Type II Alveolar Cell Dual Function: Repair versus Surfactant Synthesis

2015 ◽  
pp. 154-160 ◽  
Author(s):  
George Brumley ◽  
Judy Stevens ◽  
James Raub ◽  
Robert Mercer ◽  
James Crapo
Keyword(s):  
Dual Function ◽  
Type Ii ◽  
Alveolar Cell ◽  
Surfactant Synthesis

Inhibition of alveolar type II cell ATP and surfactant synthesis by nitric oxide

1996 ◽  
Vol 270 (6) ◽  
pp. L898-L906 ◽  
Author(s):  
I. Y. Haddad ◽  
S. Zhu ◽  
J. Crow ◽  
E. Barefield ◽  
T. Gadilhe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lipid Synthesis ◽  
Alveolar Epithelium ◽  
Alveolar Type ◽  
Type Ii ◽  
Surfactant Synthesis ◽  
Cell Energy ◽  
Type Ii Cell

Alveolar type II (ATII) cells, are often exposed to increased concentration of endogenous and exogenous nitric oxide (.NO). Exposure of freshly isolated rat ATII cells for 2 h to 1-3 microM .NO, generated by S-nitroso-N-penicillamine (SNAP), spermine NONOate, or 3-morpholino-sydnonimine (SIN-1) in the presence of superoxide dismutase, resulted in approximately 60% decrease in the rate of surfactant synthesis, as measured by the rate of incorporation of [methyl-3H]choline into phosphatidylcholine, and 60-80% inhibition of cellular ATP levels, as determined by bioluminescence. Similar results were obtained after incubation of ATII cells with authentic peroxynitrite (0.5 mM) but not SIN-1, a putative generator of peroxynitrite. Addition into the medium of oxyhemoglobin (20 microM), which scavenged .NO, or enhancement of ATII glutathione levels by preincubation with glutathione ester (5 mM) totally prevented the NONOate (100 microM) inhibition of cellular ATP. In contrast to the in vitro findings, normal levels of ATP and lipid synthesis were measured in ATII cells isolated from the lungs of rats that breathed .NO gas (80 ppm) in 21% O2 for 2 h (n = 4). This lack of effect may be due either to the presence of various antioxidants (such as glutathione) in the epithelial lining fluid or to the relatively low concentrations of .NO reaching the alveolar epithelium. We conclude that .NO and peroxynitrite, at concentrations likely to be encountered in vivo during inflammation, decrease ATII cell energy stores and surfactant synthesis, which may lead to derangement of important physiological functions.

scholarly journals Nitric Oxide Does Not Affect Surfactant Synthesis but Does Decrease Antioxidant Enzyme (AOE) Activity in Type II Pneumocytes (TII-P)

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 295A-295A
Author(s):  
Vineet Bhandari ◽  
Graham Vigliotta ◽  
Nilanjana Maulik ◽  
Avinash Chander
Keyword(s):  
Nitric Oxide ◽  
Antioxidant Enzyme ◽  
Type Ii ◽  
Surfactant Synthesis ◽  
Type Ii Pneumocytes

Roles of SP-A, SP-B, and SP-C in modulation of lipid uptake by pulmonary epithelial cells in vitro

1996 ◽  
Vol 270 (1) ◽  
pp. L69-L79 ◽  
Author(s):  
A. D. Horowitz ◽  
B. Moussavian ◽  
J. A. Whitsett
Keyword(s):  
Epithelial Cells ◽  
Lipid Vesicles ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lipid Uptake ◽  
3T3 Cells ◽  
Alveolar Cell ◽  
Pulmonary Epithelial Cells ◽  
Nih 3T3

The effects of the surfactant proteins (SP)-A, SP-B, and SP-C on binding and endocytosis of fluorescently labeled lipid vesicles were studied in rat type II epithelial cells and in MLE-12 cells, a pulmonary adenocarcinoma cell line with alveolar cell characteristics. Incorporation of SP-C in lipid vesicles markedly stimulated binding to the cell membrane at 4 degrees C and endocytosis of lipids at 37 degrees C. SP-C enhanced lipid uptake in MLE-12 cells, type II cells, and NIH 3T3 cells. SP-B stimulated lipid uptake in MLE-12 cells, but to a lesser degree. SP-B decreased the amount of lipid uptake stimulated by SP-C, SP-A did not increase endocytosis of lipids by MLE-12 cells or type II cells, but aggregates of lipid were observed associated with the cell surface in the presence of SP-A. Maintenance of active surfactant in the lung may be achieved through the selective uptake and degradation of surfactant subfractions depleted in SP-A and SP-B.

Effects of Hyperoxia on Type II Cell Surfactant Synthesis

2015 ◽  
pp. 291-293
Author(s):  
B. A. Holm ◽  
S. Matalon
Keyword(s):  
Type Ii ◽  
Surfactant Synthesis ◽  
Type Ii Cell

scholarly journals Comparative Antimicrobial Activities of the Newly Synthesized Quinolone WQ-3034, Levofloxacin, Sparfloxacin, and Ciprofloxacin against Mycobacterium tuberculosis andMycobacterium avium Complex

2000 ◽  
Vol 44 (2) ◽  
pp. 283-286 ◽  
Author(s):  
Haruaki Tomioka ◽  
Katsumasa Sato ◽  
Hiroko Kajitani ◽  
Tatsuya Akaki ◽  
Shinji Shishido
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Cell Line ◽  
Antimicrobial Activities ◽  
Dilution Method ◽  
Agar Dilution Method ◽  
Type Ii ◽  
In Vitro Activity ◽  
Alveolar Cell ◽  
Agar Dilution

ABSTRACT WQ-3034 is a newly synthesized acidic fluoroquinolone. We assessed its in vitro activity against Mycobacterium tuberculosisand M. avium complex using levofloxacin (LVFX), ciprofloxacin (CPFX), sparfloxacin (SPFX), and KRM-1648 (KRM) as reference drugs. The MICs of these agents were determined by the agar dilution method with 7H11 medium. The MICs at which 50 and 90% of the test strains were inhibited (MIC50s, and MIC90s, respectively) for the test quinolones for rifampin (RMP)-susceptible M. tuberculosis strains were in the order SPFX < LVFX ≦ WQ-3034 ≦ CPFX, while those for RMP-resistant M. tuberculosis strains were in the order SPFX ≦ WQ-3034 ≦ LVFX < CPFX. The MICs of KRM for RMP-susceptible M. tuberculosis were much lower than those of the test quinolones, while the MIC90 of KRM for RMP-resistant M. tuberculosis strains was higher than those of the quinolones. The MIC50s and MIC90s of the test drugs for M. avium were in the order KRM < SPFX < CPFX ≦ WQ-3034 ≦ LVFX, while those forM. intracellulare were in the order KRM < SPFX < WQ-3034 ≒ LVFX ≦ CPFX. Next, we compared the antimicrobial activities of the test drugs against M. tuberculosisorganisms residing in cells of the Mono Mac 6 macrophage (Mφ)-like cell line (MM6-Mφs) and of the A-549 type II alveolar cell line (A-549 cells). When drugs were added at the concentration that achieves the maximum concentration in blood, progressive killing or inhibition of the M. tuberculosis organisms residing in MM6-Mφs and A-549 cells was observed in the order KRM > SPFX ≧ LVFX > WQ-3034 > CPFX. The efficacies of all quinolones against intracellular M. tuberculosis organisms were significantly lower in A-549 cells than in MM6-Mφs. WQ-3034 at the MIC caused more marked growth inhibition of intramacrophage M. tuberculosis than did LVFX. These findings indicate that the in vitro anti-M. tuberculosis activity of WQ-3034 is greater than that of CPFX and is comparable to that of LVFX.

Effect of pentoxifylline on the inhibition of surfactant synthesis induced by TNF-alpha in human type II pneumocytes.

1994 ◽  
Vol 149 (3) ◽  
pp. 699-706 ◽  
Author(s):  
J L Balibrea-Cantero ◽  
J Arias-Diaz ◽  
C Garcia ◽  
J Torres-Melero ◽  
C Simon ◽  
...  
Keyword(s):  
Tnf Alpha ◽  
Type Ii ◽  
Human Type ◽  
Surfactant Synthesis ◽  
Type Ii Pneumocytes

Lecithin biosynthesis in a clonal line of lung adenoma cells with type II alveolar cell properties

1978 ◽  
Vol 29 (1) ◽  
pp. 102-114 ◽  
Author(s):  
Gary D. Stoner ◽  
Mikko Hallman ◽  
Mamie C. Troxell
Keyword(s):  
Type Ii ◽  
Clonal Line ◽  
Alveolar Cell

In utero nicotine exposure alters fetal rat lung alveolar type II cell proliferation, differentiation, and metabolism

2007 ◽  
Vol 292 (1) ◽  
pp. L323-L333 ◽  
Author(s):  
Virender K. Rehan ◽  
Ying Wang ◽  
Sharon Sugano ◽  
Jamie Santos ◽  
Sanjay Patel ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
In Utero ◽  
Alveolar Type ◽  
Nicotine Exposure ◽  
Concomitant Treatment ◽  
Type Ii ◽  
Ppar Γ ◽  
Atii Cell ◽  
Surfactant Synthesis

We recently suggested that alveolar interstitial fibroblast-to-myofibroblast transdifferentiation may be a key mechanism underlying in utero nicotine-induced lung injury. However, the effects of in utero nicotine exposure on fetal alveolar type II (ATII) cells have not been fully determined. Placebo, nicotine (1 mg/kg), or nicotine (1 mg/kg) + the peroxisome proliferator-activated receptor (PPAR)-γ agonist prostaglandin J2 (PGJ2, 0.3 mg/kg) was administered intraperitoneally once daily to time-mated pregnant Sprague-Dawley rats from embryonic day 6 until their death on embryonic day 20. Fetal ATII cells were isolated, and ATII cell proliferation, differentiation (surfactant synthesis), and metabolism (metabolic profiling with the stable isotope [1,2-13C2]-d-glucose) were determined after nicotine exposure in utero or in vitro. In utero nicotine exposure significantly stimulated ATII cell proliferation, differentiation, and metabolism. Although the effects on ATII cell proliferation and metabolism were almost completely prevented by concomitant treatment with PGJ2, the effects on surfactant synthesis were not. On the basis of in utero and in vitro data, we conclude that surfactant synthesis is stimulated by nicotine's direct effect on ATII cells, whereas cell proliferation and metabolism are affected via a paracrine mechanism(s) secondary to its effects on the adepithelial fibroblasts. These data provide evidence for direct and indirect effects of in utero nicotine exposure on fetal ATII cells that could permanently alter the “developmental program” of the developing lung. More importantly, concomitant administration of PPAR-γ agonists can effectively attenuate many of the effects of in utero exposure to nicotine on ATII cells.

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