upregulated in response to IFN-γstimulation during influenza. Previous studies show that CXCL10 contributes to bacteria co-infections and worse finales in influenza. However, the underlying mechanisms by which CXCL10 facilitate secondary infections remains unclear. Emerging evidences show that influenza virus infections disturb the composition and function of gut microbiota, which in turn influences the infection process. Herein, we aimed to explore whether CXCL10 could affect the progress of influenza infection and secondary infection in a gut microbiota dependent manner. Methods CXCL10 knockout mice were used to determine the role of CXCL10 in staphylococcus aureus co-infection after influenza A virus (IAV) infection. Lung tissues from CXCL10 knockout mice were collected for Transcriptomics sequencing. Feces from mice and clinicals including IAV patients and healthy individuals were collected for Metagenomic sequencing. Paired serum samples were collected for Metabolomic sequencing. QRT-PCR was performed to determine the expression of inflammatory factors in lung tissues from CXCL10 knockout mice. Elisa assays were used to measure the serum expression levels of CXCL10 and IL22. Flow cytometry was applied to detect the proportion of IL22+ cells. Fecal microbiota transplantation (FMT) was applied to confirm that CXCL10 plays an adverse role in acute lung injury and staphylococcus aureus co-infection after IAV infection by disrupting intestinal microbiome homeostasis. Results CXCL10 aggravated acute lung injury and promoted staphylococcus aureus coinfection after IAV infection. Transcriptomics sequencing results suggests improved cell membrane integrity and regeneration of epithelial cells after IAV infection in CXCL10 knockout mice with an upregulation of integrity proteins. CXCL10 knockout significantly increased the expression levels of IL22 without influencing virus duplication. rh-IL22 protects lung epithelial cell from staphylococcus aureus co-infection in influenza and increased the expression of tight junction proteins. The gut microbiome shows different structures between wild type mice and knockout mice, as well as clinical samples according to serum CXCL10 expression levels. We found some genera were markedly increased in knockout mice and patients with low serum CXCL10 expression levels including Lactobacillus, Lachnospiraceae, Oscillibacter, Odoribacter, Eubacterium. FMT from patients with low serum CXCL10 levels and healthy individuals ameliorating lung pathological damage. Conclusions This study interpreted that CXCL10 exacerbates acute lung injury and secondary infection in influenza by inducing gut dysbiosis, suggesting that balancing the gut flora could be assistant treatments to protect from acute lung injury and secondary infections in influenza. And IL22 may be a potential mediating factor between gut-lung axis to improve epithelial integrity.

Association of dietary intake with pneumothorax: A Mendelian randomization study

BackgroundAn association between dietary habits and lung disease has been demonstrated in previous studies. Employing Mendelian randomization, we aimed to explore how different dietary intakes relate to pneumothorax, shedding light on the interplay among gut flora, the lung-gut axis, and pneumothorax. MethodsEmploying both two-sample and multi-sample Mendelian randomization (MR) analyses, we investigated 24 dietary intake variables to establish a strong association with pneumothorax. Causal inferences were drawn using the inverse variance weighted (IVW) method. To fortify our findings, we employed a diverse array of methodologies, including Weighted Median Estimator (WME), Weighted Mode, Simple Mode, Mendelian Randomization Pleiotropy Residual Sum and Outlier (MR-PRESSO), MR-Egger regression, and LASSO. ResultsOur analysis identified genetic variants reliably predicting dietary intakes, meeting stringent criteria (p < 5 × 10−8) and demonstrating independence (r2 < 0.001). Causal-effect estimates derived from the IVW model unveiled a statistically significant association, indicating a causal correlation between pneumothorax and three dietary intakes. Specifically, heightened consumption of fresh fruit (OR = 0.196, 95%CI: 0.063–0.606, p = 0.004) and dried fruit (OR = 0.323, 95%CI: 0.114–0.911, p = 0.032) correlated with reduced pneumothorax risk, while increased processed meat intake (OR = 2.705, 95%CI: 1.026–7.128, p = 0.044) showed a positive correlation. ConclusionIn summary, our MR analysis yields robust evidence supporting a causal correlation between dietary elements and pneumothorax. This study significantly advances our comprehension of pneumothorax risk factors, protective agents, and the intricate mechanisms of the lung-gut axis.

The Role of Gut Microbiota as a Trigger for Exacerbations in Pulmonary Obstruction Disorder in General

Pulmonary diseases can be associated with the gastrointestinal (GI) system, particularly if an infection causes them. This relationship between organs is known as the gut-lung axis (GLA). Skin and mucosal surfaces are associated with microbiota (bacteria, fungi, viruses, macrophages, archaea, protists, helminths), which can trigger an immune response in GLA and serve a role in respiratory diseases. For instance, asthma can be inhibited by a specific antigen that is triggered by probiotics, the microorganisms found in the GI tract. Asthma incidence can be reduced by consuming fiber due to its ability to protect airways from infection. Pattern recognition receptors (PRRs) are the first immune component to identify microbial compounds in GI and lung epithelial cells. The PRRs then induce regulatory T-cell (T-reg) and Th-17 differentiation. Diet, antibiotics, and stress can all influence the structure and function of bacteria. This is known as dysbiosis. Lung microbiota can influence immune cell maturation and homeostasis. If the diversity of lung microbiota decreases, it will affect intestinal microbiota and may result in chronic respiratory disorders such as chronic obstructive pulmonary disease (COPD), asthma, and cystic fibrosis. This literature review explained how the interactions between the intestines and lungs can affect humans’ health and well-being.

Influence of Gut and Lung Microbiota and the Gut-Lung Axis on Bronchopulmonary Dysplasia

Bronchopulmonary dysplasia (BPD), also known as neonatal chronic lung disease, is a common respiratory disease in preterm infants. Preterm infants with BPD often exhibit changes in gut and lung microbiota. In recent years, with the development of high-throughput sequencing technology, more and more mechanisms of the gut-lung axis have been confirmed, helping to explore new directions for the treatment of BPD using microecological agents. This paper reviews the roles of gut microbiota, lung microbiota, and the gut-lung axis in the pathogenesis of BPD in preterm infants, providing new research avenues for the prevention and treatment of BPD.

Reducing the excessive inflammation after burn injury in aged mice by maintaining a healthier intestinal microbiome.

One in six people are projected to be 65 years or older by 2050. As the population ages, better treatments for injuries that disproportionately impact the aged population will be needed. Clinical studies show that people aged 65 and older experience higher rates of morbidity and mortality after burn injury, including a greater incidence of pulmonary complications when compared to younger burn injured adults, which we and others believe is mediated, in part, by inflammation originating in the intestines. Herein, we use our clinically relevant model of scald burn injury in young and aged mice to determine whether cohousing aged mice with young mice or giving aged mice oral gavage of fecal material from young mice is sufficient to alter the microbiome of the aged mice and protect them from inflammation in the ileum and the lungs. Aged burn injured mice have less DNA expression of Bacteroidetes in the feces and an unhealthy Firmicutes/Bacteroidetes ratio. Both Bacteroidetes and the ratio of these two phyla are restored in aged burn injured by prior cohousing for a month with younger mice but not fecal transfer from young mice. This shift in the microbiome coincides with heightened expression of danger-associated molecular patterns (DAMP), and pro-inflammatory cytokine interleukin-6 (il6) in the ileum and lung of aged, burn injured mice, and heightened antimicrobial peptide camp in the lung. Cohousing reverses DAMP expression in the ileum and lung, and cathelicidin-related antimicrobial peptide protein (camp) in the lung, while fecal transfer heightened DAMPs while reducing camp in the lung, and also increased IL-6 protein in the lungs. These results highlight the importance of the intestinal microbiome in mediating inflammation within the gut-lung axis, giving insights into potential future treatments in the clinic.