Gasdermin D in Bronchoalveolar Lavage Fluid Causes Cell Death Ex Vivo in Pulmonary Epithelial Cells

Background. This study investigated whether the 1 : 2 ω-3/ω-6 ratio may reduce proinflammatory response in human alveolar cells (A549) exposed to anex vivoinflammatory stimulus (bronchoalveolar lavage fluid (BALF) of acute respiratory distress syndrome (ARDS) patients).Methods. We exposed A549 cells to the BALF collected from 12 ARDS patients. After 18 hours, fatty acids (FA) were added as docosahexaenoic acid (DHA,ω-3) and arachidonic acid (AA,ω-6) in two ratios (1 : 2 or 1 : 7). 24 hours later, in culture supernatants were evaluated cytokines (TNF-α, IL-6, IL-8, and IL-10) and prostaglandins (PGE2and PGE3) release. The FA percentage content in A549 membrane phospholipids, content of COX-2, level of PPARγ, and NF-κB binding activity were determined.Results. The 1 : 2 DHA/AA ratio reversed the baseline predominance ofω-6 overω-3 in the cell membranes (P< 0.001). The proinflammatory cytokine release was reduced by the 1 : 2 ratio (P< 0.01 to <0.001) but was increased by the 1 : 7 ratio (P< 0.01). The 1 : 2 ratio reduced COX-2 and PGE2(P< 0.001) as well as NF-κB translocation into the nucleus (P< 0.01), while it increased activation of PPARγand IL-10 release (P< 0.001).Conclusion. This study demonstrated that shifting the FA supply fromω-6 toω-3 decreased proinflammatory mediator release in human alveolar cells exposed to BALF of ARDS patients.

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Bronchoalveolar lavage fluid gliotoxin induces mesenchymal stromal cell death: a potential explanation to the decreased protective capacity of MSCs in clinical trials

Cytotherapy ◽

10.1016/j.jcyt.2019.03.426 ◽

2019 ◽

Vol 21 (5) ◽

pp. S55

Author(s):

S. Rolandsson Enes ◽

S.C. Abreu ◽

T.H. Hampton ◽

R.A. Cramer ◽

B.A. Stanton ◽

...

Keyword(s):

Clinical Trials ◽

Cell Death ◽

Bronchoalveolar Lavage ◽

Mesenchymal Stromal Cell ◽

Stromal Cell ◽

Bronchoalveolar Lavage Fluid ◽

Lavage Fluid ◽

Protective Capacity ◽

Potential Explanation

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Changes in immunoreactivity for cathepsin H in rat type II alveolar epithelial cells and its proteolytic activity in bronchoalveolar lavage fluid over 24 hours

The Anatomical Record ◽

10.1002/ar.1092300411 ◽

1991 ◽

Vol 230 (4) ◽

pp. 519-523 ◽

Cited By ~ 7

Author(s):

Yukio Ishii ◽

Yutaka Hashizume ◽

Eiki Kominami ◽

Yasuo Uchiyama

Keyword(s):

Epithelial Cells ◽

Bronchoalveolar Lavage ◽

Proteolytic Activity ◽

Bronchoalveolar Lavage Fluid ◽

Lavage Fluid ◽

Alveolar Epithelial Cells ◽

Type Ii ◽

Alveolar Epithelial ◽

Cathepsin H

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Cystic fibrosis bronchoalveolar lavage fluid lead to human mesenchymal stromal cell death

Cytotherapy ◽

10.1016/j.jcyt.2018.02.062 ◽

2018 ◽

Vol 20 (5) ◽

pp. S25-S26

Author(s):

S.C. Abreu ◽

J. Dearborn ◽

N. Gasek ◽

C. dos Santos ◽

M.J. Wargo ◽

...

Keyword(s):

Cystic Fibrosis ◽

Cell Death ◽

Bronchoalveolar Lavage ◽

Mesenchymal Stromal Cell ◽

Stromal Cell ◽

Bronchoalveolar Lavage Fluid ◽

Lavage Fluid

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Putative Bronchopulmonary Flagellated Protozoa in Immunosuppressed Patients

BioMed Research International ◽

10.1155/2014/912346 ◽

2014 ◽

Vol 2014 ◽

pp. 1-5 ◽

Cited By ~ 6

Author(s):

Ali Ahmet Kilimcioglu ◽

Yavuz Havlucu ◽

Nogay Girginkardesler ◽

Pınar Çelik ◽

Kor Yereli ◽

...

Keyword(s):

At Risk ◽

Epithelial Cells ◽

Infectious Diseases ◽

Light Microscopy ◽

Bronchoalveolar Lavage ◽

Bronchoalveolar Lavage Fluid ◽

Lavage Fluid ◽

Adult Patients ◽

Immunosuppressed Patients

Flagellated protozoa that cause bronchopulmonary symptoms in humans are commonly neglected. These protozoal forms which were presumed to be “flagellated protozoa” have been previously identified in immunosuppressed patients in a number of studies, but have not been certainly classified so far. Since no human cases of bronchopulmonary flagellated protozoa were reported from Turkey, we aimed to investigate these putative protozoa in immunosuppressed patients who are particularly at risk of infectious diseases. Bronchoalveolar lavage fluid samples of 110 immunosuppressed adult patients who were admitted to the Department of Chest Diseases, Hafsa Sultan Hospital of Celal Bayar University, Manisa, Turkey, were examined in terms of parasites by light microscopy. Flagellated protozoal forms were detected in nine (8.2%) of 110 cases. Metronidazole (500 mgb.i.d.for 30 days) was given to all positive cases and a second bronchoscopy was performed at the end of the treatment, which revealed no parasites. In conclusion, immunosuppressed patients with bronchopulmonary symptoms should attentively be examined with regard to flagellated protozoa which can easily be misidentified as epithelial cells.

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Novel Pathway of Adenosine Generation in the Lungs from NAD+: Relevance to Allergic Airway Disease

Molecules ◽

10.3390/molecules25214966 ◽

2020 ◽

Vol 25 (21) ◽

pp. 4966

Author(s):

Richard Graeff ◽

Alonso Guedes ◽

Ruth Quintana ◽

Erin Wendt-Hornickle ◽

Caroline Baldo ◽

...

Keyword(s):

Uric Acid ◽

Epithelial Cells ◽

Bronchoalveolar Lavage ◽

Bronchoalveolar Lavage Fluid ◽

Culture Media ◽

Airway Disease ◽

Lavage Fluid ◽

Airway Epithelial Cells ◽

Allergic Airway Disease ◽

Chronic Obstructive

Adenosine and uric acid (UA) play a pivotal role in lung diseases such as asthma and chronic obstructive pulmonary disease (COPD). In the present experiments, we measured adenosine synthesis from nicotinamide adenine dinucleotide (NAD+) in membranes prepared from wild type (WT) and CD38 knockout (CD38KO) mouse lungs, from cultured airway smooth muscle and epithelial cells, and in bronchoalveolar lavage fluid after airway challenge with epidemiologically relevant allergens. Adenosine was determined using an enzymatically coupled assay that produces ATP and is detected by luminescence. Uric acid was determined by ELISA. Exposure of cultured airway epithelial cells to Alternaria alternata extract caused significant nucleotide (NAD+ and ATP) release in the culture media. The addition of NAD+ to membranes prepared from WT mice resulted in faster generation of adenosine compared to membranes from CD38KO mice. Formation of adenosine from NAD+ affected UA and ATP concentrations, its main downstream molecules. Furthermore, NAD+ and adenosine concentrations in the bronchoalveolar lavage fluid decreased significantly following airway challenge with house-dust mite extract in WT but not in CD38KO mice. Thus, NAD+ is a significant source of adenosine and UA in the airways in mouse models of allergic airway disease, and the capacity for their generation from NAD+ is augmented by CD38, a major NADase with high affinity for NAD+. This novel non-canonical NAD+-adenosine-UA pathway that is triggered by allergens has not been previously described in the airways.

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