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Hormone Molecular Biology and Clinical... Aug 2021COVID-19 is a global emergency with over 10 million cases and over 500, 000 deaths worldwide. The SARS CoV-2 is a RNA virus belonging to the family coronaviridae. It has... (Review)
Review
COVID-19 is a global emergency with over 10 million cases and over 500, 000 deaths worldwide. The SARS CoV-2 is a RNA virus belonging to the family coronaviridae. It has high infectivity. The manifestations of the disease range from asymptomatic or mild symptoms to severe pneumonia and ARDS. The CT scan of lung shows consolidation and "Ground Glass Opacities". The persons with other comorbidities are considered to be at a higher rate of acquiring the infection. Asthma and other allergies have not been identified as major risk factors for COVID-19 as the number of asthmatic patients having COVID-19 is not high enough for it to be considered so. The occurrence of COVID-19 in COPD patients can be related with smoking. The ACE-2 expression in such patients was considerably high. The relation between COVID-19 and Tuberculosis can also be reflected in terms of the stigma associated with diagnosis and treatment of such diseases in some communities, eventually increasing the chances of people's reluctance to seek medical help. Cancer patients are usually more susceptible to infections. Lung cancer is no different. Additionally, lung cancer also has strong association with smoking further increasing the risk. The risk of getting infection and its severity is high for autoimmune disorders as well as fungal infections. Currently there is no definite treatment of COVID-19. However, some of the currently used modalities are hydroxychloroquine and antiviral drugs.
Topics: COVID-19; Comorbidity; Diagnostic Imaging; Disease Management; Disease Susceptibility; Host-Pathogen Interactions; Humans; Lung; Public Health Surveillance; SARS-CoV-2; Symptom Assessment
PubMed: 34333882
DOI: 10.1515/hmbci-2020-0096 -
Medical Mycology Feb 2019Pulmonary cryptococcosis is an important opportunistic invasive mycosis in immunocompromised patients, but it is also increasingly seen in immunocompetent patients. The... (Review)
Review
Pulmonary cryptococcosis is an important opportunistic invasive mycosis in immunocompromised patients, but it is also increasingly seen in immunocompetent patients. The main human pathogens are Cryptococcus neoformans and C. gattii, which have a worldwide distribution. In contrast to cryptococcal meningitis, pulmonary cryptococcosis is still underdiagnosed because of limitations in diagnostic tools. It can mimic lung cancer, pulmonary tuberculosis, bacterial pneumonia, and other pulmonary mycoses both clinically and radiologically. Pulmonary nodules are the most common radiological feature, but these are not specific to pulmonary cryptococcosis. The sensitivity of culture of respiratory samples for Cryptococcus is poor and a positive result may also reflect colonisation. Cryptococcal antigen (CrAg) with lateral flow device is a fast and sensitive test and widely used on serum and cerebrospinal fluid, but sera from patients with pulmonary cryptococcosis are rarely positive in the absence of disseminated disease. Detection of CrAg from respiratory specimens might assist the diagnosis of pulmonary cryptococcosis but there are very few data. Molecular detection techniques such as multiplex reverse transcription polymerase chain reaction (RT-PCR) could also provide better sensitivity but these still require validation for respiratory specimens. The first line of treatment for pulmonary cryptococcosis is fluconazole, or amphotericin B and flucytosine for those with central nervous system involvement. Pulmonary cryptococcosis worsens the prognosis of cryptococcal meningitis. In this review, we summarize the biological aspects of Cryptococcus and provide an update on the diagnosis and management of pulmonary cryptococcosis.
Topics: Animals; Antifungal Agents; Clinical Laboratory Techniques; Cryptococcosis; Cryptococcus; Humans; Lung; Lung Diseases, Fungal; Prognosis; Risk Factors
PubMed: 30329097
DOI: 10.1093/mmy/myy086 -
Physiological Reviews Apr 2020Despite anti-retroviral therapy (ART), human immunodeficiency virus-1 (HIV)-related pulmonary disease continues to be a major cause of morbidity and mortality for people... (Review)
Review
Despite anti-retroviral therapy (ART), human immunodeficiency virus-1 (HIV)-related pulmonary disease continues to be a major cause of morbidity and mortality for people living with HIV (PLWH). The spectrum of lung diseases has changed from acute opportunistic infections resulting in death to chronic lung diseases for those with access to ART. Chronic immune activation and suppression can result in impairment of innate immunity and progressive loss of T cell and B cell functionality with aberrant cytokine and chemokine responses systemically as well as in the lung. HIV can be detected in the lungs of PLWH and has profound effects on cellular immune functions. In addition, HIV-related lung injury and disease can occur secondary to a number of mechanisms including altered pulmonary and systemic inflammatory pathways, viral persistence in the lung, oxidative stress with additive effects of smoke exposure, microbial translocation, and alterations in the lung and gut microbiome. Although ART has had profound effects on systemic viral suppression in HIV, the impact of ART on lung immunology still needs to be fully elucidated. Understanding of the mechanisms by which HIV-related lung diseases continue to occur is critical to the development of new preventive and therapeutic strategies to improve lung health in PLWH.
Topics: AIDS-Related Opportunistic Infections; Animals; Anti-HIV Agents; Anti-Inflammatory Agents; Asthma; Disease Models, Animal; HIV; HIV Infections; Host-Pathogen Interactions; Humans; Hypertension, Pulmonary; Immunocompromised Host; Lung; Lung Neoplasms; Prognosis; Pulmonary Disease, Chronic Obstructive; Respiratory Tract Infections; Risk Factors
PubMed: 31600121
DOI: 10.1152/physrev.00039.2018 -
Nature Jan 2015Lung diseases such as chronic obstructive pulmonary disease and pulmonary fibrosis involve the progressive and inexorable destruction of oxygen exchange surfaces and...
Lung diseases such as chronic obstructive pulmonary disease and pulmonary fibrosis involve the progressive and inexorable destruction of oxygen exchange surfaces and airways, and have emerged as a leading cause of death worldwide. Mitigating therapies, aside from impractical organ transplantation, remain limited and the possibility of regenerative medicine has lacked empirical support. However, it is clinically known that patients who survive sudden, massive loss of lung tissue from necrotizing pneumonia or acute respiratory distress syndrome often recover full pulmonary function within six months. Correspondingly, we recently demonstrated lung regeneration in mice following H1N1 influenza virus infection, and linked distal airway stem cells expressing Trp63 (p63) and keratin 5, called DASC(p63/Krt5), to this process. Here we show that pre-existing, intrinsically committed DASC(p63/Krt5) undergo a proliferative expansion in response to influenza-induced lung damage, and assemble into nascent alveoli at sites of interstitial lung inflammation. We also show that the selective ablation of DASC(p63/Krt5) in vivo prevents this regeneration, leading to pre-fibrotic lesions and deficient oxygen exchange. Finally, we demonstrate that single DASC(p63/Krt5)-derived pedigrees differentiate to type I and type II pneumocytes as well as bronchiolar secretory cells following transplantation to infected lung and also minimize the structural consequences of endogenous stem cell loss on this process. The ability to propagate these cells in culture while maintaining their intrinsic lineage commitment suggests their potential in stem cell-based therapies for acute and chronic lung diseases.
Topics: Animals; Bronchioles; Cell Differentiation; Cell Lineage; Cell Proliferation; Dogs; Humans; Influenza A Virus, H1N1 Subtype; Keratin-5; Lung; Madin Darby Canine Kidney Cells; Mice; Orthomyxoviridae Infections; Oxygen; Pedigree; Phosphoproteins; Pneumonia; Pulmonary Alveoli; Re-Epithelialization; Regeneration; Stem Cell Transplantation; Stem Cells; Trans-Activators
PubMed: 25383540
DOI: 10.1038/nature13903 -
Journal of Infection and Public Health Nov 2021Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) attacks pulmonary alveolar cells via angiotensin-converting enzyme 2 (ACE2) receptors and causes pulmonary... (Review)
Review
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) attacks pulmonary alveolar cells via angiotensin-converting enzyme 2 (ACE2) receptors and causes pulmonary infections that result in coronavirus disease (COVID-19), inducing immune responses that can result in severe pneumonia. We reviewed the clinical experiences of lung diseases during the COVID-19 pandemic to offer insights into the adaptations made by experts in the diagnosis and treatment of these comorbidities. Various lung comorbidities increase the severity of COVID-19 and associated mortality by amplifying ACE2 expression. Additionally, the COVID-19 pandemic has changed the use of routine diagnostic pulmonary imaging methods, making chest sonography scoring the most convenient, as it can be conducted bedside. Treatment protocols for SARS-CoV-2 infection and the underlying lung diseases are also affected owing to potential interactions. The optimal diagnostic methods and treatment protocols for lung diseases have been adapted worldwide to increase survival rates and attenuate acute lung injuries during the COVID-19 pandemic.
Topics: COVID-19; Humans; Lung; Pandemics; Pneumonia; SARS-CoV-2
PubMed: 34700289
DOI: 10.1016/j.jiph.2021.09.024 -
Journal of Thoracic Imaging Sep 2018Chronic cavitary lung disease is an uncommon manifestation of pulmonary infection, and is a pattern which worldwide is most commonly caused by reactivation tuberculosis.... (Review)
Review
Chronic cavitary lung disease is an uncommon manifestation of pulmonary infection, and is a pattern which worldwide is most commonly caused by reactivation tuberculosis. Other organisms, however, can cause similar radiologic patterns. Endemic fungi have long been recognized as potential causes of this pattern in North and South America, but the frequency with which these diseases present with chronic cavities in North America is relatively small. Nontuberculous mycobacteria and chronic aspergillus infections are recognized with increasing frequency as causes of this pattern. Melioidosis, a bacterial infection that can also cause chronic lung cavities, was previously understood to be relevant primarily in Southeast Asia, but is now understood to have a wider geographic range. While cultures, serologies, and other laboratory methods are key to identifying the infectious causes of chronic lung cavities, radiologic evaluation can contribute to the diagnosis. Differentiating the radiologic patterns of these diseases from reactivation tuberculosis depends on subtle differences in imaging findings and, in some cases, appreciation of underlying lung disease.
Topics: Chronic Disease; Humans; Lung; Lung Diseases; Respiratory Tract Infections; Tomography, X-Ray Computed
PubMed: 30048346
DOI: 10.1097/RTI.0000000000000346 -
Frontiers in Immunology 2021Schistosome infection is a major cause of global morbidity, particularly in sub-Saharan Africa. However, there is no effective vaccine for this major neglected tropical... (Review)
Review
Schistosome infection is a major cause of global morbidity, particularly in sub-Saharan Africa. However, there is no effective vaccine for this major neglected tropical disease, and re-infection routinely occurs after chemotherapeutic treatment. Following invasion through the skin, larval schistosomula enter the circulatory system and migrate through the lung before maturing to adulthood in the mesenteric or urogenital vasculature. Eggs released from adult worms can become trapped in various tissues, with resultant inflammatory responses leading to hepato-splenic, intestinal, or urogenital disease - processes that have been extensively studied in recent years. In contrast, although lung pathology can occur in both the acute and chronic phases of schistosomiasis, the mechanisms underlying pulmonary disease are particularly poorly understood. In chronic infection, egg-mediated fibrosis and vascular destruction can lead to the formation of portosystemic shunts through which eggs can embolise to the lungs, where they can trigger granulomatous disease. Acute schistosomiasis, or Katayama syndrome, which is primarily evident in non-endemic individuals, occurs during pulmonary larval migration, maturation, and initial egg-production, often involving fever and a cough with an accompanying immune cell infiltrate into the lung. Importantly, lung migrating larvae are not just a cause of inflammation and pathology but are a key target for future vaccine design. However, vaccine efforts are hindered by a limited understanding of what constitutes a protective immune response to larvae. In this review, we explore the current understanding of pulmonary immune responses and inflammatory pathology in schistosomiasis, highlighting important unanswered questions and areas for future research.
Topics: Animals; Disease Models, Animal; Host-Parasite Interactions; Humans; Immune Evasion; Lung; Lung Diseases, Parasitic; Mice; Protozoan Vaccines; Schistosoma; Schistosomiasis; Schistosomicides
PubMed: 33953712
DOI: 10.3389/fimmu.2021.635513 -
Clinical Microbiology and Infection :... Mar 2019Rhodococcus equi is a recognized cause of disease in humans, especially in individuals who are immunocompromised. Because diphtheroids are regarded as part of normal... (Review)
Review
BACKGROUND
Rhodococcus equi is a recognized cause of disease in humans, especially in individuals who are immunocompromised. Because diphtheroids are regarded as part of normal respiratory flora, the importance of R. equi as a pulmonary pathogen may not be fully appreciated and its prevalence may be underestimated. Most treatment recommendations for R. equi infection were established before antiretroviral drugs became available for human immunodeficiency virus/AIDS therapy, and therapeutic strategies may need to be updated.
OBJECTIVES
To review the role of R. equi as a cause of pulmonary infection; to highlight its importance for clinicians and microbiologists; and to challenge current approaches to treatment, whether in immunodeficient or immunocompetent individuals.
SOURCES
A PubMed search using combinations of the following terms: 'Rhodococcus (automatically including Corynebacterium) equi' AND 'pneumonia' OR 'pulmonary' infection, then cross-checking references in the resulting cases, case series and reviews.
CONTENT
We provide a review that details the challenges in the diagnosis, microbiology and pathogenesis of pulmonary infection caused by R. equi and the options for treatment.
IMPLICATIONS
Ten to 14 days of treatment may be effective for pneumonia due to R. equi. Our review suggests that longer courses of therapy are needed for cavitary lesions and lung masses. However, recommendations for excessively prolonged treatment of all pulmonary infections arose during a time when many cases occurred in individuals with AIDS and before effective antiretroviral therapy was available. We suggest that the rationale for prolonged therapy with multiple antibiotics needs to be re-evaluated.
Topics: AIDS-Related Opportunistic Infections; Actinomycetales Infections; Anti-Bacterial Agents; Disease Management; Humans; Immunocompromised Host; Lung; Pneumonia, Bacterial; Rhodococcus equi
PubMed: 29777923
DOI: 10.1016/j.cmi.2018.04.033 -
The Journal of Allergy and Clinical... Oct 2023The human microbiome associated with the respiratory tract is diverse, heterogeneous, and dynamic. The diversity and complexity of the microbiome and the interactions... (Review)
Review
The human microbiome associated with the respiratory tract is diverse, heterogeneous, and dynamic. The diversity and complexity of the microbiome and the interactions between microorganisms, host cells, and the host immune system are complex and multifactorial. Furthermore, the lymphatics provide a direct highway, the gut-lung axis, for the gut microbiome to affect outcomes related to respiratory disease and the host immune response. Viral infections in the airways can also alter the presence or absence of bacterial species, which might increase the risks for allergies and asthma. Viruses infect the airway epithelium and interact with the host to promote inflammatory responses that can trigger a wheezing illness. This immune response may alter the host's immune response to microbes and allergens, leading to T2 inflammation. However, exposure to specific bacteria may also tailor the host's response long before the virus has infected the airway. The frequency of viral infections, age at infection, sampling season, geographic location, population differences, and preexisting composition of the microbiota have all been linked to changes in microbiota diversity and stability. This review aims to evaluate the current reported evidence for microbiome interactions and the influences that viral infection may have on respiratory and gut microbiota, affecting respiratory outcomes in children.
Topics: Child; Humans; Microbiota; Virus Diseases; Asthma; Lung; Bacteria; Viruses
PubMed: 37607643
DOI: 10.1016/j.jaci.2023.08.008 -
Toxins Apr 2020Bacterial toxins play a key role in the pathogenesis of lung disease. Based on their structural and functional properties, they employ various strategies to modulate... (Review)
Review
Bacterial toxins play a key role in the pathogenesis of lung disease. Based on their structural and functional properties, they employ various strategies to modulate lung barrier function and to impair host defense in order to promote infection. Although in general, these toxins target common cellular signaling pathways and host compartments, toxin- and cell-specific effects have also been reported. Toxins can affect resident pulmonary cells involved in alveolar fluid clearance (AFC) and barrier function through impairing vectorial Na transport and through cytoskeletal collapse, as such, destroying cell-cell adhesions. The resulting loss of alveolar-capillary barrier integrity and fluid clearance capacity will induce capillary leak and foster edema formation, which will in turn impair gas exchange and endanger the survival of the host. Toxins modulate or neutralize protective host cell mechanisms of both the innate and adaptive immunity response during chronic infection. In particular, toxins can either recruit or kill central players of the lung's innate immune responses to pathogenic attacks, i.e., alveolar macrophages (AMs) and neutrophils. Pulmonary disorders resulting from these toxin actions include, e.g., acute lung injury (ALI), the acute respiratory syndrome (ARDS), and severe pneumonia. When acute infection converts to persistence, i.e., colonization and chronic infection, lung diseases, such as bronchitis, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF) can arise. The aim of this review is to discuss the impact of bacterial toxins in the lungs and the resulting outcomes for pathogenesis, their roles in promoting bacterial dissemination, and bacterial survival in disease progression.
Topics: Adaptive Immunity; Animals; Bacteria; Bacterial Infections; Bacterial Toxins; Disease Progression; Host-Pathogen Interactions; Humans; Immunity, Innate; Lung; Respiratory Tract Infections; Signal Transduction
PubMed: 32252376
DOI: 10.3390/toxins12040223