Tumor necrosis factor and interleukin-1 activities in free lung cells after single and repeated inhalation of bacterial endotoxin

Rochemonteix-Galve, B de; Marchat-Amoruso, B; Dayer, Jean‐Michel; Rylander, Ragnar

doi:10.1128/iai.59.10.3646-3650.1991

Cited by 28 publications

(10 citation statements)

References 22 publications

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“…Our data on the putative effect of oxidative stress on sAMs were tested by LPS-injection experiments, which were shown to induce remarkable oxidative stress in the animals (36,37). As expected, the sAMs were up-regulated after injection, but what is more interesting is that we found aged animals had a greater response to LPS administration.…”

Section: Discussionsupporting

confidence: 52%

Alteration of soluble adhesion molecules during aging and their modulation by calorie restriction

et al. 2003

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To investigate the status of soluble adhesion molecules (sAMs) during aging, the present study determined protein levels of several major sAMs in serum samples obtained from rats at different ages. These sAMs include E-selectin, P-selectin, vascular cell adhesion molecule 1 (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1). Fischer 344 rats, ages 6, 12, 18, and 24 months, fed ad libitum (AL) and calorie restricted (CR) diets were used in this study. Analysis by Western blotting showed that the levels of all sAMs studied increased during aging in AL rats, but were effectively blunted in the CR rats. Total reactive oxygen species/reactive nitrogen species (ROS/RNS) levels were measured by fluorescent probe 2',7'-dichlorofluorescin diacetate. Increased ROS/RNS levels were found to coincide with increased levels of superoxide-generating xanthine oxidase in serum during aging, but were found suppressed by CR. Increases in sAMs levels were duplicated in another experiment in which young (13-month-old) and old (31-month-old) rats were injected with proinflammatory lipopolysaccharide. These findings suggest that the altered expressions of sAMs may be due to increased oxidative stress with advanced age and that these increases were prevented by CR through its antioxidative action.

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Section: Discussionsupporting

confidence: 52%

Alteration of soluble adhesion molecules during aging and their modulation by calorie restriction

et al. 2003

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“…13 LPS inhalation has also been shown to increase the traffic of airway antigenbearing dendritic cells (DC) to regional lymph nodes (RLN), 14 where they initiate immune responses via presentation of their sequestered stores of inhaled antigens to T cells. 15,16 The principal stimulus for DC migration from the intraepithelial tissue sites to RLN appears to be TNFa , 17 the major source of w hich in the LPS-stimulated lung is alveolar macrophages (AM), 18,19 and we suggest the latter as a likely mechanism for LPS enhancement of the anti-OVA antibody response in these experiments.…”

Section: Discussionmentioning

confidence: 68%

(1 →3)‐ β ‐D‐Glucan and endotoxin modulate immune response to inhaled allergen

Rylander

Holt

1998

Mediators of Inflammation

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Exposure to dust may involve co-exposure to agents which are allergens, together with those which are pro-inflammatory. To study the effects of such a co-exposure, the humoral and inflammatory responses were studied in guinea pigs inhaling the T-cell-dependent antigen ovalbumin (OVA) and the inflammatory agents (1 --> 3)-beta-D-glucan and lipopolysaccharide (LPS). The effects were evaluated as inflammatory cells in the lung and serum antibodies to OVA. LPS caused a stimulation of the OVA-induced antibody production which was abolished by simultaneous exposure to (1 --> 3)-beta-D-glucan. An increase of eosinophils after OVA exposure was decreased by co-exposure to (1 --> 3)-beta-D-glucan. The results demonstrate a complex interaction between adaptive and innate immune mechanisms in the lung, determined by exposure to common contaminants in airborne dust.

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“…TNF-α release was not influenced by pre-exposure to LPS. In line, TNF-α release by alveolar macrophages was not significantly increased upon ex vivo LPS stimulation following intravenous LPS challenge 16 and no increase in TNF-α was found in BALF of guinea pigs after recurrent intranasal administration of LPS 37 . The differential results on TNF-α production and that of IL-1β and IL-6 by LPS-AM might be influenced by augmented gene transcription and/or prolonged mRNA stability [38][39][40][41] .…”

Section: Discussionmentioning

confidence: 83%

Priming of Alveolar Macrophages upon Instillation of Lipopolysaccharide in the Human Lung

Hoogerwerf¹,

Vos²,

Veer³

et al. 2010

Am J Respir Cell Mol Biol

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The airways are continuously exposed to respiratory pathogens, which may result in bacterial pneumonia, one of the most common infectious diseases and the leading cause of sepsis. Considering that recurrent exposure to microbial products can lead to tolerance of immune cells, and that this might contribute to the susceptibility to nosocomial infection, we investigated the effect of in vivo lipopolysaccharide (LPS) instillation on the responsiveness of alveolar macrophages. In eight healthy humans, sterile saline was instilled into a lung segment by bronchoscope, followed by instillation of LPS into the contralateral lung; 6 hours later, a bilateral bronchoalveolar lavage was performed, and purified alveolar macrophages were ex vivo stimulated with LPS or lipoteichoic acid (LTA), triggering Toll-like receptor (TLR)-4 and -2, respectively. In vivo LPS-exposed alveolar macrophages were primed, as reflected by increased ex vivo LPS- and LTA-induced IL-1 beta and IL-6 gene expression and production compared with in vivo saline-exposed alveolar macrophages. LPS instillation did not influence the surface expression of TLR4 or TLR2. Furthermore, LPS instillation did not impact on the expression of a number of extracellular and intracellular regulators of TLR signaling. However, p38 mitogen-activated protein kinase remained phosphorylated in alveolar macrophages upon LPS instillation. The current data demonstrate that LPS instillation in the human lung primes alveolar macrophages for further stimulation with either LPS or LTA, possibly by sustained p38 mitogen-activated protein kinase activation.

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Tumor necrosis factor and interleukin-1 activities in free lung cells after single and repeated inhalation of bacterial endotoxin

Cited by 28 publications

References 22 publications

Alteration of soluble adhesion molecules during aging and their modulation by calorie restriction

Alteration of soluble adhesion molecules during aging and their modulation by calorie restriction

(1 →3)‐ β ‐D‐Glucan and endotoxin modulate immune response to inhaled allergen

Priming of Alveolar Macrophages upon Instillation of Lipopolysaccharide in the Human Lung

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