• ARDS
• PEEP
• driving pressure
• mechanical power
• mechanical ventilation
• modeling
• power
• tidal volume

• KL2 TR002542 NCATS NIH HHS
• R01 EB017205 NIBIB NIH HHS

• Adaptive immunity
• Airway smooth muscle
• Allergen
• Asthma
• Cytokine
• Dendritic cell
• Eosinophil
• Epithelial cell
• Extracellular matrix (ECM)
• Fibroblast
• Innate lymphoid cell
• Lung remodeling
• Lymphocyte
• Mast cell
• Matrix metalloproteinase
• Mucins
• Neutrophil

• Humans
• Airway Remodeling
• Lung
• Asthma
• Extracellular Matrix/physiology
• Adaptive Immunity

The immunologic mechanisms that contribute to the response to Mycobacterium tuberculosis infection still represent a challenge in the clinical management and scientific understanding of tuberculosis disease. In this scenario, the role of the different cells involved in the host response, either in terms of innate or adaptive immunity, remains key for defeating this disease. Among this coordinated cell response, mast cells remain key for defeating tuberculosis infection and disease. Together with its effector’s molecules, membrane receptors as well as its anatomical locations, mast cells play a crucial role in the establishment and perpetuation of the inflammatory response that leads to the generation of the granuloma during tuberculosis. This review highlights the current evidences that support the notion of mast cells as key link to reinforce the advancements in tuberculosis diagnosis, disease progression, and novel therapeutic strategies. Special focus on mast cells capacity for the modulation of the inflammatory response among patients suffering multidrug resistant tuberculosis or in co-infections such as current COVID-19 pandemic.

• anti-TB therapy
• biomarker
• co-infection
• disease control
• disease progression
• histamine
• mast cells
• tuberculosis

Mast cells (MCs) are known to be involved in the pathogenesis of idiopathic pulmonary fibrosis (IPF), although their role in acute exacerbations of IPF has not been investigated. The aims of the study were to evaluate the numbers of MCs in fibrotic and non-fibrotic areas of lung tissue specimens of idiopathic pulmonary fibrosis (IPF) patients with or without an acute exacerbation of IPF, and to correlate the MC density with clinical parameters. MCs of IPF patients were quantified from surgical lung biopsy (SLB) specimens (n = 47) and lung tissue specimens taken at autopsy (n = 7). MC density was higher in the fibrotic areas of lung tissue compared with spared alveolar areas or in controls. Female gender, low diffusion capacity for carbon monoxide, diffuse alveolar damage, and smoking were associated with a low MC density. MC densities of fibrotic areas had declined significantly in five subjects in whom both SLB in the stable phase and autopsy after an acute exacerbation of IPF had been performed. There were no correlations of MC densities with survival time or future acute exacerbations. The MC density in fibrotic areas was associated with several clinical parameters. An acute exacerbation of IPF was associated with a significant decline in MC counts. Further investigations will be needed to clarify the role of these cells in IPF and in the pathogenesis of acute exacerbation as this may help to identify some potential targets for medical treatment for this serious disease.

• acute exacerbation
• alveolar parenchyma.
• fibrosis
• idiopathic pulmonary fibrosis
• mast cells

• Cell Count
• Female
• Fibrosis
• Humans
• Idiopathic Pulmonary Fibrosis/pathology
• Lung/pathology
• Mast Cells/pathology

• Suomen Tuberkuloosin Vastustamisyhdistyksen Säätiö
• Hengityssairauksien Tutkimussäätiö
• Jalmari ja Rauha Ahokkaan Säätiö
• Research Foundation of North Finland
• Tampereen Tuberkuloosisäätiö
• Väinö ja Laina Kiven Säätiö
• University of Oulu including Oulu University Hospital

• ARDS
• Cytokine storm
• Inflammation
• Nimbolide
• Oxidative stress
• iRGD-NIMLip

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes coronavirus disease 2019 (COVID-19). SARS-CoV-2 binds the angiotensin-converting enzyme 2 (ACE2) on the cell surface and this complex is internalized. ACE2 serves as an endogenous inhibitor of inflammatory signals associated with four major regulator systems: the renin-angiotensin-aldosterone system (RAAS), the complement system, the coagulation cascade, and the kallikrein-kinin system (KKS). Understanding the pathophysiological effects of SARS-CoV-2 on these pathways is needed, particularly given the current lack of proven, effective treatments. The vasoconstrictive, prothrombotic and pro-inflammatory conditions induced by SARS-CoV-2 can be ascribed, at least in part, to the activation of these intersecting physiological networks. Moreover, patients with immune deficiencies, hypertension, diabetes, coronary heart disease, and kidney disease often have altered activation of these pathways, either due to underlying disease or to medications, and may be more susceptible to SARS-CoV-2 infection. Certain characteristic COVID-associated skin, sensory, and central nervous system manifestations may also be linked to viral activation of the RAAS, complement, coagulation, and KKS pathways. Pharmacological interventions that target molecules along these pathways may be useful in mitigating symptoms and preventing organ or tissue damage. While effective anti-viral therapies are critically needed, further study of these pathways may identify effective adjunctive treatments and patients most likely to benefit.

• COVID-19
• SARS-CoV-2
• angiotensin II
• bradykinin
• coagulation
• pharmacotherapy
• renin-angiotensin-aldosterone system
• substance P

The COVID-19 pandemic is posing an unprecedented sanitary threat. In the absence of specific vaccines and anti-SARS-CoV-2 drugs, medicines that may assist in tackling the emergency and limiting the high number of fatalities are urgently needed. The repositioning of available drugs to treat COVID-19 is the only and rapid option in the face of the lack of direct antiviral agents and vaccines available. In this light it is important to focus on available drugs, which, based on their pharmacodynamics, could plausibly attenuate viral growth as well as COVID-19’s worst complications. This is the case of chloroquine and tocilizumab which seem to limit virus replication and the severity of interstitial pneumonia, respectively. However, these treatments, particularly those aimed at containing inflammation, are still reserved for the most severe cases. This commentary elaborates on the pharmacological rationale of repositioning the mast cell stabilizer chromones as an adjunctive treatment for SARS‐CoV‐2 infection, and proposes their practical clinical testing as an early, safe, and cost-effective anti-inflammatory intervention in COVID-19 to limit the eventual secondary progression toward life-threatening respiratory complications.

• COVID-19
• chromones
• inflammation
• lung injury
• mast cells

• Mast cells
• eosinophils
• histamine concentration
• trinitrobenzene sulfonic acid
• ulcerative colitis

• Diabetes mellitus
• E-cadherin
• Epithelial–mesenchymal transition
• N-cadherin
• Transforming growth factor-β
• α-smooth muscle actin

• ARDS
• H1N1
• azithromycin
• pirfenidone
• prednisolone
• pulmonary fibrosis

• acute respiratory distress syndrome
• cardiac fibrosis
• heart
• heart failure
• idiopathic pulmonary hypertension
• lung
• myocardial infarction
• pulmonary fibrosis

Diffuse alveolar damage (DAD), which is the histological surrogate for acute respiratory distress syndrome (ARDS), has a multifactorial aetiology. Therefore it is possible that the immunopathology differs among the various presentations of DAD. The aim of this study is to compare lung immunopathology of viral (influenza A(H1N1)pdm09) to non-viral, extrapulmonary aetiologies in autopsy cases with DAD.

The lung tissue of 44 patients, was divided in the H1N1 group (n = 15) characterized by severe pulmonary injury due to influenza A(H1N1)pdm09 infection; the ARDS group (n = 13), characterized by patients with DAD due to non-pulmonary causes; and the Control group (n = 16), consisting of patients with non-pulmonary causes of death. Immunohistochemistry and image analysis were used to quantify, in the parenchyma and small airways, several immune cell markers.

Both DAD groups had higher expression of neutrophils and macrophages in parenchyma and small airways. However, there was a higher expression of CD4+ and CD8+ T lymphocytes, CD83+ dendritic cells, granzyme A+ and natural killer + cell density in the lung parenchyma of the H1N1 group (p < 0.05). In the small airways, there was a lower cell density of tryptase + mast cells and dendritic + cells and an increase of IL-17 in both DAD groups (p < 0.05).

DAD due to viral A(H1N1)pdm09 is associated with a cytotoxic inflammatory phenotype, with partially divergent responses in the parenchyma relative to the small airways. In non-viral DAD, main immune cell alterations were found at the small airway level, reinforcing the role of the small airways in the pathogenesis of the exudative phase of DAD.

The online version of this article (doi:10.1186/s12931-017-0630-x) contains supplementary material, which is available to authorized users.

• ARDS
• Autopsy
• Diffuse alveolar damage
• Human Influenza
• Pathology

Acute respiratory distress syndrome (ARDS) is characterized by acute hypoxemia respiratory failure, bilateral pulmonary infiltrates, and pulmonary edema of non-cardiac origin. Effective treatments for ARDS patients may arise from experimental studies with translational mouse models of this disease that aim to delineate the mechanisms underlying the disease pathogenesis. Mouse models of ARDS, however, can be limited by their rapid progression from injured to recovery state, which is in contrast to the course of ARDS in humans. Furthermore, current mouse models of ARDS do not recapitulate certain prominent aspects of the pathogenesis of ARDS in humans. In this study, we developed an improved endotoxemic mouse model of ARDS resembling many features of clinical ARDS including extended courses of injury and recovery as well as development of fibrosis following i.p. injection of lipopolysaccharide (LPS) to corn oil-preloaded mice. Compared with mice receiving LPS alone, those receiving corn oil and LPS exhibited extended course of lung injury and repair that occurred over a period of >2 weeks instead of 3–5days. Importantly, LPS challenge of corn oil-preloaded mice resulted in pulmonary fibrosis during the repair phase as often seen in ARDS patients. In summary, this simple novel mouse model of ARDS could represent a valuable experimental tool to elucidate mechanisms that regulate lung injury and repair in ARDS patients.

• Animals
• Apoptosis/drug effects
• Cell Proliferation/drug effects
• Corn Oil/pharmacology
• Disease Models, Animal
• Endotoxemia/complications
• Endotoxemia/etiology
• Female
• Lipopolysaccharides/pharmacology
• Lung Injury/chemically induced
• Male
• Mice
• Mice, Inbred C57BL
• Pulmonary Fibrosis/chemically induced
• Real-Time Polymerase Chain Reaction
• Respiratory Distress Syndrome/etiology

• P01 HL077806 NHLBI NIH HHS
• R01 HL125350 NHLBI NIH HHS
• R01 HL133951 NHLBI NIH HHS
• R01 HL123957 NHLBI NIH HHS
• R01 HL104092 NHLBI NIH HHS
• National Heart, Lung, and Blood Institute

Swine flu influenza had spread the world over in 2009. The main pathology was bilateral pneumonia. Majority of these cases recovered from pneumonia fully. Though in some cases, pulmonary fibrosis was reported as a sequel. However, long-term progression of such pulmonary fibrosis is uncertain. We are hereby reporting two cases of swine flu that showed residual pulmonary fibrosis. The clinical and laboratory parameters were also recorded. In both the cases, radiological shadows and spirometric values did not show deterioration. We conclude that swine flu pulmonary fibrosis is not a progressive condition.

• Interstitial lung disease
• pulmonary fibrosis
• swine flu

• angiotensin-converting enzyme
• lung injury
• mechanical ventilation

Most patients with sepsis and acute lung injury require mechanical ventilation to improve oxygenation and facilitate organ repair. Mast cells are important in response to infection and resolution of tissue injury. Since tryptase secreted from mast cells has been associated with tissue fibrosis, we hypothesized that tryptase would be involved in the early development of ventilator-induced pulmonary fibrosis in a clinically relevant model of sepsis-induced lung injury.

Prospective, randomized, controlled animal study using Sprague-Dawley rats. Sepsis was induced by cecal ligation and perforation. Animals were randomized to spontaneous breathing or two ventilatory strategies for 4 h: protective ventilation with tidal volume (VT) = 6 ml/kg plus 10 cmH₂O positive end-expiratory pressure (PEEP) or injurious ventilation with VT = 20 ml/kg plus 2 cmH₂O PEEP. Healthy, non-ventilated animals served as non-septic controls. We studied the following end points: histology, serum cytokine levels, hydroxyproline content, tryptase and proteinase-activated receptor-2 (PAR-2) protein level in lung homogenates, and tryptase and PAR-2 immunohistochemical localization in the lungs.

All septic animals developed acute lung injury. Animals ventilated with high VT had a significant increase of pulmonary fibrosis, hydroxyproline content, tryptase and PAR-2 protein levels compared to septic controls (P <0.0001). However, protective ventilation attenuated sepsis-induced lung injury and decreased lung tryptase and PAR-2 protein levels. Immunohistochemical staining confirmed the presence of tryptase and PAR-2 in the lungs.

Mechanical ventilation modified tryptase and PAR-2 in injured lungs. Increased levels of these proteins were associated with development of sepsis and ventilator-induced pulmonary fibrosis early in the course of sepsis-induced lung injury.

Pulmonary sarcoidosis involves an intense leukocyte infiltration of the lung with the formation of non-necrotizing granulomas. CC chemokines (chemokine (C-C motif) ligand 2 (CCL2)-CCL5) are chemoattractants of mononuclear cells and act through seven transmembrane G-coupled receptors. Previous studies have demonstrated conflicting results with regard to the associations of these chemokines with sarcoidosis. In an effort to clarify previous discrepancies, we performed the largest observational study to date of CC chemokines in bronchoalveolar lavage fluid (BALF) from patients with pulmonary sarcoidosis.

BALF chemokine levels from 72 patients affected by pulmonary sarcoidosis were analyzed by enzyme-linked immunosorbent assay (ELISA) and compared to 8 healthy volunteers. BALF CCL3 and CCL4 levels from pulmonary sarcoidosis patients were not increased compared to controls. However, CCL2 and CCL5 levels were elevated, and subgroup analysis showed higher levels of both chemokines in all stages of pulmonary sarcoidosis. CCL2, CCL5, CC chemokine receptor type 1 (CCR1), CCR2 and CCR3 were expressed from mononuclear cells forming the lung granulomas, while CCR5 was only found on mast cells.

These data suggest that CCL2 and CCL5 are important mediators in recruiting CCR1, CCR2, and CCR3 expressing mononuclear cells as well as CCR5-expressing mast cells during all stages of pulmonary sarcoidosis.

• Adult
• Airway Remodeling/physiology
• Autopsy
• Case-Control Studies
• Extracellular Matrix/metabolism
• Female
• Humans
• Lung/pathology
• Male
• Middle Aged
• Respiratory Distress Syndrome/physiopathology
• Retrospective Studies

• Actins/genetics
• Adult
• Aged
• Bronchoalveolar Lavage Fluid/chemistry
• Cell Differentiation/physiology
• Collagen Type III/genetics
• Female
• Fibroblasts/cytology
• Gene Expression/physiology
• Hospital Mortality
• Humans
• Male
• Middle Aged
• Polymerase Chain Reaction
• Prognosis
• RNA, Messenger/genetics
• Respiratory Distress Syndrome/mortality
• Respiratory Distress Syndrome/physiopathology
• Survival Rate
• Transforming Growth Factor beta1/genetics

• 1K12RR017707-02 NCRR NIH HHS
• ES013995 NIEHS NIH HHS
• HL067835 NHLBI NIH HHS
• M01 RR-00048 NCRR NIH HHS

• Animals
• Blood-Air Barrier/physiology
• Capillary Permeability/physiology
• Fibrinolytic Agents/therapeutic use
• Genetic Therapy/methods
• Humans
• Prognosis
• Respiratory Distress Syndrome/metabolism
• Respiratory Distress Syndrome/therapy
• Respiratory Mucosa/metabolism
• Thrombolytic Therapy/methods

• ES013995 NIEHS NIH HHS
• HL48129 NHLBI NIH HHS
• P0171643 PHS HHS

• Acute Disease
• Adult
• Biopsy
• Bronchi/cytology
• Bronchi/physiology
• Bronchoalveolar Lavage Fluid
• Female
• Gene Expression/physiology
• Humans
• Lung Transplantation/physiology
• Male
• Mast Cells/physiology
• Middle Aged
• Postoperative Complications
• Proto-Oncogene Proteins c-kit/metabolism
• RNA, Messenger/analysis
• Respiratory Mucosa/cytology
• Respiratory Mucosa/physiology
• Serine Endopeptidases/metabolism
• Stem Cell Factor/blood
• Stem Cell Factor/genetics
• Tryptases

• Actins/metabolism
• Adult
• Aged
• Apoptosis
• Bronchoalveolar Lavage Fluid/cytology
• Bronchoscopy
• Cell Proliferation
• Cell Survival/physiology
• Female
• Fibroblasts/metabolism
• Flow Cytometry
• Fluorescent Antibody Technique
• Forkhead Box Protein O1
• Forkhead Transcription Factors/metabolism
• Humans
• Leukocyte Common Antigens/metabolism
• Male
• Middle Aged
• Procollagen-Proline Dioxygenase/metabolism
• Proto-Oncogene Proteins c-akt/metabolism
• Proto-Oncogene Proteins c-bcl-2/metabolism
• Pulmonary Alveoli/metabolism
• Pulmonary Alveoli/pathology
• Respiratory Distress Syndrome/metabolism
• Respiratory Distress Syndrome/pathology
• Signal Transduction/physiology

• P50 HL-81059 NHLBI NIH HHS
• L30 HL081881 NHLBI NIH HHS
• K08 HL-81059 NHLBI NIH HHS
• R01 HL067967 NHLBI NIH HHS
• K08 HL081059 NHLBI NIH HHS
• P50 HL074024 NHLBI NIH HHS
• R01-HL-67967 NHLBI NIH HHS

• Cell Differentiation/genetics
• Cell Differentiation/immunology
• Cell Line
• Cytokines/analysis
• Flow Cytometry/methods
• Gene Expression Profiling/methods
• Humans
• Immunohistochemistry/methods
• Immunophenotyping/methods
• Lung/immunology
• Lung/pathology
• Lung Diseases, Interstitial/genetics
• Lung Diseases, Interstitial/immunology
• Lung Diseases, Interstitial/pathology
• Lymphangioleiomyomatosis/genetics
• Lymphangioleiomyomatosis/immunology
• Lymphangioleiomyomatosis/pathology
• Mast Cells/chemistry
• Metalloproteases/genetics
• Proto-Oncogene Proteins c-kit/analysis
• Pulmonary Fibrosis/genetics
• Pulmonary Fibrosis/immunology
• Pulmonary Fibrosis/pathology
• Sarcoidosis/genetics
• Sarcoidosis/immunology
• Sarcoidosis/pathology
• Scleroderma, Systemic/genetics
• Scleroderma, Systemic/immunology
• Scleroderma, Systemic/pathology
• Signal Transduction/genetics
• Signal Transduction/immunology
• Transcription, Genetic/genetics
• Transcription, Genetic/immunology

• HL-64897 NHLBI NIH HHS

• Animals
• Apoptosis/physiology
• Cholestasis/immunology
• Cholestasis/pathology
• Common Bile Duct/pathology
• Epithelial Cells/pathology
• Epithelial Cells/ultrastructure
• In Situ Nick-End Labeling
• Ligation
• Liver/immunology
• Liver/pathology
• Liver/ultrastructure
• Mast Cells/immunology
• Microscopy, Electron, Transmission
• Rats
• Rats, Wistar

• Airway Resistance/drug effects
• Animals
• Bronchoconstriction/physiology
• Collagen/drug effects
• Elasticity/drug effects
• Herbicides/pharmacology
• Lung/pathology
• Lung/physiopathology
• Lung/ultrastructure
• Lung Compliance/drug effects
• Microscopy, Electron
• Paraquat/pharmacology
• Rats
• Rats, Wistar
• Respiratory Mechanics/drug effects
• Time Factors

Historically, mast cells were known as a key cell type involved in type I hypersensitivity. Until last two decades, this cell type was recognized to be widely involved in a number of non-allergic diseases including inflammatory bowel disease (IBD). Markedly increased numbers of mast cells were observed in the mucosa of the ileum and colon of patients with IBD, which was accompanied by great changes of the content in mast cells such as dramatically increased expression of TNF-α, IL-16 and substance P. The evidence of mast cell degranulation was found in the wall of intestine from patients with IBD with immunohistochemistry technique. The highly elevated histamine and tryptase levels were detected in mucosa of patients with IBD, strongly suggesting that mast cell degranulation is involved in the pathogenesis of IBD. However, little is known of the actions of histamine, tryptase, chymase and carboxypeptidase in IBD. Over the last decade, heparin has been used to treat IBD in clinical practice. The low molecular weight heparin (LMWH) was effective as adjuvant therapy, and the patients showed good clinical and laboratory response with no serious adverse effects. The roles of PGD2, LTC4, PAF and mast cell cytokines in IBD were also discussed. Recently, a series of experiments with dispersed colon mast cells suggested there should be at least two pathways in man for mast cells to amplify their own activation-degranulation signals in an autocrine or paracrine manner. The hypothesis is that mast cell secretogogues induce mast cell degranulation, release histamine, then stimulate the adjacent mast cells or positively feedback to further stimulate its host mast cells through H₁ receptor. Whereas released tryptase acts similarly to histamine, but activates mast cells through its receptor PAR-2. The connections between current anti-IBD therapies or potential therapies for IBD with mast cells were discussed, implicating further that mast cell is a key cell type that is involved in the pathogenesis of IBD. In conclusion, while pathogenesis of IBD remains unclear, the key role of mast cells in this group of diseases demonstrated in the current review implicates strongly that IBD is a mast cell associated disease. Therefore, close attentions should be paid to the role of mast cells in IBD.

• Cell Degranulation
• Humans
• Inflammatory Bowel Diseases/etiology
• Inflammatory Bowel Diseases/pathology
• Inflammatory Bowel Diseases/physiopathology
• Mast Cells/metabolism
• Mast Cells/pathology

• Animals
• Biopsy, Needle
• Disease Models, Animal
• Female
• Immunohistochemistry
• Injections, Intravenous
• Lung/drug effects
• Lung/pathology
• Male
• Methylprednisolone/administration & dosage
• Probability
• Pulmonary Alveoli/drug effects
• Pulmonary Alveoli/pathology
• Rats
• Rats, Wistar
• Reference Values
• Respiratory Distress Syndrome/drug therapy
• Respiratory Distress Syndrome/pathology
• Respiratory Function Tests
• Respiratory Mechanics
• Treatment Outcome

• Animals
• Asthma/immunology
• Asthma/physiopathology
• Humans
• Inflammation Mediators/physiology
• Mast Cells/physiology

• Humans
• Lung/diagnostic imaging
• Respiratory Distress Syndrome/diagnostic imaging
• Respiratory Distress Syndrome/etiology
• Respiratory Distress Syndrome/physiopathology
• Tomography, X-Ray Computed

• Acute Disease
• Analysis of Variance
• Animals
• Biomechanical Phenomena
• Collagen/metabolism
• Collagen/physiology
• Contractile Proteins/physiology
• Elastic Tissue/injuries
• Elastic Tissue/pathology
• Elastic Tissue/physiology
• Elastic Tissue/physiopathology
• Elastin/metabolism
• Elastin/physiology
• Extracellular Matrix
• Herbicides/administration & dosage
• Herbicides/toxicity
• Histological Techniques
• Injections, Intraperitoneal
• Lung/metabolism
• Lung/pathology
• Lung/physiopathology
• Lung Compliance
• Lung Injury
• Paraquat/administration & dosage
• Paraquat/toxicity
• Pulmonary Alveoli/injuries
• Pulmonary Alveoli/physiopathology
• Rats
• Rats, Wistar
• Time Factors

• Animals
• Female
• Histamine/analysis
• Immunohistochemistry
• Lung/pathology
• Male
• Mannheimia haemolytica
• Mast Cells/pathology
• Pasteurellosis, Pneumonic/etiology
• Pasteurellosis, Pneumonic/immunology
• Pasteurellosis, Pneumonic/pathology
• Sheep
• Sheep Diseases/etiology
• Sheep Diseases/immunology
• Sheep Diseases/pathology
• Substance P/isolation & purification

• Cell Division
• Exudates and Transudates
• Fibrosis
• Humans
• Immunohistochemistry
• Lung/blood supply
• Lung/pathology
• Pulmonary Alveoli/pathology
• Respiratory Distress Syndrome/pathology

• Animals
• Apoptosis
• Collagen/metabolism
• Epithelium/physiology
• Humans
• Inflammation
• Lung/physiology
• Pulmonary Alveoli/physiology
• Regeneration
• Respiratory Distress Syndrome/immunology
• Respiratory Distress Syndrome/pathology
• Severity of Illness Index

• P50-HL50152 NHLBI NIH HHS

• Blood Platelets/pathology
• Cell Adhesion Molecules/metabolism
• Cytokines/immunology
• Cytokines/metabolism
• Eosinophils/cytology
• Eosinophils/metabolism
• Humans
• Lung/pathology
• Macrophages/cytology
• Mast Cells/cytology
• Neutrophils/pathology
• Respiratory Distress Syndrome/immunology
• Respiratory Distress Syndrome/metabolism
• Respiratory Distress Syndrome/pathology