Secretion of cytokines by rat alveolar epithelial cells: possible regulatory role for SP-A

Blau, Hannah; Riklis, S.; Kravtsov, Vladimir; Kalina, Moshe

doi:10.1152/ajplung.1994.266.2.l148

Cited by 46 publications

(40 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent work done with human nasal epithelial cells shows that O 3 exposure resulted in NF-B activation and increased production of TNF-␣ by these cells (55). Thus the same may be true for the alveolar epithelial cells (8). In such a situation, the alveolar epithelial cells in response to O 3 may initiate an inflammatory cascade by increasing the local levels of inflammatory cytokines, and this may influence the activity of resident alveolar macrophages as well as affect the influx of circulatory inflammatory cells.…”

Section: Discussionmentioning

confidence: 89%

Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

Janic

Umstead

Phelps

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

, a major component of air pollution and a strong oxidizing agent, can lead to lung injury associated with edema, inflammation, and epithelial cell damage. The effects of O 3 on pulmonary immune cells have been studied in various in vivo and in vitro systems. We have shown previously that O 3 exposure of surfactant protein (SP)-A decreases its ability to modulate proinflammatory cytokine production by cells of monocyte/macrophage lineage (THP-1 cells). In this report, we exposed THP-1 cells and/or native SP-A obtained from bronchoalveolar lavage of patients with alveolar proteinosis to O 3 and studied cytokine production and NF-B signaling. The results showed 1) exposure of THP-1 cells to O 3 significantly decreased their ability to express TNF-␣ in response to SP-A; TNF-␣ production, under these conditions, was still significantly higher than basal (unstimulated) levels in filtered air-exposed THP-1 cells; 2) exposure of both THP-1 cells and SP-A to O 3 did not result in any significant differences in TNF-␣ expression compared with basal levels; 3) O 3 exposure of SP-A resulted in a decreased ability of SP-A to activate the NF-B pathway, as assessed by the lack of significant increase and decrease of the nuclear p65 subunit of NF-B and cytoplasmic I B␣, respectively; and 4) O 3 exposure of THP-1 cells resulted in a decrease in SP-A-mediated THP-1 cell responsiveness, which did not seem to be mediated via the classic NF-B pathway. These findings indicate that O 3 exposure may mediate its effect on macrophage function both directly and indirectly (via SP-A oxidation) and by involving different mechanisms.inflammation; tumor necrosis factor-␣; nuclear factor-B; I B␣; surfactant protein A OZONE (O 3 ) IS A MAJOR COMPONENT of photochemical air pollution. Approximately 113 million people live in areas with O 3 levels above the National Ambient Air Quality (NAAQ) standards for the daily exposure limit, noted as a maximum of 0.12 ppm for 1 h or 0.08 ppm cumulative for 8 consecutive hours (1). O 3 is a strong oxidizing agent that can be rapidly converted into a number of reactive oxygen species (ROS). O 3 exposure has been associated with impaired lung function (53) and with the majority of pathological changes localized in the lower airways. Due to its very low water solubility, O 3 cannot effectively penetrate through the thick epithelial lining fluid in the upper airways. However, the thinner lining in the lower airways allows O 3 to interact with various elements of the fluid and the underlying cells.O 3 and other oxidants exhibit their toxicity by reacting with cell proteins and lipids. This interaction often results in edema, inflammation, and epithelial cell damage causing lung injury and surfactant derangement (66, 67). Furthermore, both morphological (6, 7) and biochemical (26, 27) changes in surfactant are observed following O 3 exposure. An extensive body of work has been generated by various groups to support the hypothesis that O 3 -induced changes lead to a compromised immune response in the lung. However,...

show abstract

Section: Discussionmentioning

confidence: 89%

Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

Janic

Umstead

Phelps

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

“…Recent reports focused on immunoregulatory functions of SP-A, mostly directed towards monocytes and macrophages [5][6][7][8][9][10][11][12][13][14][15][16][17]. SP-A can stimulate macrophage antibacterial functions, in particular phagocytosis of several bacteria [8][9][10][11]14] including Mycobacterium tuberculosis [6].…”

Section: Discussionmentioning

confidence: 99%

“…In fact, SP-A enhances attachment [5][6][7], chemotaxis, phagocytosis, and oxygen-dependent killing [8][9][10][11][12][13][14] of specific respiratory pathogens in monocytes and alveolar macrophages. In addition, SP-A stimulates the production of many pro-inflammatory cytokines by human type-II cells or monocytes [15,16] and the release of tumour necrosis factor (TNF)-a, interleukin (IL)-1b, IL-6 and IL-8 by the monocytic THP-1 cell line [17]. The effect of SP-A on TNF-a release was inhibited by surfactant lipids, suggesting that in physiological conditions the effect of SP-A might be counteracted by other surfactant components.…”

mentioning

confidence: 99%

Surfactant apoprotein A modulates interleukin-8 and monocyte chemotactic peptide-1 production

Meloni¹,

Albertí²,

Bulgheroni³

et al. 2002

European Respiratory Journal

View full text Add to dashboard Cite

Previous studies have shown that surfactant apoprotein A (SP-A) and natural or synthetic surfactant can modulate the release of pro-inflammatory cytokines from alveolar mononuclear phagocytes.The aim of this study was to assess whether SP-A or Surfactant (Surf) from patients with pulmonary alveolar proteinosis (PAP) can affect the release of two chemokines (interleukin (IL)-8 and monocyte chemtactic peptide (MCP)-1) from human monocytes and rat lung type-II cells. In addition IL-8 and MCP-1 levels were assessed in the brochoalveolar lavage fluid (BALF) of seven patients with PAP and compared with those in a group of control subjects (n=5).SP-A, tested over a wide range of concentrations, significantly increased IL-8 and MCP-1 release from monocytes. SP-A retained its activity after collagenase digestion, but was not active after heat treatment. The release of IL-8 by monocytes was also stimulated by Surf. Finally, median BALF IL-8 and MCP-1 levels in PAP patients were significantly higher than in controls (9.50 and 9.51 pg?mL -1 in controls versus 151.95 and 563.70 pg?mL -1 in PAP, respectively) and significantly correlated with SP-A concentrations in BALF.Overall the results of this study support the view that the high content of alveolar surfactant apoprotein A may contribute to the upregulation of chemokine release in pulmonary alveolar proteinosis, thus contributing to airway inflammation.

show abstract

“…18 Recent findings demonstrate that type II and other respiratory epithelial cells are capable of synthesizing GM-CSF. 19 The fact that regression of this process has been achieved in GMϪ/Ϫ mice using BMT suggests that this disorder may be haematopoietic in nature, involving AM. In the aforementioned animal model, the donor origin of AM was demonstrated.…”

mentioning

confidence: 99%

“…6 The role of BMT in human PAP is as yet undefined, but preliminary observations of abnormal AM have also been made in the human PAP. 19 Dirksen et al 13 …”

mentioning

confidence: 99%

Haematopoietic transplantation in pulmonary alveolar proteinosis associated with chronic myelogenous leukaemia

Rodríguez-Luaces

Lafuente

Martin

et al. 1997

Bone Marrow Transplant

View full text Add to dashboard Cite

Summary:generated by gene targeting: these mutant mice developed pulmonary disease characteristic of PAP. In these animal models haematopoietic development and function were not Pulmonary alveolar proteinosis (PAP) is a disease of unknown etiopathogenesis sometimes associated with disturbed. [4][5][6] When found in association with haematological dismalignant haematological disorders. The potential reversibility of the process in these cases seems to be orders, PAP has been considered a secondary form. 7 In a series of haematology patients with respiratory failure, the related to recovery from the underlying disease. GM-CSF has acquired an important, potentially pathogenic incidence of PAP was 5.3%. 8 It has been suggested that in such cases, PAP may be the result of a disease-related role and BMT presents one therapeutic option effective in certain forms of human PAP. We present the case of defect in the AM function 9 and/or due to treatment (chemotherapy, radiotherapy, steroids). 10 The most signifia 43-year-old female patient with Ph؉ CML. During pretransplantation evaluation, unexpected pulmonary cant complication in both primary and secondary cases is superinfection, particularly by opportunistic organisms. The infiltrates were noted in the chest X-ray, PAP being diagnosed on biopsy. In view of the progressive respirpreferred diagnostic method both in primary 11 and secondary 8 PAP is bronchoalveolar lavage (BAL). atory symptomatology and her CML being in accelerated phase, the patient underwent haematopoietic transSpontaneous remission of idiopathic primary PAP has occasionally been described. 12 The use of BAL as therapy plantation. She died on day ؉12 from invasive pulmonary aspergillosis before a response could be has improved the prognosis considerably. However, the potential reversibility of the process in secondary PAP is observed. Pathogenic implications in PAP and the role of haematopoietic transplantation in this disease are related to prior recovery from the haematological condition. 8 The possible part played by a deficiency of GMdiscussed. Keywords: pulmonary alveolar proteinosis; CML; PBSC CSF in the pathogenesis of human PAP opens up new therapeutic possibilities, such as BMT 13 or treatment with transplantation; aspergillosis GM-CSF. 14 We present a case of PAP diagnosed in a female with CML. The patient underwent allogeneic haematopoietic Pulmonary alveolar proteinosis (PAP) is a heterogenous transplantation with the objective of achieving recovery and group of congenital and acquired diseases. It is characsubsequent control of the respiratory symptomatology. terized by deposition of extracellular granular material consisting of a mixture of phospholipids and surfactant proteins within the alveoli and airways. In humans, a fatal form of Case report congenital PAP arises from a mutation resulting in surfactant protein-B (SP-B) deficiency. 1 Acquired forms may be A 43-year-old female was diagnosed with CML Phϩ in found in previously healthy patients, but the pathogenic chronic phase during ho...

show abstract

Secretion of cytokines by rat alveolar epithelial cells: possible regulatory role for SP-A

Cited by 46 publications

References 0 publications

Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

Surfactant apoprotein A modulates interleukin-8 and monocyte chemotactic peptide-1 production

Haematopoietic transplantation in pulmonary alveolar proteinosis associated with chronic myelogenous leukaemia

Contact Info

Product

Resources

About