ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Acute pulmonary lipopolysaccharide tolerance decreases TNF-alpha without reducing neutrophil recruitment.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Disease tolerance: a protective mechanism of lung infections.Frontiers in cellular and infection microbiology · 2023Review
- Serum- and Glucocorticoid-Inducible Kinase 1 Promotes Alternative Macrophage Polarization and Restrains Inflammation through FoxO1 and STAT3 Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- JAK3 restrains inflammatory responses and protects against periodontal disease through Wnt3a signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- S100A8/A9 and S100A9 reduce acute lung injury.Immunology and cell biology · 2017Article
- The Pig: A Relevant Model for Evaluating the Neutrophil Serine Protease Activities during Acute Pseudomonas aeruginosa Lung Infection.PloS one · 2016Article
- Substance P mediates reduced pneumonia rates after traumatic brain injury.Critical care medicine · 2014Article
- Chemokines mediate ethanol-induced exacerbations of murine cockroach allergen asthma.Clinical and experimental immunology · 2013Article
- Cecal ligation and puncture-induced murine sepsis does not cause lung injury.Critical care medicine · 2013Article
- Article
- Mannose-capped Lipoarabinomannan from Mycobacterium tuberculosis induces soluble tumor necrosis factor receptor production through tumor necrosis factor alpha-converting enzyme activation.Infection and immunity · 2012Article
- Pulmonary endotoxin tolerance protects against cockroach allergen-induced asthma-like inflammation in a mouse model.International archives of allergy and immunology · 2012Article
- Diesel exhaust particulates exacerbate asthma-like inflammation by increasing CXC chemokines.The American journal of pathology · 2011Article
- Corticotropin-releasing hormone receptor-1 and 2 activity produces divergent resistance against stress-induced pulmonary Streptococcus pneumoniae infection.Journal of neuroimmunology · 2011Article
- Rectal administration of lipopolysaccharide and ovalbumin ameliorates acute murine colitis.Digestive diseases and sciences · 2011Article
- Sources of alveolar soluble TNF receptors during acute lung injury of different etiologies.Journal of applied physiology (Bethesda, Md. : 1985) · 2011Article
- A rat model of exercise-induced asthma: a nonspecific response to a specific immunogen.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Endotoxin, coliform, and dust levels in various types of rodent bedding.Journal of the American Association for Laboratory Animal Science : JAALAS · 2010Article
- Chronic pulmonary LPS tolerance induces selective immunosuppression while maintaining the neutrophilic response.Shock (Augusta, Ga.) · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pulmonary LPS exposure plays a key role in exacerbation of lung diseases such as chronic obstructive pulmonary disease and asthma. However, little is known about the effects of repeated LPS exposure in the lung microenvironment. We have developed a novel murine model of pulmonary LPS tolerance induced by intratracheal (i.t.) administration of LPS. First, we show that pulmonary LPS exposure does not induce whole-body refractoriness to systemic LPS, because i.t. administration followed by i.p. administration did not decrease plasma TNF-alpha. However, a local refractory state can be induced with two i.t. LPS exposures. Pulmonary LPS tolerance was induced by i.t. administration of 100 ng LPS at time 0 and 48 h. Nontolerant mice received PBS at time 0 and LPS at 48 h. Bronchoalveolar lavage levels of TNF-alpha were significantly attenuated in tolerant mice vs nontolerant mice (1597 pg/ml vs 7261 pg/ml). TNF-alpha mRNA was significantly reduced in bronchoalveolar lavage cells (5-fold) and lung tissue (10-fold). No reduction was seen in neutrophil numbers in the bronchoalveolar lavage fluid, myeloperoxidase activity, or expression of neutrophil chemoattractants CXCL1 and CXCL2, reflecting the specificity of the response. The reduction in TNF-alpha was accompanied by a significant increase in soluble receptors, TNF-SRI (159 pg/ml vs 206 pg/ml) and TNF-SRII (1366 pg/m vs 2695 pg/ml). In conclusion, pulmonary LPS tolerance results in a specific reduction in TNF-alpha expression, while the neutrophilic response is unaffected. This response may be a mechanism to limit tissue damage by reducing TNF-alpha levels, while still maintaining the antimicrobial capacity of the lung.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.