Airway Interleukin‐8 in Elderly Patients with Bacterial Lower Respiratory Tract Infections

P, Ponglertnapagorn; Oishi, Kazunori; Iwagaki, Akitaka; Sonoda, Fuminari; Watanabe, Kiwao; Nagatake, Tsuyoshi; Matsushima, Kouji; Matsumoto, Keizō

doi:10.1111/j.1348-0421.1996.tb03322.x

Cited by 8 publications

(4 citation statements)

References 21 publications

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“…Another possible mechanism for the release of this enzyme might involve administration of bactericidal antibiotics to these patients (2,20). We have previously reported that a variety of respiratory pathogens induce IL-8 production in the airway of patients with lower respiratory tract infections (31). Therefore, further investigations to determine which respiratory pathogens possess Pseudomonas nitrite reductase and induce inflammatory cytokines, including IL-8, in human respiratory cells are required.…”

Section: Discussionmentioning

confidence: 99%

Nitrite reductase from Pseudomonas aeruginosa induces inflammatory cytokines in cultured respiratory cells

et al. 1997

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Persistent infection with Pseudomonas aeruginosa increases interleukin-8 (IL-8) levels and causes dense neutrophil infiltrations in the airway of patients with chronic airway diseases. To investigate the role of P. aeruginosa infection in IL-8 production in the airway of these patients, we examined whether cell lysates of P. aeruginosa could cause IL-8 production from human bronchial epithelial cells. Diluted sonicated supernatants of P. aeruginosa (SSPA) with a mucoid or nonmucoid phenotype stimulated human bronchial epithelial (BET-1A) cells to produce IL-8. In this study, we have purified a 59-kDa heat-stable protein with IL-8-inducing activity from the SSPA by sequential ion-exchange chromatography. The N-terminal sequence of this purified protein completely matched a sequence at the N-terminal part of the mature protein of nitrite reductase from P. aeruginosa. In addition, immunoblotting with a polyclonal immunoglobulin G (IgG) against recombinant Pseudomonas nitrite reductase demonstrated a specific binding to the purified protein. Furthermore, the immunoprecipitates of the SSPA with a polyclonal IgG against recombinant nitrite reductase induced a twofold-higher IL-8 production in the BET-1A cell culture than did the immunoprecipitates of the SSPA with a control IgG. These lines of evidence confirmed that Pseudomonas nitrite reductase was responsible for IL-8 production in the BET-1A cells. The purified nitrite reductase induced maximal expression of IL-8 mRNA in the BET-1A cells at 1 to 3 h after stimulation, and the IL-8 mRNA expression declined by 8 h after stimulation. New protein translation was not required for nitrite reductase-mediated IL-8 mRNA expression in the BET-1A cells. Nitrite reductase stimulated the BET-1A cells, as well as human alveolar macrophages, pulmonary fibroblasts, and neutrophils, to produce IL-8. In contrast, nitrite reductase induced significant levels of tumor necrosis factor alpha and IL-1␤ protein only in human alveolar macrophages. These data support the notion that nitrite reductase from P. aeruginosa induces the production of inflammatory cytokines by respiratory cells and may contribute to the pathogenesis of chronic airway diseases and persistent P. aeruginosa infection.

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Section: Discussionmentioning

confidence: 99%

Nitrite reductase from Pseudomonas aeruginosa induces inflammatory cytokines in cultured respiratory cells

et al. 1997

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“…Many patients eventually harbor Pseudomonas aeruginosa in their lower respiratory tract which accounts for significant morbidity. The role of some proinflammatory mediators, such as interleukin-1 (IL-1), IL-8, tumor necrosis factor-alpha (TNF-␣ ), and leukotriene B4 (LTB4), in recruiting neutrophils into the tracheobronchial tree has been recently established (1,(2)(3)(4)(5)(6)(7). As there is no gold standard in measuring inflammatory activities in bronchiectasis, concentrations of these proinflammatory mediators might act as surrogate end points in disease monitoring.…”

mentioning

confidence: 99%

Inhaled Fluticasone Reduces Sputum Inflammatory Indices in Severe Bronchiectasis

Tsang

Lam

et al. 1998

Am J Respir Crit Care Med

159

147

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Although corticosteroid therapy might be clinically beneficial for bronchiectasis, very little is known of its effects on the inflammatory and infective markers in bronchiectasis. We have therefore performed a double-blind, placebo-controlled study to evaluate the effects of a 4-wk administration of inhaled fluticasone in bronchiectasis. Twenty-four patients (12 female; mean age 51 yr) were randomized into receiving either inhaled fluticasone (500 microgram twice daily) via the Accuhaler device (n = 12) or placebo. At each visit, spirometry, 24-h sputum volume, sputum leukocyte density, bacterial densities, and concentrations of interleukin (IL)-1beta, IL-8, tumor necrosis factor-alpha (TNF-alpha), and leukotriene B4 (LTB4) were determined. There was a significant (p < 0.05) decrease in sputum leukocyte density and IL-1beta, IL-8, and LTB4 after fluticasone treatment. The fluticasone group had one and the placebo group three episodes of exacerbation. There were no significant changes in spirometry (p > 0.05) or any reported adverse reactions in either group. The results of this study show that high-dose fluticasone is effective in reducing the sputum inflammatory indices in bronchiectasis. Large-scale and long-term studies are indicated to evaluate the effects of inhaled steroid therapy on the inflammatory components in bronchiectasis.

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“…These several lines of evidence suggest that PNR released from P. aeruginosa by antimicrobial agents or complement may induce IL-8 production and neutrophil migration in the airways of patients with bronchopulmonary infections. We have previously reported that the levels of IL-8 and the number of neutrophils in expectorated sputum from patients with bacterial bronchopulmonary infections have decreased after treatment with the appropriate antimicrobial agents (33). Therefore, antibiotic-induced PNR release and neutrophil migration through induction of IL-8 production in the airways may begin after initiation of therapy and gradually decrease during successful antimicrobial chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Nitrite Reductase from Pseudomonas aeruginosa Released by Antimicrobial Agents and Complement Induces Interleukin-8 Production in Bronchial Epithelial Cells

Sar¹,

Oishi²,

Wada

et al. 1999

Antimicrob Agents Chemother

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We have recently reported that nitrite reductase, a bifunctional enzyme located in the periplasmic space of Pseudomonas aeruginosa, could induce interleukin-8 (IL-8) generation in a variety of respiratory cells, including bronchial epithelial cells (K. Oishi et al. Infect. Immun. 65:2648–2655, 1997). In this report, we examined the mode of nitrite reductase (PNR) release from a serum-sensitive strain of live P. aeruginosa cells during in vitro treatment with four different antimicrobial agents or human complement. Bacterial killing ofP. aeruginosa by antimicrobial agents induced PNR release and mediated IL-8 production in human bronchial epithelial (BET-1A) cells. Among these agents, imipenem demonstrated rapid killing of P. aeruginosa as well as rapid release of PNR and resulted in the highest IL-8 production. Complement-mediated killing of P. aeruginosa was also associated with PNR release and enhanced IL-8 production. The immunoprecipitates of the aliquots of bacterial culture containing imipenem or complement with anti-PNR immunoglobulin G (IgG) induced a twofold-higher IL-8 production than did the immunoprecipitates of the aliquots of bacterial culture with a control IgG. These pieces of evidence confirmed that PNR released in the aliquots of bacterial culture was responsible for IL-8 production in the BET-1A cells. Furthermore, the culture supernatants of the BET-1A cells stimulated with aliquots of bacterial culture containing antimicrobial agents or complement similarly mediated neutrophil migration in vitro. These data support the possibility that a potent inducer of IL-8, PNR, could be released fromP. aeruginosa after exposure to antimicrobial agents or complement and contributes to neutrophil migration in the airways during bronchopulmonary infections with P. aeruginosa.

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Airway Interleukin‐8 in Elderly Patients with Bacterial Lower Respiratory Tract Infections

Cited by 8 publications

References 21 publications

Nitrite reductase from Pseudomonas aeruginosa induces inflammatory cytokines in cultured respiratory cells

Nitrite reductase from Pseudomonas aeruginosa induces inflammatory cytokines in cultured respiratory cells

Inhaled Fluticasone Reduces Sputum Inflammatory Indices in Severe Bronchiectasis

Nitrite Reductase from Pseudomonas aeruginosa Released by Antimicrobial Agents and Complement Induces Interleukin-8 Production in Bronchial Epithelial Cells

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