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The Microbiome in Multiple Sclerosis
Published in David Perlmutter, The Microbiome and the Brain, 2019
Helen Tremlett, Emmanuelle Waubant
We found few published studies assessing the microbiome in body sites other than the gut or for Kingdoms other than Bacteria and Archaea in people with multiple sclerosis or at risk of developing multiple sclerosis. Briefly, groups are actively pursuing these areas by sampling from the mouth, nasal passages, cerebrospinal fluid65 (which “bathes” the brain and spinal cord) and autopsied brain tissue66. Animal studies have also included lung tissue samples to assess the microbiome, as lung tissue may be an important site of immune activation.67 Because smoking in adults and passive smoking in children is a potential risk factor for the onset of multiple sclerosis,25 combined with some animal studies,67 there is a biological rationale for further exploration of the lung microbiome, even though it is a challenging site from which to harvest samples for study.
The Role of the Microbiome on Human Health
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Rodney R. Dietert, Janice M. Dietert
While the gastrointestinal microbiome has the most extensive research, it is important to recognize that many different tissues have their own microbiome and that these are distinct from that of the gut. Each body site such as the airways, skin, breast tissue, placenta, and urogenital tract has its own healthy and dysfunctional microbiome profiles. For example, Yu et al. (2016) recently described the human lung microbiome and reported that the lung microbiota are distinct from the microbial communities in oral, nasal, stool, vagina, and skin. In lung, Proteobacteria were the dominant phylum (60%).
Respiratory infections
Published in Louis-Philippe Boulet, Applied Respiratory Pathophysiology, 2017
In individuals suffering from chronic obstructive pulmonary disease (COPD), the respiratory tract can be colonized without the actual presence of an active infection. The implantation of new bacterial strains or the proliferation of strains already present in the airway greatly facilitates the risk of infections which can initiate acute exacerbations of COPD, also called acute exacerbations of chronic bronchitis or emphysema. It has been clearly established that exposure to microorganisms, such as viruses or bacteria, is related to the occurrence of exacerbation in COPD patients, [15,16]. In fact, it has been demonstrated that a change in the lung microbiome is associated with COPD exacerbation and is potentially implicated in mediating host inflammatory responses at least in some subjects [17,18]. Moreover, recent studies in COPD patients revealed that the microbiome composition of the lung fluctuates with the severity of COPD [19]. In about 50% of cases, the pathogens are bacteria (Table 8.2). The type of bacteria involved depends on the severity of the underlying obstructive pulmonary disease, the frequency of exacerbations, the presence of associated comorbidities, and if the individual has recently received antibiotic treatment.
Impact of aging on immune function in the pathogenesis of pulmonary diseases: potential for therapeutic targets
Published in Expert Review of Respiratory Medicine, 2023
Sadiya Bi Shaikh, Chiara Goracci, Ariel Tjitropranoto, Irfan Rahman
Studies have shown that the maturation of the respiratory immune system in the postnatal environment depends on the type and abundance of antigen exposure to the host [19]. The lung microbiota helps in the development, induction, homeostasis, and tolerance of the respiratory immune system [20]. Numerous modifications take place in the pulmonary aging environment that influences the function of the innate immune system and host defenses against lung infections. One of the examples is the mucociliary barrier, which is a major defense against the pathogens in the bronchioles and the upper respiratory of the lung, both of which supply a physical barrier against a broad range of debris and microbes on top of the airways [17]. Studies have demonstrated a reductionmucociliary clearance in aged individuals donating to microbial invasion of the alveoli and lower airways [17,21,22]. The lung residential epithelial cells, innate lymphoid cells (ILCs), alveolar macrophages (AMs), and other pulmonary immune cells are vital to maintaining a stable state in the lungs [20]. Nevertheless, the capacity of these immune cells to identify different airway allergens and pathogens leads to the activation of inflammatory alterations in the lungs. There are some situations under which these lung inflammatory alterations are gentle and self-resolving, but during a respiratory condition such as acute lung injury (ALI) or sepsis, these pulmonary changes may show harmful effects on the host depending on the severity of the inflammatory innate immune response [18].
COVID-19: Immunology, Immunopathogenesis and Potential Therapies
Published in International Reviews of Immunology, 2022
Asha Bhardwaj, Leena Sapra, Chaman Saini, Zaffar Azam, Pradyumna K. Mishra, Bhupendra Verma, Gyan C. Mishra, Rupesh K. Srivastava
It is also reported that like gut, lung also has its own microbiota denoted as lung microbiota. Lung microbe is dominated by Firmicutes, Bacteroidetes and Proteobacteria. Surprisingly, it has been revealed that GM regulates pulmonary health and there is effect of lung inflammation on GM also. Thus, GM and lung interconnect with each other and affect each other’s development. This bidirectional interconnection between the GM and lung is referred as gut-lung axis. Gut-lung axis increases the likelihood that SARS-CoV-2 infection might affect the GM. It was also observed that GM also has role in ARDS which further increase the possibility that GM has role in COVID-19 [280]. Interestingly, a study has reported that GM colonization in germ free mice reduced the expression of colonic ACE2 [281]. This again confirms the role of GM in SARS-CoV-2 pathogenesis.
Rapid diagnostic tests in the management of pneumonia
Published in Expert Review of Molecular Diagnostics, 2022
Eleonora Riccobono, Linda Bussini, Maddalena Giannella, Pierluigi Viale, Gian Maria Rossolini
According to recent studies on lung microbiome, lower airways and alveoli are no longer considered a sterile environment, while they are settled by a commensal microbiota mainly composed by anaerobic bacteria like Prevotella, Veillonella, Fusobacterium, and by Haemophilus and Streptococci [28]. An antecedent or simultaneous viral infection may disrupt this microbial homeostasis favoring the overgrowth of bacteria causing CAP [9]. Moreover, some studies suggested that clinical severity of CAP may be determined by interactions between microbiota dysbiosis and the immune system [14]. This revised pathogenetic model may affect current statements on CAP therapeutic management concerning, for example, the role of antibiotics versus reconstitution of normal microbiota or immunomodulation as potential therapeutic target.