scholarly journals Influence of Hypoxia on the Epithelial-Pathogen Interactions in the Lung: Implications for Respiratory Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Lee K. Page ◽  
Karl J. Staples ◽  
C. Mirella Spalluto ◽  
Alastair Watson ◽  
Tom M. A. Wilkinson
Keyword(s):  
Airway Epithelium ◽  
Lung Diseases ◽  
Respiratory Diseases ◽  
Molecular Mechanisms ◽  
Complex Disease ◽  
Tissue Hypoxia ◽  
Current Evidence ◽  
Chronic Obstructive ◽  
Respiratory Pathogens

Under normal physiological conditions, the lung remains an oxygen rich environment. However, prominent regions of hypoxia are a common feature of infected and inflamed tissues and many chronic inflammatory respiratory diseases are associated with mucosal and systemic hypoxia. The airway epithelium represents a key interface with the external environment and is the first line of defense against potentially harmful agents including respiratory pathogens. The protective arsenal of the airway epithelium is provided in the form of physical barriers, and the production of an array of antimicrobial host defense molecules, proinflammatory cytokines and chemokines, in response to activation by receptors. Dysregulation of the airway epithelial innate immune response is associated with a compromised immunity and chronic inflammation of the lung. An increasing body of evidence indicates a distinct role for hypoxia in the dysfunction of the airway epithelium and in the responses of both innate immunity and of respiratory pathogens. Here we review the current evidence around the role of tissue hypoxia in modulating the host-pathogen interaction at the airway epithelium. Furthermore, we highlight the work needed to delineate the role of tissue hypoxia in the pathophysiology of chronic inflammatory lung diseases such as asthma, cystic fibrosis, and chronic obstructive pulmonary disease in addition to novel respiratory diseases such as COVID-19. Elucidating the molecular mechanisms underlying the epithelial-pathogen interactions in the setting of hypoxia will enable better understanding of persistent infections and complex disease processes in chronic inflammatory lung diseases and may aid the identification of novel therapeutic targets and strategies.

scholarly journals A Review of The Role of The Microbiome on Immune Responses and Its Association With Cystic Fibrosis

2021 ◽  
Vol 3 (2) ◽  
pp. 75-88
Author(s):  
Mahtab Ghorban Movahed ◽  
◽  
Ahya Abdi Ali ◽  
Keyword(s):  
Cystic Fibrosis ◽  
Immune Responses ◽  
Lung Diseases ◽  
Complex Disease ◽  
Pulmonary Complications ◽  
Host Susceptibility ◽  
Chronic Obstructive ◽  
Chronic Lung Diseases ◽  
The Impact

In recent years, the microbiome has been recognized as a key regulator of immune responses. Evidence suggests that changes in the microbiome can lead to chronic disease and even exacerbation of the disease. Impairment of innate immunity resulting from microbial incompatibility may worsen host susceptibility to infection and exacerbate chronic lung diseases. Specific microbes play a key role in improving immune responses and microbial incompatibility is involved in chronic lung diseases such as asthma, chronic obstructive pulmonary disease, and Cystic Fibrosis (CF). CF is an extremely complex disease that results from a gene mutation. Lack of expression of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) has late complications. Incompatibility in lung microbiota is associated with chronic lung diseases, but it is not determined whether this incompatibility can cause health problems or ineffective regulation of immune response create the disease and its progression. In the CF, due to the deficiency of the immune system, many opportunistic microorganisms, including Pseudomonas. aeruginosa or Staphylococcus aureus are colonized in the patient’s lung and due to an immunodeficiency causedby a defect in the system CFTR, lungs are unable to clear the bacteria that leads to severe pulmonary complications and respiratory and digestive problems in such patients. Therefore, in these patients, the microbiome contributes to dysfunctional immune responses and disease exacerbations. This review summarizes the impact of the microbiome on host immune responses and its relationship with CF to explore the role of the microbiome in causing CF.

scholarly journals Relationships Between Oral Microecosystem and Respiratory Diseases

2022 ◽  
Vol 8 ◽  
Author(s):  
Jiajia Dong ◽  
Wei Li ◽  
Qi Wang ◽  
Jiahao Chen ◽  
Yue Zu ◽  
...  
Keyword(s):  
Oral Health ◽  
Respiratory Infection ◽  
Respiratory Diseases ◽  
Oral Microbiome ◽  
Chronic Obstructive ◽  
Oral Microbiota ◽  
Respiratory Pathogens ◽  
Oral Diseases ◽  
Oral Microbes

Oral microecosystem is a very complicated ecosystem that is located in the mouth and comprises oral microbiome, diverse anatomic structures of oral cavity, saliva and interactions between oral microbiota and between oral microbiota and the host. More and more evidence from studies of epidemiology, microbiology and molecular biology is establishing a significant link between oral microecosystem and respiratory diseases. Microbiota settling down in oral microecosystem is known as the main source of lung microbiome and has been associated with the occurrence and development of respiratory diseases like pneumonia, chronic obstructive pulmonary disease, lung cancer, cystic fibrosis lung disease and asthma. In fact, it is not only indigenous oral microbes promote or directly cause respiratory infection and inflammation when inhaled into the lower respiratory tract, but also internal environment of oral microecosystem serves as a reservoir for opportunistic respiratory pathogens. Moreover, poor oral health and oral diseases caused by oral microecological dysbiosis (especially periodontal disease) are related with risk of multiple respiratory diseases. Here, we review the research status on the respiratory diseases related with oral microecosystem. Potential mechanisms on how respiratory pathogens colonize oral microecosystem and the role of indigenous oral microbes in pathogenesis of respiratory diseases are also summarized and analyzed. Given the importance of oral plaque control and oral health interventions in controlling or preventing respiratory infection and diseases, we also summarize the oral health management measures and attentions, not only for populations susceptible to respiratory infection like the elderly and hospitalized patients, but also for dentist or oral hygienists who undertake oral health care. In conclusion, the relationship between respiratory diseases and oral microecosystem has been established and supported by growing body of literature. However, etiological evidence on the role of oral microecosystem in the development of respiratory diseases is still insufficient. Further detailed studies focusing on specific mechanisms on how oral microecosystem participate in the pathogenesis of respiratory diseases could be helpful to prevent and treat respiratory diseases.

scholarly journals Current Evidence for a Role of Neuropeptides in the Regulation of Autophagy

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Elisabetta Catalani ◽  
Clara De Palma ◽  
Cristiana Perrotta ◽  
Davide Cervia
Keyword(s):  
Molecular Mechanisms ◽  
Current Evidence ◽  
Pathological Conditions ◽  
Organ Systems ◽  
Intercellular Signalling ◽  
Physiological Homeostasis ◽  
Response To Stress ◽  
Autophagic Process ◽  
Regulatory Functions

Neuropeptides drive a wide diversity of biological actions and mediate multiple regulatory functions involving all organ systems. They modulate intercellular signalling in the central and peripheral nervous systems as well as the cross talk among nervous and endocrine systems. Indeed, neuropeptides can function as peptide hormones regulating physiological homeostasis (e.g., cognition, blood pressure, feeding behaviour, water balance, glucose metabolism, pain, and response to stress), neuroprotection, and immunomodulation. We aim here to describe the recent advances on the role exerted by neuropeptides in the control of autophagy and its molecular mechanisms since increasing evidence indicates that dysregulation of autophagic process is related to different pathological conditions, including neurodegeneration, metabolic disorders, and cancer.

scholarly journals Research Progress in the Mechanism of Effect of PRP in Bone Deficiency Healing

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Ning Zhang ◽  
Yong-Ping Wu ◽  
Sheng-Jun Qian ◽  
Chong Teng ◽  
Shuai Chen ◽  
...  
Keyword(s):  
Bone Repair ◽  
Molecular Mechanisms ◽  
Platelet Rich Plasma ◽  
Autologous Blood ◽  
Research Progress ◽  
Current Evidence ◽  
Clinical Settings ◽  
Bone Deficiency ◽  
Defect Repair

Platelet-rich plasma (PRP) therapy is a recently developed technique that uses a concentrated portion of autologous blood to try to improve and accelerate the healing of various tissues. There is a considerable interest in using these PRP products for the treatment used in bone deficiency healing. Because PRP products are safe and easy to prepare and administer, there has been increased attention toward using PRP in numerous clinical settings. The benefits of PRP therapy appear to be promising, and many investigators are exploring the ways in which this therapy can be used in the clinical setting. At present, the molecular mechanisms of bone defect repair studies have focused on three aspects of the inflammatory cytokines, growth factors and angiogenic factors. The role of PRP works mainly through these three aspects of bone repair. The purpose of this paper is to review the current evidence on the mechanism of the effect of PRP in bone deficiency healing.

MicroRNA: Potential biomarker and target of therapy in acute lung injury

2020 ◽  
Vol 39 (11) ◽  
pp. 1429-1442
Author(s):  
Z-F Jiang ◽  
L Zhang ◽  
J Shen
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Respiratory Diseases ◽  
Current Evidence ◽  
Biological Processes ◽  
Fatal Disease ◽  
Small Noncoding Rnas ◽  
Potential Biomarker ◽  
Indirect Injury

MicroRNAs (miRNAs) are small noncoding RNAs stretching over 18–22 nucleotides and considered to be modifiers of many respiratory diseases. They are highly evolutionary conserved and have been implicated in several biological processes, including cell proliferation, apoptosis, differentiation, among others. Acute lung injury (ALI) is a fatal disease commonly caused by direct or indirect injury factors and has a high mortality rate in intensive care unit. Changes in expression of several types of miRNAs have been reported in patients with ALI. Some miRNAs suppress cellular injury and accelerate the recovery of ALI by targeting specific molecules and decreasing excessive immune response. For this reason, miRNAs are proposed as potential biomarkers for ALI and as therapeutic targets for this disease. This review summarizes current evidence supporting the role of miRNAs in ALI.

scholarly journals Mechanisms of phagocytosis and host clearance ofPseudomonas aeruginosa

2014 ◽  
Vol 306 (7) ◽  
pp. L591-L603 ◽  
Author(s):  
Rustin R. Lovewell ◽  
Yash R. Patankar ◽  
Brent Berwin
Keyword(s):  
Molecular Mechanisms ◽  
Bacterial Pathogen ◽  
Chronic Obstructive ◽  
Flagellar Motility ◽  
Obstructive Pulmonary Disease ◽  
Clinical Observations ◽  
High Incidence ◽  
Cellular Recruitment ◽  
Sterilizing Immunity

Pseudomonas aeruginosa is an opportunistic bacterial pathogen responsible for a high incidence of acute and chronic pulmonary infection. These infections are particularly prevalent in patients with chronic obstructive pulmonary disease and cystic fibrosis: much of the morbidity and pathophysiology associated with these diseases is due to a hypersusceptibility to bacterial infection. Innate immunity, primarily through inflammatory cytokine production, cellular recruitment, and phagocytic clearance by neutrophils and macrophages, is the key to endogenous control of P. aeruginosa infection. In this review, we highlight recent advances toward understanding the innate immune response to P. aeruginosa, with a focus on the role of phagocytes in control of P. aeruginosa infection. Specifically, we summarize the cellular and molecular mechanisms of phagocytic recognition and uptake of P. aeruginosa, and how current animal models of P. aeruginosa infection reflect clinical observations in the context of phagocytic clearance of the bacteria. Several notable phenotypic changes to the bacteria are consistently observed during chronic pulmonary infections, including changes to mucoidy and flagellar motility, that likely enable or reflect their ability to persist. These traits are likewise examined in the context of how the bacteria avoid phagocytic clearance, inflammation, and sterilizing immunity.

scholarly journals Rhinoviruses as Pathogens of the Lower Respiratory Tract

2000 ◽  
Vol 7 (5) ◽  
pp. 409-414 ◽  
Author(s):  
Nikolaos G Papadopoulos ◽  
Sebastian L Johnson
Keyword(s):  
Airway Disease ◽  
Current Evidence ◽  
Lower Airway ◽  
Respiratory Pathogens ◽  
Local Inflammatory Response ◽  
Upper Respiratory ◽  
Polymerase Chain ◽  
Serious Disease ◽  
The Individual

Rhinoviruses (RVs) are the most common upper respiratory pathogens, inducing the majority of common colds worldwide. RV-related morbidity, although significant cumulatively, has been considered trivial for the individual patient. However, recent strong epidemiological associations of RVs with asthma exacerbations, including severe episodes requiring hospitalization, indicate that RV infections can result in serious disease. Current evidence supports the possibility that RVs infect the lower airways, inducing a local inflammatory response. Such evidence suggests that the role of RVs in other lower respiratory diseases, such as pneumonia, bronchitis, bronchiolitis and cystic fibrosis, should be re-examined with polymerase chain reaction-based methodologies, which are considerably more sensitive than traditional, cell culture-based techniques. The mechanisms through which RVs induce lower airway disease are studied to understand the relative contributions of the epithelial, neurogenic and immune components in the antiviral response, and to permit the design and implementation of specific treatments.

scholarly journals Smoking and interstitial lung diseases

2015 ◽  
Vol 24 (137) ◽  
pp. 428-435 ◽  
Author(s):  
George A. Margaritopoulos ◽  
Eirini Vasarmidi ◽  
Joseph Jacob ◽  
Athol U. Wells ◽  
Katerina M. Antoniou
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Langerhans Cell Histiocytosis ◽  
Lung Diseases ◽  
Interstitial Lung Diseases ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Pulmonary Langerhans Cell Histiocytosis

For many years has been well known that smoking could cause lung damage. Chronic obstructive pulmonary disease and lung cancer have been the two most common smoking-related lung diseases. In the recent years, attention has also focused on the role of smoking in the development of interstitial lung diseases (ILDs). Indeed, there are three diseases, namely respiratory bronchiolitis-associated ILD, desquamative interstitial pneumonia and pulmonary Langerhans cell histiocytosis, that are currently considered aetiologically linked to smoking and a few others which are more likely to develop in smokers. Here, we aim to focus on the most recent findings regarding the role of smoking in the pathogenesis and clinical behaviour of ILDs.

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