ArticleAmerican journal of respiratory cell and molecular biology2008
Tumor necrosis factor-alpha from macrophages enhances LPS-induced clara cell expression of keratinocyte-derived chemokine.
Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- Age-dependent inflammatory response is altered in an ex vivo model of bacterial pneumonia.Respiratory research · 2024Article
- Pulmonary Inflammation and KRAS Mutation in Lung Cancer.Advances in experimental medicine and biology · 2021Article
- Expression of Piwi protein MIWI2 defines a distinct population of multiciliated cells.The Journal of clinical investigation · 2017Article
- Fraction of MHCII and EpCAM expression characterizes distal lung epithelial cells for alveolar type 2 cell isolation.Respiratory research · 2017Article
- Myb permits multilineage airway epithelial cell differentiation.Stem cells (Dayton, Ohio) · 2014Article
- Article
- Depletion of tumor-associated macrophages slows the growth of chemically induced mouse lung adenocarcinomas.Frontiers in immunology · 2014Article
- LPS-treated macrophage cytokines repress surfactant protein-B in lung epithelial cells.American journal of respiratory cell and molecular biology · 2013Article
- ADAM17 activation in circulating neutrophils following bacterial challenge impairs their recruitment.Journal of leukocyte biology · 2012Article
- Characterization of the cytokine expression profiles of the aorta and liver of young tumor necrosis factor alpha mutant mice.Molecular and cellular biochemistry · 2012Article
- Age-related defects in TLR2 signaling diminish the cytokine response by alveolar macrophages during murine pneumococcal pneumonia.Experimental gerontology · 2012Article
- Lipopolysaccharide-induced cyclooxygenase-2 expression in mouse transformed Clara cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2012Article
- Leukocyte ADAM17 regulates acute pulmonary inflammation.PloS one · 2011Article
- Clara cells attenuate the inflammatory response through regulation of macrophage behavior.American journal of respiratory cell and molecular biology · 2010Article
- Endogenous lung stem cells and contribution to disease.The Journal of pathology · 2009Review
- Keratinocyte growth factor protects against Clara cell injury induced by naphthalene.The European respiratory journal · 2008Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Tumor necrosis factor (TNF)-alpha is a cytokine produced by alveolar macrophages in response to LPS in the lung. Clara cells are bronchiolar epithelial cells that produce a variety of proinflammatory cytokines in response to LPS but not to TNF-alpha. In this study, we examined whether TNF-alpha affects Clara cell cytokine production in the setting of LPS stimulation. Using a transformed murine Clara cell line (C22), we observed that both LPS and TNF-alpha induced production of keratinocyte-derived chemokine (KC) and monocyte chemoattractant protein (MCP)-1. We also found that simultaneous LPS and TNF-alpha stimulation is synergistic for KC production, but additive for MCP-1 production. By using a Transwell coculture system of RAW264.7 macrophages and Clara cells isolated from C57Bl/6 mice, we found that macrophages produce a soluble factor that enhances Clara cell KC production in response to LPS. Cocultures of Clara cells from mice deficient in TNF-alpha receptors with RAW264.7 macrophages demonstrated that the effect of macrophages on Clara cells is mediated primarily via TNF-alpha. To determine whether these findings occur in vivo, we treated wild-type and TNF receptor-deficient mice intratracheally with LPS and examined the expression of KC. LPS-treated, TNF receptor-deficient mice showed much less KC mRNA in airway epithelial cells compared with wild-type mice. In contrast, a similar number of KC-expressing cells was seen in the lung periphery. Thus, upregulation of KC by Clara cells in the setting of LPS stimulation is largely dependent on TNF-alpha originating from alveolar macrophages. These findings shed light on macrophage-Clara cell interactions in regulating the pulmonary inflammatory response to LPS.
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Registered trials
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