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1.
Int J Mol Sci ; 23(6)2022 Mar 17.
Article in English | MEDLINE | ID: covidwho-1753505

ABSTRACT

As the global SARS-CoV-2 pandemic continues to plague healthcare systems, it has become clear that opportunistic pathogens cause a considerable proportion of SARS-CoV-2-associated mortality and morbidity cases. Of these, Covid-Associated Pulmonary Aspergilliosis (CAPA) is a major concern with evidence that it occurs in the absence of traditional risk factors such as neutropenia and is diagnostically challenging for the attending physician. In this review, we focus on the immunopathology of SARS-CoV-2 and how this potentiates CAPA through dysregulation of local and systemic immunity as well as the unintended consequences of approved COVID treatments including corticosteroids and IL-6 inhibitors. Finally, we will consider how knowledge of the above may aid in the diagnosis of CAPA using current diagnostics and what treatment should be instituted in probable and confirmed cases.


Subject(s)
COVID-19/complications , COVID-19/immunology , Disease Susceptibility/immunology , Host-Pathogen Interactions/immunology , Pulmonary Aspergillosis/etiology , SARS-CoV-2/immunology , Antifungal Agents/therapeutic use , Biomarkers , COVID-19/virology , Disease Management , Humans , Immunocompromised Host , Pulmonary Aspergillosis/diagnosis , Pulmonary Aspergillosis/therapy , Reproducibility of Results , Serologic Tests/methods , Serologic Tests/standards , Treatment Outcome
3.
Front Immunol ; 12: 774776, 2021.
Article in English | MEDLINE | ID: covidwho-1581334

ABSTRACT

Both RNA N6-methyladenosine (m6A) modification of SARS-CoV-2 and immune characteristics of the human body have been reported to play an important role in COVID-19, but how the m6A methylation modification of leukocytes responds to the virus infection remains unknown. Based on the RNA-seq of 126 samples from the GEO database, we disclosed that there is a remarkably higher m6A modification level of blood leukocytes in patients with COVID-19 compared to patients without COVID-19, and this difference was related to CD4+ T cells. Two clusters were identified by unsupervised clustering, m6A cluster A characterized by T cell activation had a higher prognosis than m6A cluster B. Elevated metabolism level, blockage of the immune checkpoint, and lower level of m6A score were observed in m6A cluster B. A protective model was constructed based on nine selected genes and it exhibited an excellent predictive value in COVID-19. Further analysis revealed that the protective score was positively correlated to HFD45 and ventilator-free days, while negatively correlated to SOFA score, APACHE-II score, and crp. Our works systematically depicted a complicated correlation between m6A methylation modification and host lymphocytes in patients infected with SARS-CoV-2 and provided a well-performing model to predict the patients' outcomes.


Subject(s)
Adenosine/analogs & derivatives , COVID-19/immunology , COVID-19/virology , Host-Pathogen Interactions/immunology , Leukocytes/immunology , RNA, Viral/genetics , SARS-CoV-2/physiology , Adenosine/metabolism , Cluster Analysis , Computational Biology/methods , Disease Susceptibility/immunology , Gene Expression Profiling , Humans , Leukocytes/metabolism , RNA, Viral/metabolism , ROC Curve
5.
Neuromolecular Med ; 23(4): 561-571, 2021 12.
Article in English | MEDLINE | ID: covidwho-1525619

ABSTRACT

The current SARS-CoV-2 outbreak, which causes COVID-19, is particularly devastating for individuals with chronic medical conditions, in particular those with Down Syndrome (DS) who often exhibit a higher prevalence of respiratory tract infections, immune dysregulation and potential complications. The incidence of Alzheimer's disease (AD) is much higher in DS than in the general population, possibly increasing further the risk of COVID-19 infection and its complications. Here we provide a biological overview with regard to specific susceptibility of individuals with DS to SARS-CoV-2 infection as well as data from a recent survey on the prevalence of COVID-19 among them. We see an urgent need to protect people with DS, especially those with AD, from COVID-19 and future pandemics and focus on developing protective measures, which also include interventions by health systems worldwide for reducing the negative social effects of long-term isolation and increased periods of hospitalization.


Subject(s)
COVID-19/epidemiology , COVID-19/virology , Disease Susceptibility , Down Syndrome/epidemiology , Adolescent , Adult , Alzheimer Disease/complications , Alzheimer Disease/epidemiology , Alzheimer Disease/immunology , COVID-19/complications , COVID-19/prevention & control , COVID-19 Vaccines/administration & dosage , COVID-19 Vaccines/immunology , Comorbidity , Disease Susceptibility/immunology , Disease Susceptibility/virology , Down Syndrome/complications , Down Syndrome/immunology , Female , Hospitalization , Humans , Immune System/abnormalities , Incidence , Male , Pandemics/prevention & control , Prevalence , Risk Factors , Vaccination/methods
6.
J Infect Dev Ctries ; 15(10): 1384-1387, 2021 10 31.
Article in English | MEDLINE | ID: covidwho-1518650

ABSTRACT

Occurrence and recurrence of COVID-19 cases have been observed globally. The complex relationship of host-pathogen and the environment plays a vital role in understanding the widespread recurrence of the SARS-CoV-2 among humans. Though the pathobiology of the disease is not completely understood, it is well established that COVID-19 poses a greater threat to individuals with co-morbidities and a weakened immune system. The article deals with the notion of innate immunity, natural selection, and the survival of the fittest during the COVID-19 outbreak. The article also attempts to introduce the concept of "lifestyle and cultural immunity" that needs to be addressed and incorporated at an early stage of childhood to boost up the human immune system. The communication further discusses the role of vaccination and micro-organisms pre-existing in the environment which are required to enhance the immunity of an individual.


Subject(s)
COVID-19/immunology , COVID-19/mortality , Immunity, Innate , SARS-CoV-2/pathogenicity , Selection, Genetic/genetics , COVID-19/prevention & control , Disease Outbreaks , Disease Susceptibility/immunology , Host-Pathogen Interactions , Humans , SARS-CoV-2/immunology , Selection, Genetic/immunology , Vaccination
7.
Immunity ; 54(10): 2172-2176, 2021 Oct 12.
Article in English | MEDLINE | ID: covidwho-1433404

ABSTRACT

The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its associated disease, coronavirus disease 2019 (COVID-19), has caused a devastating pandemic worldwide. Here, we explain basic concepts underlying the transition from an epidemic to an endemic state, where a pathogen is stably maintained in a population. We discuss how the number of infections and the severity of disease change in the transition from the epidemic to the endemic phase and consider the implications of this transition in the context of COVID-19.


Subject(s)
COVID-19/epidemiology , COVID-19/immunology , Endemic Diseases , COVID-19/prevention & control , Disease Susceptibility/epidemiology , Disease Susceptibility/immunology , Epidemics , Humans , Immunity , Prevalence , SARS-CoV-2/immunology , Severity of Illness Index , Vaccination
9.
J Exp Med ; 218(8)2021 08 02.
Article in English | MEDLINE | ID: covidwho-1387679

ABSTRACT

Initial replication of SARS-CoV-2 in the upper respiratory tract is required to establish infection, and the replication level correlates with the likelihood of viral transmission. Here, we examined the role of host innate immune defenses in restricting early SARS-CoV-2 infection using transcriptomics and biomarker-based tracking in serial patient nasopharyngeal samples and experiments with airway epithelial organoids. SARS-CoV-2 initially replicated exponentially, with a doubling time of ∼6 h, and induced interferon-stimulated genes (ISGs) in the upper respiratory tract, which rose with viral replication and peaked just as viral load began to decline. Rhinovirus infection before SARS-CoV-2 exposure accelerated ISG responses and prevented SARS-CoV-2 replication. Conversely, blocking ISG induction during SARS-CoV-2 infection enhanced viral replication from a low infectious dose. These results show that the activity of ISG-mediated defenses at the time of SARS-CoV-2 exposure impacts infection progression and that the heterologous antiviral response induced by a different virus can protect against SARS-CoV-2.


Subject(s)
COVID-19/immunology , COVID-19/virology , Immunity, Innate/physiology , Nasopharynx/virology , Adult , Aged , Aged, 80 and over , Angiotensin-Converting Enzyme 2/genetics , Case-Control Studies , Chemokine CXCL10/metabolism , Disease Susceptibility/immunology , Female , Gene Expression Profiling , Host-Pathogen Interactions/physiology , Humans , Interferons/genetics , Interferons/immunology , Interferons/metabolism , Male , Middle Aged , Picornaviridae Infections/immunology , Picornaviridae Infections/virology , SARS-CoV-2/genetics , SARS-CoV-2/physiology , Viral Load , Virus Replication
10.
Immunol Lett ; 234: 16-32, 2021 06.
Article in English | MEDLINE | ID: covidwho-1173426

ABSTRACT

Inflammasomes are cytosolic multiprotein complexes that crucially contribute to host defense against pathogens but are also involved in the pathogenesis of autoinflammatory diseases. Inflammasome formation leads to activation of effector caspases (caspase-1, 4, 5, or 11), the proteolytic maturation of IL-1ß and IL-18 as well as cleavage of the pore-forming protein Gasdermin D. Dendritic cells are major regulators of immune responses as they bridge innate and adaptive immunity. We here summarize the current knowledge on inflammasome expression and formation in murine bone marrow-, human monocyte-derived as well as murine and human primary dendritic cells. Further, we discuss both, the beneficial and detrimental, involvement of inflammasome activation in dendritic cells in cancer, infections, and autoimmune diseases. As inflammasome activation is typically accompanied by Gasdermin d-mediated pyroptosis, which is an inflammatory form of programmed cell death, inflammasome formation in dendritic cells seems ill-advised. Therefore, we propose that hyperactivation, which is inflammasome activation without the induction of pyroptosis, may be a general model of inflammasome activation in dendritic cells to enhance Th1, Th17 as well as cytotoxic T cell responses.


Subject(s)
Dendritic Cells/immunology , Dendritic Cells/metabolism , Inflammasomes/metabolism , Animals , Biomarkers , Cell Communication/genetics , Cell Communication/immunology , Cytokines/metabolism , Disease Susceptibility/immunology , Humans , Immunomodulation , Inflammation/etiology , Inflammation/metabolism , Inflammation/pathology , T-Lymphocyte Subsets/immunology , T-Lymphocyte Subsets/metabolism
11.
Front Immunol ; 12: 681449, 2021.
Article in English | MEDLINE | ID: covidwho-1314554

ABSTRACT

Immunosenescence is a process associated with aging that leads to dysregulation of cells of innate and adaptive immunity, which may become dysfunctional. Consequently, older adults show increased severity of viral and bacterial infections and impaired responses to vaccinations. A better understanding of the process of immunosenescence will aid the development of novel strategies to boost the immune system in older adults. In this review, we focus on major alterations of the immune system triggered by aging, and address the effect of chronic viral infections, effectiveness of vaccination of older adults and strategies to improve immune function in this vulnerable age group.


Subject(s)
Aging/immunology , Host-Pathogen Interactions/immunology , Immunity , Virus Diseases/immunology , Adaptive Immunity , Age Factors , Animals , Clinical Decision-Making , Disease Management , Disease Susceptibility/immunology , Humans , Immune System/immunology , Immune System/metabolism , Immunity, Innate , Virus Diseases/therapy , Virus Diseases/virology
12.
PLoS Pathog ; 17(7): e1009753, 2021 07.
Article in English | MEDLINE | ID: covidwho-1309967

ABSTRACT

To understand the diversity of immune responses to SARS-CoV-2 and distinguish features that predispose individuals to severe COVID-19, we developed a mechanistic, within-host mathematical model and virtual patient cohort. Our results suggest that virtual patients with low production rates of infected cell derived IFN subsequently experienced highly inflammatory disease phenotypes, compared to those with early and robust IFN responses. In these in silico patients, the maximum concentration of IL-6 was also a major predictor of CD8+ T cell depletion. Our analyses predicted that individuals with severe COVID-19 also have accelerated monocyte-to-macrophage differentiation mediated by increased IL-6 and reduced type I IFN signalling. Together, these findings suggest biomarkers driving the development of severe COVID-19 and support early interventions aimed at reducing inflammation.


Subject(s)
COVID-19/immunology , Models, Immunological , SARS-CoV-2 , Biomarkers/metabolism , CD8-Positive T-Lymphocytes/immunology , COVID-19/virology , Cohort Studies , Computational Biology , Computer Simulation , Disease Susceptibility/immunology , Host Microbial Interactions/immunology , Humans , Immunity, Innate , Interferons/metabolism , Interleukin-6/metabolism , Macrophages/immunology , Pandemics , SARS-CoV-2/immunology , Severity of Illness Index , User-Computer Interface
13.
Int J Mol Sci ; 22(13)2021 Jun 24.
Article in English | MEDLINE | ID: covidwho-1304660

ABSTRACT

The liver is an organ with impressive regenerative potential and has been shown to heal sizable portions after their removal. However, certain diseases can overstimulate its potential to self-heal and cause excessive cellular matrix and collagen buildup. Decompensation of liver fibrosis leads to cirrhosis, a buildup of fibrotic ECM that impedes the liver's ability to efficiently exchange fluid. This review summarizes the complex immunological activities in different liver diseases, and how failure to maintain liver homeostasis leads to progressive fibrotic tissue development. We also discuss a variety of pathologies that lead to liver cirrhosis, such as alcoholic liver disease and chronic hepatitis B virus (HBV). Mesenchymal stem cells are widely studied for their potential in tissue replacement and engineering. Herein, we discuss the potential of MSCs to regulate immune response and alter the disease state. Substantial efforts have been performed in preclinical animal testing, showing promising results following inhibition of host immunity. Finally, we outline the current state of clinical trials with mesenchymal stem cells and other cellular and non-cellular therapies as they relate to the detection and treatment of liver cirrhosis.


Subject(s)
Disease Susceptibility , Liver Diseases/etiology , Liver Diseases/metabolism , Animals , Biomarkers , Combined Modality Therapy , Disease Management , Disease Progression , Disease Susceptibility/immunology , Host-Pathogen Interactions/genetics , Host-Pathogen Interactions/immunology , Humans , Liver Diseases/diagnosis , Liver Diseases/therapy
14.
Gac Med Mex ; 157(2): 174-180, 2021.
Article in English | MEDLINE | ID: covidwho-1285646

ABSTRACT

INTRODUCTION: Whether there is an influence of the ABO blood system on SARS-CoV-2 infection is unknown. OBJECTIVE: To analyze if there is an association between the ABO system antigens and susceptibility to and severity of SARS-CoV-2 infection. MATERIAL AND METHODS: The frequency of ABO system antigens was compared in 73 confirmed cases of SARS-CoV-2 infection and 52 clinically healthy donors. Infection severity was assessed by comparing the frequency of antigens by disease severity and mortality. RESULTS: The risk of suffering from SARS-CoV-2 infection increases in subjects with A vs. non-A antigen (OR = 1.45; 95 % CI: 1.061-1.921). Blood phenotype O reduces the risk of SARS-CoV-2 infection (OR = 0.686; 95 % CI: 0.522-0.903). No differences were found regarding disease severity. In critically ill patients, the risk of mortality increased in subjects with A vs. non-A antigen (OR = 3.34; 95 % CI: 1.417-8.159). CONCLUSION: Blood group A is a risk factor for SARS-CoV-2 infection, but not for disease severity, although in critically ill patients it is a risk factor for mortality.


INTRODUCCIÓN: Se desconoce si existe una influencia del sistema sanguíneo ABO en susceptibilidad y gravedad de la enfermedad. OBJETIVO: Analizar si existe una asociación entre los antígenos del sistema ABO y la susceptibilidad y gravedad de la infección por SARS-CoV-2. MATERIAL Y MÉTODOS: Se compararon las frecuencias de los antígenos del sistema ABO en 73 casos confirmados de infección por SARS-CoV-2 y 52 donadores clínicamente sanos. La gravedad de la infección se evaluó comparando la frecuencia de los antígenos por gravedad de la enfermedad y la mortalidad. RESULTADOS: El riesgo de padecer infección por SARS-CoV-2 se incrementa en sujetos con antígeno A vs los no-A (OR=1.45; IC95 %:1.061-1.921). El fenotipo sanguíneo O disminuye el riesgo de padecer infección por SARS-CoV-2 (OR=0.686; IC95 %: 0.522-0.903). No se encontraron diferencias entre la gravedad de la enfermedad. En los pacientes graves, el riesgo de mortalidad se incrementó en sujetos con antígeno A vs los no-A (OR= 3.34; IC95 %: 1.417-8.159). CONCLUSIÓN: El grupo sanguíneo A es un factor de riesgo para padecer infección por SARS-CoV-2, no así en la gravedad de la enfermedad, pero en los pacientes graves fue un factor de riesgo para la mortalidad.


Subject(s)
ABO Blood-Group System/immunology , COVID-19/immunology , Severity of Illness Index , ABO Blood-Group System/adverse effects , Adult , Aged , COVID-19/blood , COVID-19/epidemiology , COVID-19/mortality , Case-Control Studies , Confidence Intervals , Critical Illness , Disease Susceptibility/blood , Disease Susceptibility/immunology , Female , Humans , Male , Middle Aged , Odds Ratio , Risk Factors , Young Adult
15.
J Med Virol ; 93(7): 4585-4591, 2021 07.
Article in English | MEDLINE | ID: covidwho-1263090

ABSTRACT

Since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in China at the end of 2019, the virus has spread rapidly across the globe leading to millions of infections and subsequent deaths. Although the virus infects those exposed indiscriminately, there are groups in society at an increased risk of severe infection, leading to increased morbidity. Patients suffering from hematological cancers, particularly leukemia, lymphoma, and myeloma, may be one such group and previous studies have suggested that they may be at a three to four times greater risk of severe COVID-19 after SARS-CoV-2 infection, leading to admissions to ICU, mechanical ventilation, and death compared to those without such malignancies. Serological testing for IgG seroconversion has been extensively studied in the immunocompetent, but fewer publications have characterized this process in large series of immunocompromised patients. This study described 20 patients with hematological cancers who tested positive for SARS-CoV-2 via PCR with 12 of the patients receiving further serological testing. We found that of the 12 patients screened for SARS-CoV-2 IgG antibodies, only 2 (16.6%) were able to generate an immune response to the infection. Yet despite this low seroconversion rate in this cohort, none of these patients died or became particularly unwell with COVID-19 or its related complications.


Subject(s)
Antibodies, Viral/blood , COVID-19/pathology , Hematologic Neoplasms/immunology , Immunocompromised Host/immunology , SARS-CoV-2/immunology , Aged , Aged, 80 and over , Antibodies, Neutralizing/blood , COVID-19/diagnosis , COVID-19/immunology , COVID-19 Testing , Disease Susceptibility/immunology , Disease Susceptibility/virology , Female , Hematologic Neoplasms/drug therapy , Humans , Immunoglobulin G/blood , Immunoglobulin M/blood , Male , Middle Aged , Retrospective Studies , Seroconversion
16.
Clin Transl Sci ; 14(6): 2111-2116, 2021 11.
Article in English | MEDLINE | ID: covidwho-1247160

ABSTRACT

This review describes the evidence for the potential benefit of vitamin D supplementation in people with respiratory diseases who may have a higher susceptibility to coronavirus disease 2019 (COVID-19) infection and its consequences. Clinical evidence indicates that vitamin D may reduce the risk of both upper and lower respiratory tract infections and offers benefit particularly in people with vitamin D deficiency. Some evidence exists for a higher incidence of active tuberculosis (TB) in patients who are deficient in vitamin D. An association between low levels of 25(OH)D (the active form of vitamin D) and COVID-19 severity of illness and mortality has also been reported. In addition, low 25(OH)D levels are associated with poor outcomes in acute respiratory distress syndrome (ARDS). The cytokine storm experienced in severe COVID-19 infections results from excessive release of pro-inflammatory cytokines. Due to its immunomodulatory effects, adequate vitamin D levels may cause a decrease in the pro-inflammatory cytokines and an increase in the anti-inflammatory cytokines during COVID-19 infections. Vitamin D deficiency was found in 82.2% of hospitalized COVID-19 cases and 47.2% of population-based controls (p < 0.0001). The available evidence warrants an evaluation of vitamin D supplementation in susceptible populations with respiratory diseases, such as TB, and particularly in those who are deficient in vitamin D. This may mitigate against serious complications of COVID-19 infections or reduce the impact of ARDS in those who have been infected.


Subject(s)
COVID-19/immunology , Dietary Supplements , Tuberculosis/immunology , Vitamin D Deficiency/diet therapy , Vitamin D/administration & dosage , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/prevention & control , Comorbidity , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/prevention & control , Cytokine Release Syndrome/virology , Disease Susceptibility/blood , Disease Susceptibility/immunology , Humans , Pandemics , Respiratory Distress Syndrome/immunology , Respiratory Distress Syndrome/prevention & control , Risk Factors , Severity of Illness Index , Tuberculosis/blood , Tuberculosis/epidemiology , Vitamin D/blood , Vitamin D Deficiency/complications , Vitamin D Deficiency/epidemiology , Vitamin D Deficiency/immunology
17.
Zool Res ; 42(3): 335-338, 2021 May 18.
Article in English | MEDLINE | ID: covidwho-1231642

ABSTRACT

The global outbreak of coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as of 8 May 2021, has surpassed 150 700 000 infections and 3 279 000 deaths worldwide. Evidence indicates that SARS-CoV-2 RNA can be detected on particulate matter (PM), and COVID-19 cases are correlated with levels of air pollutants. However, the mechanisms of PM involvement in the spread of SARS-CoV-2 remain poorly understood. Here, we found that PM exposure increased the expression level of angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) in several epithelial cells and increased the adsorption of the SARS-CoV-2 spike protein. Instillation of PM in a hACE2 mouse model significantly increased the expression of ACE2 and Tmprss2 and viral replication in the lungs. Furthermore, PM exacerbated the pulmonary lesions caused by SARS-CoV-2 infection in the hACE2 mice. In conclusion, our study demonstrated that PM is an epidemiological factor of COVID-19, emphasizing the necessity of wearing anti-PM masks to cope with this global pandemic.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/chemically induced , COVID-19/immunology , Particulate Matter/adverse effects , SARS-CoV-2 , Adsorption/drug effects , Animals , Disease Susceptibility/chemically induced , Disease Susceptibility/immunology , Epithelial Cells/metabolism , Mice , Mice, Inbred Strains , Particulate Matter/chemistry , RNA, Viral/analysis , SARS-CoV-2/genetics , Serine Endopeptidases/metabolism , Spike Glycoprotein, Coronavirus/metabolism , Virus Internalization/drug effects
19.
Immunity ; 54(6): 1200-1218.e9, 2021 06 08.
Article in English | MEDLINE | ID: covidwho-1213288

ABSTRACT

Tissue macrophages self-renew during homeostasis and produce inflammatory mediators upon microbial infection. We examined the relationship between proliferative and inflammatory properties of tissue macrophages by defining the impact of the Wnt/ß-catenin pathway, a central regulator of self-renewal, in alveolar macrophages (AMs). Activation of ß-catenin by Wnt ligand inhibited AM proliferation and stemness, but promoted inflammatory activity. In a murine influenza viral pneumonia model, ß-catenin-mediated AM inflammatory activity promoted acute host morbidity; in contrast, AM proliferation enabled repopulation of reparative AMs and tissue recovery following viral clearance. Mechanistically, Wnt treatment promoted ß-catenin-HIF-1α interaction and glycolysis-dependent inflammation while suppressing mitochondrial metabolism and thereby, AM proliferation. Differential HIF-1α activities distinguished proliferative and inflammatory AMs in vivo. This ß-catenin-HIF-1α axis was conserved in human AMs and enhanced HIF-1α expression associated with macrophage inflammation in COVID-19 patients. Thus, inflammatory and reparative activities of lung macrophages are regulated by ß-catenin-HIF-1α signaling, with implications for the treatment of severe respiratory diseases.


Subject(s)
COVID-19/immunology , COVID-19/virology , Cell Self Renewal/immunology , Host-Pathogen Interactions/immunology , Macrophages/immunology , SARS-CoV-2/immunology , Biomarkers , COVID-19/metabolism , Cytokines/metabolism , Disease Susceptibility/immunology , Humans , Hypoxia-Inducible Factor 1, alpha Subunit/metabolism , Inflammation Mediators/metabolism , Macrophages/cytology , Macrophages/metabolism , Macrophages, Alveolar/immunology , Macrophages, Alveolar/metabolism , Signal Transduction
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