scholarly journals Mucus, Microbiomes and Pulmonary Disease

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 675
Author(s):  
Oliver W. Meldrum ◽  
Sanjay H. Chotirmall

The respiratory tract harbors a stable and diverse microbial population within an extracellular mucus layer. Mucus provides a formidable defense against infection and maintaining healthy mucus is essential to normal pulmonary physiology, promoting immune tolerance and facilitating a healthy, commensal lung microbiome that can be altered in association with chronic respiratory disease. How one maintains a specialized (healthy) microbiome that resists significant fluctuation remains unknown, although smoking, diet, antimicrobial therapy, and infection have all been observed to influence microbial lung homeostasis. In this review, we outline the specific role of polymerizing mucin, a key functional component of the mucus layer that changes during pulmonary disease. We discuss strategies by which mucin feed and spatial orientation directly influence microbial behavior and highlight how a compromised mucus layer gives rise to inflammation and microbial dysbiosis. This emerging field of respiratory research provides fresh opportunities to examine mucus, and its function as predictors of infection risk or disease progression and severity across a range of chronic pulmonary disease states and consider new perspectives in the development of mucolytic treatments.

2019 ◽  
Vol 316 (6) ◽  
pp. F1211-F1217 ◽  
Author(s):  
Gerren P. Hobby ◽  
Oleg Karaduta ◽  
Giuseppina F. Dusio ◽  
Manisha Singh ◽  
Boris L. Zybailov ◽  
...  

The gut microbiome is composed of a diverse population of bacteria that have beneficial and adverse effects on human health. The microbiome has recently gained attention and is increasingly noted to play a significant role in health and a number of disease states. Increasing urea concentration during chronic kidney disease (CKD) leads to alterations in the intestinal flora that can increase production of gut-derived toxins and alter the intestinal epithelial barrier. These changes can lead to an acceleration of the process of kidney injury. A number of strategies have been proposed to interrupt this pathway of injury in CKD. The purpose of this review is to summarize the role of the gut microbiome in CKD, tools used to study this microbial population, and attempts to alter its composition for therapeutic purposes.


2020 ◽  
Vol 48 (3) ◽  
pp. 915-931 ◽  
Author(s):  
Aline C. Fenneman ◽  
Elena Rampanelli ◽  
Yue S. Yin ◽  
Jesse Ames ◽  
Martin J. Blaser ◽  
...  

Type 1 diabetes (T1D) and Hashimoto's thyroiditis (HT) are the two most common autoimmune endocrine diseases that have rising global incidence. These diseases are caused by the immune-mediated destruction of hormone-producing endocrine cells, pancreatic beta cells and thyroid follicular cells, respectively. Both genetic predisposition and environmental factors govern the onset of T1D and HT. Recent evidence strongly suggests that the intestinal microbiota plays a role in accelerating or preventing disease progression depending on the compositional and functional profile of the gut bacterial communities. Accumulating evidence points towards the interplay between the disruption of gut microbial homeostasis (dysbiosis) and the breakdown of host immune tolerance at the onset of both diseases. In this review, we will summarize the major recent findings about the microbiome alterations associated with T1D and HT, and the connection of these changes to disease states. Furthermore, we will discuss the potential mechanisms by which gut microbial dysbiosis modulates the course of the disease, including disruption of intestinal barrier integrity and microbial production of immunomodulatory metabolites. The aim of this review is to provide broad insight into the role of gut microbiome in the pathophysiology of these diseases.


2020 ◽  
Vol 319 (4) ◽  
pp. L675-L682 ◽  
Author(s):  
Jay H. Lipinski ◽  
Bethany B. Moore ◽  
David N. O’Dwyer

Mucosal surfaces are constantly exposed to a microbiome consisting of microorganisms that heavily influence human immunity and health. In the lung these microorganisms consist of bacteria, viruses, and fungi and exist in a relatively low biomass state. Bacterial communities of the lung modulate local inflammation and correlate with changes in pulmonary physiology and clinical outcomes in patients with lung disease. Instrumental to this progress has been the study of these bacterial communities in the pathogenesis of pulmonary fibrosis, a fatal and progressive disease culminating in respiratory failure. Key pathophysiological mechanisms in pulmonary fibrosis include recurrent idiopathic alveolar epithelial injury, unchecked collagen deposition, mucociliary dysfunction due to muc5b overexpression, hypoxia, and altered host defense. These key mechanisms and their related consequences promote severe progressive architectural lung destruction and loss of local homeostasis. As such, pulmonary fibrosis is an appropriate target disease for the study of the lung microbiome. Herein, we discuss recent advances in our understanding of the role of the lung microbiome in the pathogenesis of pulmonary fibrosis. We highlight fundamental clinical observations and mechanistic insights and identify crucial areas for further discovery science. An improved understanding of how the lung microbiome acts to influence outcomes in patients with pulmonary fibrosis will lead to enhanced therapies for this devastating lung disease.


2017 ◽  
Vol 203 (2) ◽  
pp. 99-104 ◽  
Author(s):  
Jo-Maree Courtney ◽  
Patricia L. Spafford

Chronic obstructive pulmonary disease (COPD) is a major cause of mortality worldwide, and there is currently no treatment that can halt the progression of the disease. Over the last decade there has been increasing interest in the idea that epithelial-mesenchymal transition (EMT) may be active in COPD. Here we review the evidence for EMT in COPD as well as the current progress being made on understanding the drivers and mechanisms involved. Finally, we discuss the potential benefits that understanding EMT may bring to the field of chronic respiratory disease.


2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Junying Lu ◽  
Lingxin Xiong ◽  
Xiaohao Zhang ◽  
Zhongmin Liu ◽  
Shiji Wang ◽  
...  

With the development of culture-independent techniques, numerous studies have demonstrated that the lower airway is not sterile in health and harbors diverse microbial communities. Furthermore, new evidence suggests that there is a distinct lower airway microbiome in those with chronic respiratory disease. To understand the role of lower airway dysbiosis in the pathogenesis of asthma, in this article, we review the published reports about the lung microbiome of healthy controls, provide an outlook on the contribution of lower airway dysbiosis to asthma, especially steroid-resistant asthma, and discuss the potential therapies targeted for lower airway dysbiosis.


2010 ◽  
Vol 151 (51) ◽  
pp. 2083-2088 ◽  
Author(s):  
Balázs Antus

A kilégzett levegőben mérhető nitrogén-monoxid a legszélesebb körben vizsgált légúti biomarker. A stabil állapotú krónikus obstruktív tüdőbetegségben a kilégzett nitrogén-monoxid-szint hasonló vagy csak kismértékben emelkedett az egészségesekhez képest. Mivel a nitrogén-monoxid-szint szoros összefüggést mutat a légúti eosinophilia mértékével, és mivel az eosinophil típusú légúti gyulladás szteroidokra érzékenyebb, az emelkedett nitrogén-monoxid-szinttel rendelkező betegek jobb válaszkészséget mutatnak az inhalációs vagy szisztémás kortikoszteroidkezelésre. A krónikus obstruktív tüdőbetegség akut exacerbatiója során a kilégzett nitrogén-monoxid szintje megemelkedik, majd ennek kezelése után csökken. Mivel a nitrogén-monoxid-szint és a kezelés során elért légzésfunkciós javulás szoros korrelációt mutat egymással, a nitrogén-monoxid-méréssel a terápiás válasz megjósolható. Összefoglalva: a nitrogén-monoxid-méréssel a krónikus obstruktív tüdőbetegségben szenvedő betegek olyan alcsoportját lehet elkülöníteni, amelynek szteroidérzékenysége nagyobb. Orv. Hetil., 2010, 151, 2083–2088.


2020 ◽  
Vol 28 (3) ◽  
pp. 360-370
Author(s):  
Stanislav N. Kotlyarov ◽  
Anna A. Kotlyarova

Despite all achievements of the modern medicine, the problem of chronic obstructive pulmonary disease (COPD) does not lose its relevance. The current paradigm suggests a key role of macrophages in inflammation in COPD. Macrophages are known to be heterogeneous in their functions. This heterogeneity is determined by their immunometabolic profile and also by peculiarities of lipid homeostasis of cells. Aim. To analyze the role of the ABCA1 transporter, a member of the ABC A subfamily, in the pathogenesis of COPD. The expression of ABCA1 in lung tissues is on the second place after the liver, which shows the important role of the carrier and of lipid homeostasis in the function of lungs. Analysis of the literature shows that participation of the transporter in inflammation consists in regulation of the content of cholesterol in the lipid rafts of the membranes, in phagocytosis and apoptosis. Conclusion. Through regulation of the process of reverse transport of cholesterol in macrophages of lungs, ABCA1 can change their inflammatory response, which makes a significant contribution to the pathogenesis of COPD.


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