Abstract:The Human Microbiome Project began 10 years ago, leading to a signifi cant growth in understanding of the role the human microbiome plays in health and disease. In this article, we explain with an emphasis on the lung, the origins of microbiome research. We discuss how 16S rRNA gene sequencing became the fi rst major molecular tool to examine the bacterial communities present within the human body. We highlight the pitfalls of molecular-based studies, such as false fi ndings resulting from contamination, and t… Show more
“…Our results reinforce the previously known particularities of the lung microbiota, which considerably differ from oral and stool microbial communities [29]. One important concern is the theoretical risk of contamination with the upper microbiota during the bronchoscopy, but our results allowed us to rule out significant contamination, as other authors had previously suggested [30][31][32]. Data analysis by various methodologies highlighted the particularities of the microbiota associated with cancer, but also defined the respiratory microbiota core in healthy conditions.…”
Background: Dysbiosis has been scarcely explored in the respiratory tract with cancer. We aimed to define the bacterial and fungal microbiota of the bronchi in cancer versus a healthy state, also defining the microbiota core, and their correlation with that in saliva and feces; and to detect markers for the early diagnosis of central lung cancer. For this purpose, twenty-five patients with central lung cancer and sixteen healthy controls without antimicrobial intake during the previous month were recruited. Bacterial and fungi distribution was determined by massive sequencing in bronchial biopsies. Complex computational analysis was performed to define for the first time the lung microbiota core.Results: A greater abundance of Streptococcus, Rothia, Gemella and Lactobacillus distinguish the saliva of patients. Affected and contralateral bronchi of these patients have almost identical microbiota dominated by Streptococcus, whereas Pseudomonas was the major genera in controls. Oral and pulmonary ecosystems were significantly more similar in patients, probably due to microaspirations. Streptococcal bronchial abundance differentiates patients from controls by an ROC curve (90.9% sensitivity, 83.3% specificity, AUC=0.897). The mycobiome of controls (Candida) was significantly different from that of patients (Malassezia), with the cancer-affected bronchi similar to their saliva, but different from their contralateral bronchi. Conclusions: Central lung cancer is highly enriched with Streptococcus, and shows significantly differences in their composition from healthy subjects. Alterations are not restricted to the tumor tissue, and seem to be the consequence of microaspirations from the oral cavity. These findings could be useful in the screening and even diagnosis of this pathology.
“…Our results reinforce the previously known particularities of the lung microbiota, which considerably differ from oral and stool microbial communities [29]. One important concern is the theoretical risk of contamination with the upper microbiota during the bronchoscopy, but our results allowed us to rule out significant contamination, as other authors had previously suggested [30][31][32]. Data analysis by various methodologies highlighted the particularities of the microbiota associated with cancer, but also defined the respiratory microbiota core in healthy conditions.…”
Background: Dysbiosis has been scarcely explored in the respiratory tract with cancer. We aimed to define the bacterial and fungal microbiota of the bronchi in cancer versus a healthy state, also defining the microbiota core, and their correlation with that in saliva and feces; and to detect markers for the early diagnosis of central lung cancer. For this purpose, twenty-five patients with central lung cancer and sixteen healthy controls without antimicrobial intake during the previous month were recruited. Bacterial and fungi distribution was determined by massive sequencing in bronchial biopsies. Complex computational analysis was performed to define for the first time the lung microbiota core.Results: A greater abundance of Streptococcus, Rothia, Gemella and Lactobacillus distinguish the saliva of patients. Affected and contralateral bronchi of these patients have almost identical microbiota dominated by Streptococcus, whereas Pseudomonas was the major genera in controls. Oral and pulmonary ecosystems were significantly more similar in patients, probably due to microaspirations. Streptococcal bronchial abundance differentiates patients from controls by an ROC curve (90.9% sensitivity, 83.3% specificity, AUC=0.897). The mycobiome of controls (Candida) was significantly different from that of patients (Malassezia), with the cancer-affected bronchi similar to their saliva, but different from their contralateral bronchi. Conclusions: Central lung cancer is highly enriched with Streptococcus, and shows significantly differences in their composition from healthy subjects. Alterations are not restricted to the tumor tissue, and seem to be the consequence of microaspirations from the oral cavity. These findings could be useful in the screening and even diagnosis of this pathology.
“…We found that, in addition to Staphylococcus nepalensis strain CNDG, sequences similar to corisin are highly conserved in several transglycosylases from other Staphylococcus species and some members of the microbial community that inhabit the normal or fibrotic lungs, including strains of Streptococcus pneumoniae and Mycobacterium abscessus 51,[58][59][60] . This observation suggests that a broad range of bacteria may be the source of corisin in pulmonary fibrosis.…”
Idiopathic pulmonary fibrosis (IPF) is a chronic and fatal disease of unknown etiology; however, apoptosis of lung alveolar epithelial cells plays a role in disease progression. This intractable disease is associated with increased abundance of Staphylococcus and Streptococcus in the lungs, yet their roles in disease pathogenesis remain elusive. Here, we report that Staphylococcus nepalensis releases corisin, a peptide conserved in diverse staphylococci, to induce apoptosis of lung epithelial cells. The disease in mice exhibits acute exacerbation after intrapulmonary instillation of corisin or after lung infection with corisin-harboring S. nepalensis compared to untreated mice or mice infected with bacteria lacking corisin. Correspondingly, the lung corisin levels are significantly increased in human IPF patients with acute exacerbation compared to patients without disease exacerbation. Our results suggest that bacteria shedding corisin are involved in acute exacerbation of IPF, yielding insights to the molecular basis for the elevation of staphylococci in pulmonary fibrosis.
“…To date, the majority of metagenomic sequencing assays have targeted amplicons within the 16S or 28S rRNA subunits, allowing detection of pulmonary bacteria or fungi, but not both, and not viruses [31]. Recently, unbiased mNGS assays have allowed detection of both bacterial and viral nucleic acid but have lacked ideal sensitivity for detecting filamentous mold [11,12].…”
An optimized mNGS assay for pulmonary microbes demonstrates significant inoculation of the lower airways of immunocompromised children with diverse bacteria, fungi, and viruses. Potential pathogens can be identified based on absolute and relative abundance. Ongoing investigation is needed to determine the pathogenic significance of outlier microbes in the lungs of immunocompromised children with pulmonary disease.
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