Airway hyperresponsiveness after endotoxin inhalation depends on leukocyte infiltration.

Horie, Takashi; Ohmori, C; Koyama, Shozo; Saitoh, Osamu; Mutoh, Takashi; Okuma, Akiharu; Okayasu, Masahito

doi:10.1620/tjem.156.109

Cited by 4 publications

(4 citation statements)

References 26 publications

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“…In our LPStreated animals, infiltration of polymorphonuclear leukocytes could have participated in the develop ment of hyperreactivity of airway smooth muscle. In contrast to our results, some previous reports demon strated that LPS did not induce an apparent structural damage to epithelial cells [12,13]. This descrepancy might be accounted for by the differences of quantity, frequency, and mode of LPS administration.…”

Section: Discussioncontrasting

confidence: 99%

“…It has been shown that neutrophils invade into the airways after inhalation of LPS [25,26], and that the LPS-induced airway hyperresponsiveness might be associated with leukocyte migration [13]. In our LPStreated animals, infiltration of polymorphonuclear leukocytes could have participated in the develop ment of hyperreactivity of airway smooth muscle.…”

Section: Discussionmentioning

confidence: 59%

“…Recently, the inhalation of lipopolysaccharide (LPS) was reported to cause bronchoconstriction in patients with asthma but not in healthy subjects [11]. Also, the inhalation and intraperitoneal administra tion of LPS has been shown to increase the contractile responses of airway smooth muscle in experimental animals [12][13][14], In the present study, to elucidate the mechanisms of airway hyperreactivity induced by LPS, we studied isolated tracheal segments from guin ea pigs under isometric conditions in vitro. …”

Section: Introductionmentioning

confidence: 93%

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Effects of Lipopolysaccharide from <i>Pseudomonas aeruginosa</i> on Airway Smooth Muscle Functions in Guinea Pigs

Yamawaki¹,

Tamaoki²,

Kanemura³

et al. 1990

Respiration

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To elucidate the mechanisms of airway hyperreactivity induced by lipopolysaccharide (LPS), we studied isolated tracheal segments from guinea pigs under isometric conditions in vitro. Guinea pigs were injected intraperitoneally with endotoxin (1 mg/kg; LPS from Pseudomonas aeruginosa, serotype 10) for 4 days, and animals treated with sterile nonpyrogenic saline served as controls. Histological examination of trachea revealed moderate structural damage of epithelial layer in the LPS-treated group. Treatment with LPS potentiated the contractile responses of tracheal smooth muscle to acetylcholine, causing a leftward displacement of dose-response curves so that the EC₅₀ values decreased from 1.1 ± 3.7 × 10^-5 to 4.4 ± 3.7 × 10^-7M(mean ± SE, p < 0.01). Likewise, LPS shifted the dose-response curves for histamine and substance P to lower concentrations by approximately 0.5–1.0 log U. Each of these potentiations was not affected by pretreatment of tissues with indomethacin or propranolol. Addition of isoproterenol to tracheal segments precontracted with acetylcholine caused concentration-dependent relaxation, an effect that was significantly greater in controls than in the LPS-treated group. These results suggest that airway hyperreactivity induced by LPS in guinea pigs may be attributed to a decreased ability of respiratory epithelial cells to generate a relaxing factor

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 93%

See 1 more Smart Citation

Effects of Lipopolysaccharide from <i>Pseudomonas aeruginosa</i> on Airway Smooth Muscle Functions in Guinea Pigs

Yamawaki¹,

Tamaoki²,

Kanemura³

et al. 1990

Respiration

View full text Add to dashboard Cite

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“…As an important pro-infl ammatory factor, LPS was once considered to induce AHR by the recruiting neutrophils and macrophages in some studies [25,26]. However, subsequent studies showed that the infl ammation is not essential for the development of AHR [27,28].…”

Section: Discussionmentioning

confidence: 99%

Airway hyperresponsiveness induced by repetitive intraperitoneal injection of lipopolysacharide and the involvement of inflammation and nitric oxide in guinea pigs

Jiang

Jian

et al. 2006

Inflamm. res.

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Adenovirus IL-13–Induced Airway Disease in Mice

Therien¹,

Bernier²,

Weicker³

et al. 2008

Am J Respir Cell Mol Biol

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Interleukin 13 (IL-13) is considered to be a key driver of the development of airway allergic inflammation and remodeling leading to airway hyperresponsiveness (AHR). How precisely IL-13 leads to the development of airway inflammation, AHR, and mucus production is not fully understood. In order to identify key mediators downstream of IL-13, we administered adenovirus IL-13 to specifically induce IL-13-dependent inflammation in the lungs of mice. This approach was shown to induce cardinal features of lung disease, specifically airway inflammation, elevated cytokines, AHR, and mucus secretion. Notably, the model is resistant to corticosteroid treatment and is characterized by marked neutrophilia, two hallmarks of more severe forms of asthma. To identify IL-13-dependent mediators, we performed a limited-scale two-dimensional SDS-PAGE proteomic analysis and identified proteins significantly modulated in this model. Intriguingly, several identified proteins were unique to this model, whereas others correlated with those modulated in a mouse ovalbumin-induced pulmonary inflammation model. We corroborated this approach by illustrating that proteomic analysis can identify known pathways/mediators downstream of IL-13. Thus, we have characterized a murine adenovirus IL-13 lung model that recapitulates specific disease traits observed in human asthma, and have exploited this model to identify effectors downstream of IL-13. Collectively, these findings will enable a broader appreciation of IL-13 and its impact on disease pathways in the lung.

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Airway hyperresponsiveness after endotoxin inhalation depends on leukocyte infiltration.

Cited by 4 publications

References 26 publications

Effects of Lipopolysaccharide from <i>Pseudomonas aeruginosa</i> on Airway Smooth Muscle Functions in Guinea Pigs

Effects of Lipopolysaccharide from <i>Pseudomonas aeruginosa</i> on Airway Smooth Muscle Functions in Guinea Pigs

Airway hyperresponsiveness induced by repetitive intraperitoneal injection of lipopolysacharide and the involvement of inflammation and nitric oxide in guinea pigs

Adenovirus IL-13–Induced Airway Disease in Mice

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