Alveolar Epithelial Cells Secrete Chemokines in Response to IL-1β and Lipopolysaccharide but Not to Ozone

Manzer, Rizwan; Wang, Jieru; Nishina, Kahoru; McConville, Glen; Mason, Robert J.

doi:10.1165/rcmb.2005-0205oc

Cited by 46 publications

(51 citation statements)

References 48 publications

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“…As shown in Fig. 6, when rat type II cells are cultured on plastic for 2 and 4 days, the expression of LPCAT and SP-A (a type II cell marker) decreased, whereas the expression of T1␣ increased (16). These results strongly suggest that LPCAT is involved with surfactant production and not general membrane biogenesis.…”

Section: Kgf Increases Lpcat Expression In Cultured Adultmentioning

confidence: 81%

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Identification and characterization of a lysophosphatidylcholine acyltransferase in alveolar type II cells

Chen

Hyatt

Mucenski

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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175

187

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Pulmonary surfactant is a complex of lipids and proteins produced and secreted by alveolar type II cells that provides the low surface tension at the air-liquid interface. The phospholipid most responsible for providing the low surface tension in the lung is dipalmitoylphosphatidylcholine. Dipalmitoylphosphatidylcholine is synthesized in large part by phosphatidylcholine (PC) remodeling, and a lysophosphatidylcholine (lysoPC) acyltransferase is thought to play a critical role in its synthesis. However, this acyltransferase has not yet been identified. We have cloned full-length rat and mouse cDNAs coding for a lysoPC acyltransferase (LPCAT). LPCAT encodes a 535-aa protein of Ϸ59 kDa that contains a transmembrane domain and a putative acyltransferase domain. When transfected into COS-7 cells and HEK293 cells, LPCAT significantly increased lysoPC acyltransferase activity. LPCAT preferred lysoPC as a substrate over lysoPA, lysoPI, lysoPS, lysoPE, or lysoPG and prefers palmitoyl-CoA to oleoyl-CoA as the acyl donor. This LPCAT was preferentially expressed in the lung, specifically within alveolar type II cells. Expression in the fetal lung and in rat type II cells correlated with the expression of the surfactant proteins. LPCAT expression in fetal lung explants was sensitive to dexamethasone and FGFs. KGF was a potent stimulator of LPCAT expression in cultured adult type II cells. We hypothesize that LPCAT plays a critical role in regulating surfactant phospholipid biosynthesis and suggest that understanding the regulation of LPCAT will offer important insight into surfactant phospholipid biosynthesis.biochemistry ͉ lung ͉ surfactant ͉ phosphatidylcholine

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Section: Kgf Increases Lpcat Expression In Cultured Adultmentioning

confidence: 81%

“…Rat alveolar type II cells were isolated and cultured as described (15,27). A type I-like cell phenotype was generated by culturing type II cells on plastic dishes in DMEM plus 10% FBS without KGF (16). Freshly isolated mouse alveolar type II cells were isolated from adult C57BL͞6 mice as described (28).…”

Section: Methodsmentioning

confidence: 99%

Identification and characterization of a lysophosphatidylcholine acyltransferase in alveolar type II cells

Chen

Hyatt

Mucenski

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

175

187

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“…In our previous studies in vitro, we found that exposure to ozone induces toxicity in alveolar epithelial cells but without a substantial increase in chemokine production (8)(9)(10). Isolated human alveolar macrophages and THP-1 cells derived from monocytic leukemic cells also fail to secrete chemokines in response to ozone (11,12).…”

mentioning

confidence: 87%

“…Alveolar type II cells were isolated from pathogen-free adult male Sprague-Dawley rats (Harlan, Indianapolis, IN) by dissociation with porcine pancreatic elastase (Roche Molecular Biochemicals, Indianapolis, IN) and partial purification on discontinuous density gradients by standard methods (10,17). Type II cells were plated on 6-well tissue culture plastic plates.…”

Section: Rat Alveolar Epithelial Cell Isolation and Culturementioning

confidence: 99%

“…This information was recorded by a Macintosh G-3 computer and sent to the Sierra Instruments flow box, which automatically adjusted the flow of ozone to achieve the desired concentration. For the exposure, 2.0 to 3.0 ml serum-free media was added on top of 150-mm culture dishes and the cultures were rocked to minimize the fluid over the cell layer as described previously (10). Cultured cells were exposed to different concentrations of ozone or air for 1 hour.…”

Section: In Vitro Ozone Exposurementioning

confidence: 99%

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Ozone Exposure of Macrophages Induces an Alveolar Epithelial Chemokine Response through IL-1α

Manzer

Dinarello²,

McConville³

et al. 2008

Am J Respir Cell Mol Biol

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Ozone is known to produce an acute influx of neutrophils, and alveolar epithelial cells can secrete chemokines and modulate inflammatory processes. However, direct exposure of alveolar epithelial cells and macrophages to ozone (O 3 ) produces little chemokine response. To determine if cell-cell interactions might be responsible, we investigated the effect of alveolar macrophage-conditioned media after ozone exposure (MO 3 CM) on alveolar epithelial cell chemokine production. Serum-free media were conditioned by exposing a rat alveolar macrophage cell line NR8383 to ozone for 1 hour. Ozone stimulated secretion of IL-1a, IL-1b, and IL-18 from NR8383 cells, but there was no secretion of chemokines or TNF-a. Freshly isolated type II cells were cultured, so as to express the biological markers of type I cells, and these cells are referred to as type I-like cells. Type I-like cells were exposed to diluted MO 3 CM for 24 hours, and this conditioned medium stimulated secretion of cytokine-induced neutrophil chemattractant-1 (CXCL1) and monocyte chemoattractant protein-1 (CCL2). Secretion of these chemokines was inhibited by the IL-1 receptor antagonist. Although both recombinant IL-1a and IL-1b stimulated alveolar epithelial cells to secrete chemokines, recombinant IL-1a was 100-fold more potent than IL-1b. Furthermore, neutralizing anti-rat IL-1a antibodies inhibited the secretion of chemokines by alveolar epithelial cells, whereas neutralizing anti-rat IL-1b antibodies had no effect. These observations indicate that secretion of IL-1a from macrophages stimulates alveolar epithelial cells to secrete chemokines that can elicit an inflammatory response.

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Temporal Changes in Expression of FoxA1 and Wnt7A in Isolated Adult Human Alveolar Epithelial Cells Enhanced by Heparin

Apparao

Newman

Zhang

et al. 2010

The Anatomical Record

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Pre- and postnatal developmental studies of the lung have provided compelling evidence demonstrating multiple factors that orchestrate alveolar epithelial cell differentiation. The extent to which reactivation of certain developmental pathways in the adult might influence the course of differentiation of alveolar type 2 cells (AT2) into AT1 cells is not known. In this study, we examined selected members of the forkhead (Fox) family of transcription factors and the Wnt (wingless) family of signaling proteins for expression during human alveolar cell differentiation in vitro and determined their potential responses to sulfated components of extracellular matrix (ECM), like those shed from cell surfaces or found in basement membrane and modeled by heparin. Isolated adult human AT2 cells cultured over a nine day period were used to define the temporal profile of expression of targeted factors during spontaneous differentiation to AT1 cells. FoxA1 protein was up-regulated at early to intermediate time points, where it was strongly elevated by heparin. Gene expression of Wnt7A increased dramatically beginning on day 3 and was enhanced even further on days 7 and 9 by heparin, while protein expression appeared at days 7 and 9. These temporal changes of expression suggest that sulfated ECMs may act to enhance the increase in FoxA1 at the critical juncture when AT2 cells commence the differentiation process to AT1 cells, in addition to enhancing the increase in Wnt7A when the AT1 cell phenotype stabilizes. Collectively, these factors may act to modulate differentiation and stabilize cell numbers in the adult human pulmonary alveolus.

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Alveolar Epithelial Cells Secrete Chemokines in Response to IL-1β and Lipopolysaccharide but Not to Ozone

Cited by 46 publications

References 48 publications

Identification and characterization of a lysophosphatidylcholine acyltransferase in alveolar type II cells

Identification and characterization of a lysophosphatidylcholine acyltransferase in alveolar type II cells

Ozone Exposure of Macrophages Induces an Alveolar Epithelial Chemokine Response through IL-1α

Temporal Changes in Expression of FoxA1 and Wnt7A in Isolated Adult Human Alveolar Epithelial Cells Enhanced by Heparin

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