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Background Recently, it has been found that the gut microbiota may affect the development of lung cancer through the “gut‐lung axis.” To investigate this relationship, we performed this study to determine whether the gut microbiota in non‐small‐cell lung cancer (NSCLC) patients is different from that in healthy adults. Methods Quantitative PCR (qPCR) was used to detect the expression levels of eight gut butyrate‐producing bacteria in healthy adults and NSCLC patients. We enrolled 30 patients with NSCLC and 30 subjects from 100 healthy adults after matching for age and sex. Results Compared to healthy adults, most of the gut butyrate‐producing bacteria in NSCLC patients were significantly decreased; these included Faecalibacterium prausnitzii, Clostridium leptum, Clostridial cluster I, Ruminococcus spp., Clostridial Cluster XIVa, and Roseburia spp. Among the gut butyrate‐producing bacteria, we analyzed Clostridial cluster IV and Eubacterium rectale were not decreased in NSCLC patients. Conclusions We conclude that NSCLC patients had gut butyrate‐producing bacteria dysbiosis. Further studies should be performed to investigate the underlying mechanisms of how these specific bacteria affect lung cancer progression and prognosis.

Background Gut microbiota are closely related to the development and regulation of the host immune system by regulating the maturation of immune cells and the resistance to pathogens, which affects the host immunity. Early use of antibiotics disrupts the homeostasis of gut microbiota and increases the risk of asthma. Gut microbiota actively interact with the host immune system via the gut‐lung axis, a bidirectional communication pathway between the gut and lung. The manipulation of gut microbiota through probiotics, helminth therapy, and fecal microbiota transplantation (FMT) to combat asthma has become a hot research topic. Body This review mainly describes the current immune pathogenesis of asthma, gut microbiota and the role of the gut‐lung axis in asthma. Moreover, the potential of manipulating the gut microbiota and its metabolites as a treatment strategy for asthma has been discussed. Conclusion The gut‐lung axis has a bidirectional effect on asthma. Gut microecology imbalance contributes to asthma through bacterial structural components and metabolites. Asthma, in turn, can also cause intestinal damage through inflammation throughout the body. The manipulation of gut microbiota through probiotics, helminth therapy, and FMT can inform the treatment strategies for asthma by regulating the maturation of immune cells and the resistance to pathogens.

Sepsis frequently progresses to acute lung injury (ALI), characterised by inflammation, extracellular matrix degradation, and mitochondrial dysfunction. This study identifies Enterococcus faecalis as a gut‐derived bacterium that exploits the host fibrinolytic system for pulmonary translocation, resulting in mitochondrial damage and exacerbating lung injury. Utilising the cecal ligation and puncture (CLP) mouse model combined with E. faecalis pulmonary infection, we demonstrated that E. faecalis exacerbates lung injury by activating fibrinolysis, disrupting intestinal barrier integrity, and impairing mitochondrial function. Key findings include elevated plasmin activity, increased fibrin degradation products (FDP), and reduced expression of tight junction proteins ZO‐1 and occludin. Mitochondrial dysfunction was confirmed by disrupted ultrastructure, impaired ATP synthesis, and increased ROS levels. Histological analyses revealed severe alveolar damage, neutrophil infiltration, and edema. Treatment with the fibrinolysis inhibitor aminocaproic acid or the mitochondrial protector MitoTEMPO alleviated fibrinolytic activity, preserved mitochondrial function, and reduced lung damage. Notably, combination therapy showed the most significant protective effects, improving lung histology and decreasing inflammation markers. This study provides novel insights into sepsis‐induced lung injury, highlighting E. faecalis and the fibrinolytic system as potential therapeutic targets.

Objectives Acute lung injury (ALI) not only affects pulmonary function but also leads to intestinal dysfunction, which in turn contributes to ALI. Mesenchymal stem cell (MSC) transplantation can be a potential strategy in the treatment of ALI. However, the mechanisms of synergistic regulatory effects by MSCs on the lung and intestine in ALI need more in‐depth study. Materials and methods We evaluated the therapeutic effects of MSCs on the murine model of lipopolysaccharide (LPS)‐induced ALI through survival rate, histopathology and bronchoalveolar lavage fluid. Metagenomic sequencing was performed to assess the gut microbiota. The levels of pulmonary and intestinal inflammation and immune response were assessed by analysing cytokine expression and flow cytometry. Results Mesenchymal stem cells significantly improved the survival rate of mice with ALI, alleviated histopathological lung damage, improved intestinal barrier integrity, and reduced the levels of inflammatory cytokines in the lung and gut. Furthermore, MSCs inhibited the inflammatory response by decreasing the infiltration of CD8+ T cells in both small‐intestinal lymphocytes and Peyer's patches. The gut bacterial community diversity was significantly altered by MSC transplantation. Furthermore, depletion of intestinal bacterial communities with antibiotics resulted in more severe lung and gut damages and mortality, while MSCs significantly alleviated lung injury due to their immunosuppressive effect. Conclusions The present research indicates that MSCs attenuate lung and gut injury partly via regulation of the immune response in the lungs and intestines and gut microbiota, providing new insights into the mechanisms underlying the therapeutic effects of MSC treatment for LPS‐induced ALI. This study focuses on the protective effects of mesenchymal stem cells (MSCs) in the lung and gut of Lipopolysaccharide‐induced acute lung injury mice. The data suggest that MSCs improved intestinal barrier function and reduced intestinal infiltration of CD8+ T cells. Further, depletion of intestinal bacterial communities with antibiotics significantly improved the therapeutic effects of MSCs.

Bronchopulmonary dysplasia (BPD) is a severe respiratory condition that affects preterm infants, which is frequently associated with a poor long-term prognosis. The gut-lung axis is a bidirectional communication pathway mediated by microbial communities and shared immune mechanisms that has emerged as a important area of research. It has been indicated that gut microbiota can influence the progression of various pulmonary diseases, where the gut-lung axis can affect the progression of BPD through various mechanisms, such as bacterial translocation, microbial metabolite exchange, inflammatory cytokine spillover and immune cell migration. Although the relationship between the gut-lung axis and BPD remains under exploration, understanding this interaction may identify early warning markers and novel therapeutic strategies for BPD. The present review summarizes the influence of the gut-lung axis on BPD, focusing on the bidirectional communication and gut microenvironmental changes during BPD and the possible immunoregulatory mechanisms involved. By elucidating these associations, the present review aims to provide novel insights into the prevention and treatment of BPD.

Abstract Background Gastrointestinal microbiota can be influenced by several factors, including diet and systemic inflammation, and in turn could act as a modulator of the allergic response. Fecal microbiota of horses with asthma has not been described. Hypothesis/Objectives Analyze the bacterial fecal microbiota of horses with and without asthma under different environment and diet conditions, during both remission and exacerbation. Methods Prospective observational study. Feces from 6 asthmatic and 6 healthy horses were collected under 3 different conditions: on pasture, housed indoors receiving good quality hay (“good hay”), and housed indoors receiving poor quality hay (“dusty hay”). Sequencing was performed using an Illumina MiSeq platform and data were processed using the software mothur v.1.41.3 and LEfSe. Results In horses with asthma, low-abundance bacteria were more affected by changes in environment and diet (ie, when horses were experiencing an exacerbation), as shown by changes in membership and results from the LEfSe analysis. There was a significant increase in the relative abundance of Fibrobacter in healthy horses eating hay, a change that was not observed in horses with asthma. Conclusions and Clinical Importance The intestinal microbiota of horses with asthma does not adapt in the same way to changes in diet and environment compared to the microbiota of healthy horses. Mechanisms explaining how airway obstruction and inflammation could influence the intestinal microbiota and how in turn this microbiota could modulate systemic inflammation in asthmatic horses deserves further investigation.

Fungal pneumonia is a serious disease with great harm and high prevalence, presenting significant challenges in diagnosis and treatment. The gut and respiratory microbiota play a critical role in protecting lung health against fungal pneumonia. Here, it is established fungal pneumonia by infection via the sinopulmonary route with Fusarium graminearum (F. graminearum) to investigate the influence of gut microbiota state on susceptibility to fungal pneumonia in BALB/c mice. This findings revealed that F. graminearum spore exposure not only impaired pulmonary clearance mechanisms but also significantly upregulated the expression of proinflammatory cytokines, including interleukin‐6 (IL‐6), interleukin‐1β (IL‐1β), and tumor necrosis factor‐α (TNF‐α). Moreover, spore invasion led to an increase in Staphylococcus abundance and activation of both triglyceride and galactose metabolic pathways. Antibiotic treatment disrupted the gut and respiratory microbiota, facilitating F. graminearum lung colonization, which is evidenced by elevated inflammatory markers in alveolar fluid and dysregulated lung metabolism. It is demonstrated that the gut microbiota influences susceptibility to fungal pneumonia by acting as an intermediary in the gut‐lung axis through the bloodstream, thereby modulating lung metabolism and inflammatory responses. These findings open avenues for novel therapeutic strategies, such as gut microbiota modulation, for the prevention and treatment of fungal pneumonia. Fungal pneumonia induces inflammation, shown by heightened IL‐6, IL‐1β, TNF‐α levels and a growth in Staphylococcus in the alveolar flora. The gut microbiota, acting through the gut‐lung axis via blood, impacts fungal pneumonia susceptibility by altering lung metabolism and inflammatory responses.

The pathogenesis of asthma has been partially linked to lung and gut microbiome. We utilized a steroid‐resistant chronic model of cockroach antigen‐induced (CRA) asthma with corticosteroid (fluticasone) treatment to examine lung and gut microbiome during disease. The pathophysiology assessment demonstrated that mucus and airway hyperresponsiveness were increased in the chronic CRA with no alteration in the fluticasone (Flut)‐treated group, demonstrating steroid resistance. Analysis of mRNA from lungs showed no decrease of MUC5AC or Gob5 in the Flut‐treated group. Furthermore, flow‐cytometry in lung tissue showed eosinophils and neutrophils were not significantly reduced in the Flut‐treated group compared to the chronic CRA group. When the microbiome profiles were assessed, data showed that only the Flut‐treated animals were significantly different in the gut microbiome. Finally, a functional analysis of cecal microbiome metabolites using PiCRUSt showed several biosynthetic pathways were significantly enriched in the Flut‐treated group, with tryptophan pathway verified by ELISA with increased kynurenine in homogenized cecum samples. While the implications of these data are unclear, they may suggest a significant impact of steroid treatment on future disease pathogenesis through microbiome and associated metabolite pathway changes.

Patients in intensive care units, especially those immunocompromised, are prone to opportunistic infections, such as respiratory and urinary tract infections. Extended antibiotic use disrupts the production of microbiome‐derived metabolites, including those involved in colonization resistance to Pseudomonas aeruginosa, which is known for its multidrug resistance. Hence, prior antibiotic treatment has been shown to increase susceptibility to P. aeruginosa infection, but the role of microbiota‐derived metabolic cues in this context is still elusive. This study investigates how tryptophan metabolites from the indigenous microbiota affect P. aeruginosa virulence. In vitro tests on motility, biofilm production, and pigment quantification (pyocyanin and pyoverdine) were performed on P. aeruginosa strains (PAO1, PA103, PA14) and clinical isolates. Additionally, gene expression related to virulence was analyzed, and the effects of tryptophan metabolites on experimental lung infection in mice were evaluated. Indole, indoleacetic acid (IAA), and indoleacrylic acid (IA) reduced motility and pigment production. IAA and indole promoted biofilm formation, with indole having a stronger effect. Clinical isolates showed significant phenotypic diversity, and IAA was more effective at inhibiting virulence traits than indole or IA. Mice infected with bacteria grown in the presence of IAA had lower lethality and fewer polymorphonuclear leukocyte influx compared to the control group. This suggests that tryptophan metabolites, especially IAA, can modulate P. aeruginosa virulence and may help control infection progression. Screening for anti‐virulence activity exerted by tryptophan catabolites on laboratory and clinical strains of Pseudomonas aeruginosa showed that Indoleacetic acid (IAA) inhibits motility and pigment production, downregulates PQS gene expression, while increases oxidative stress sensitivity. These changes led to reduced inflammation and improved survival in mice infected with IAA‐exposed bacteria.

Background Numerous studies have characterized the gut microbiome (GM) in lung cancer (LC). Yet, the causality between GM and LC and its subtypes remain uncharacterized. Methods Two‐sample Mendelian randomization (MR) was designed to investigate the causal relationship between the GM and LC and its subtypes, using publicly available summary data of genome‐wide association studies. The researchers ran two groups of MR analyses, including the genome‐wide statistical significance threshold (5 × 10−8) and the locus‐wide significance level (1 × 10−5). Results Using MR analysis, we ascertained 42 groups of GM that are intimately linked to LC and its subtypes at the locus‐wide significance level. Of the 42 groups, 12 were in LC, nine in non‐small cell lung cancer (NSCLC), six in small cell lung cancer (SCLC), two in lung adenocarcinomas, and 13 in lung squamous carcinomas. After false discovery rate correction, we still found a remarkable causal interaction between the Eubacterium ruminantium group and SCLC. Moreover, five groups of GM closely linked to LC and its subtypes were recognised at the genome‐wide statistical significance threshold. This finding included one group each in LC, NSCLC and SCLC, two groups in lung adenocarcinoma and none in lung squamous carcinoma. None of the foregoing findings were heterogeneous or horizontal pleiotropy. Reverse MR revealed that genetic susceptibility to LC and its subtypes caused significant changes in three groups of GM. Conclusion Our findings substantiate the causality between GM and LC and its subtypes. This study offers fresh insights into the function of GM in mediating the progression of LC. Overview of Mendelian randomization (MR) analysis process and major assumptions.