Virus-induced Airway Hyperresponsiveness and Asthma

Folkerts, Gert; Busse, William W.; Nijkamp, Frans P.; Sorkness, Ronald L.; Gern, James E.

doi:10.1164/ajrccm.157.6.9707163

Cited by 253 publications

(200 citation statements)

References 160 publications

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“…The pathogenesis of airway inflammation caused by respiratory viruses is complex and involves multiple inflammatory cells, cytokines, and mediators (1,2). Airway epithelial cells are the initial site of respiratory virus infection and have the capacity to produce a variety of biologically active molecules including cytokines (4).…”

Section: R Espiratory Virus Infection Causes Airway Inflammation and mentioning

confidence: 99%

“…Airway epithelial cells are the initial site of respiratory virus infection and have the capacity to produce a variety of biologically active molecules including cytokines (4). Influenza virus (IV), 3 which is one of the major respiratory viruses, also causes airway inflammation and exacerbates asthma (1,2,5). The mechanism of the production of airway inflammation and asthma exacerbation has been investigated, and IV-infected airway epithelial cells, at least in part, participate in it by expressing various cytokines that promote inflammatory cell infiltration (6 -8).…”

Section: R Espiratory Virus Infection Causes Airway Inflammation and mentioning

confidence: 99%

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p38 Mitogen-Activated Protein Kinase and c-Jun-NH2-Terminal Kinase Regulate RANTES Production by Influenza Virus-Infected Human Bronchial Epithelial Cells

Kujime

Hashimoto

Gon

et al. 2000

The Journal of Immunology

166

142

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Airway epithelial cells which are the initial site of influenza virus (IV) infection are suggested to participate in airway inflammatory response by expressing various cytokines including RANTES; however, the intracellular signal that regulates RANTES expression has not been determined. In the present study, we examined the role of p38 mitogen-activated protein (MAP) kinase, extracellular signal-regulated kinase (Erk), and c-Jun-NH2-terminal kinase (JNK) in RANTES production by IV-infected human bronchial epithelial cells. The results showed that IV infection induced increases in p38 MAP kinase, and Erk and JNK phosphorylation and activity. SB 203580, PD 98059, and CEP-1347 attenuated IV-infection induced p38 MAP kinase activity, Erk activity, and JNK activity, respectively. SB 203580 and CEP-1347 attenuated RANTES production by 45.3% and 45.2%, respectively, but a combination of these inhibitors additively attenuated by 69.1%. In contrast, PD 98059 did not attenuate. Anti-IL-1α mAb, anti-IL-1β mAb, anti-TNF-α mAb, anti-IL-8 mAb, anti-IFN-β mAb, anti-RANTES mAb, and a combination of these mAbs did not affect IV infection-induced increases in p38 MAP kinase, Erk, and JNK phosphorylation, indicating that each cytokine neutralized by corresponding Ab was not involved in IV infection-induced phosphorylation of MAP kinases. N-acetylcysteine (NAC) did not affect IV infection-induced increases in MAP kinase phosphorylation, whereas NAC attenuated RANTES production by 18.2%, indicating that reactive oxygen species may act as a second messenger leading to RANTES production via p38 MAP kinase- and JNK-independent pathway. These results indicate that p38 MAP kinase and JNK, at least in part, regulate RANTES production by bronchial epithelial cells.

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Section: R Espiratory Virus Infection Causes Airway Inflammation and mentioning

confidence: 99%

Section: R Espiratory Virus Infection Causes Airway Inflammation and mentioning

confidence: 99%

p38 Mitogen-Activated Protein Kinase and c-Jun-NH2-Terminal Kinase Regulate RANTES Production by Influenza Virus-Infected Human Bronchial Epithelial Cells

Kujime

Hashimoto

Gon

et al. 2000

The Journal of Immunology

166

142

View full text Add to dashboard Cite

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“…Several potential mechanisms have been suggested including LRT inflammation (reviewed by FOLKERTS et al [29]), impairment of b-adrenoceptor and M 2 -muscarinic receptors leading to smooth muscle constriction [30], and persistence of virus in the LRT [31]. How these potential mechanisms relate to one another in the pathogenesis of LRT symptoms and changes in lung function during common respiratory virus infections, are still largely unknown.…”

Section: Airway Physiologymentioning

confidence: 99%

A model of viral wheeze in nonasthmatic adults: symptoms and physiology

McKean

Leech²,

Lambert³

et al. 2001

Eur Respir J

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Episodic wheezing associated with viral infections of the upper respiratory tract (URT) is a common problem in young children but also occurs in adults. It is hypothesized that an experimental infection with human coronavirus (HCoV), the second most prevalent common cold virus, would cause lower respiratory tract (LRT) changes in adults with a history of viral wheeze.Twenty-four viral wheezers (15 atopic) and 19 controls (seven atopic) were inoculated with HCoV 229E and monitored for the development of symptoms, changes in airway physiology and provocative concentration of methacholine causing a 20% fall in forced expiratory volume in one second (FEV1) (PC20). At baseline, viral wheezers were similar to controls in PC20 (mean¡SD log 2 PC20: 5.1¡1.9 and 5.8¡1.4 g?L -1 , respectively) but had a lower FEV1 than controls (mean¡SD 85.8¡11.4 and 95.6¡13.2% predicted, respectively pv0.05). Nineteen viral wheezers and 11 controls developed colds. Viral wheezers with colds reported significantly more URT symptoms than controls (median scores (interquartile range): 24 (10 -37) and 6 (4 -15), respectively p~0.014). Sixteen viral wheezers and no controls reported LRT symptoms (wheeze, chest tightness and shortness of breath). The viral wheezers with colds had small (3 -4%) reductions in FEV1 and peak expiratory flow on days with LRT symptoms (days 3 -6), but a progressive reduction in PC20 from baseline on days 2, 4 and 17 after inoculation (by 0.82, 1.35 and 1.82 doubling concentrations, respectively). The fall in PC20 affected both atopic and nonatopic subjects equally. There were no changes in FEV1 or PC20 in controls.An adult model of viral wheeze that is independent of atopy and therefore, of classical atopic asthma was established.

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“…Respiratory syncytial virus and parainfluenza virus are common viruses in young children, whereas rhinovirus is a frequent etiological agent in older children and adults (reviewed in Refs. [3][4][5]. However, any virus capable of eliciting an acute respiratory infection has the potential to exacerbate asthma (6).…”

mentioning

confidence: 99%

Murine Cytomegalovirus Infection Alters Th1/Th2 Cytokine Expression, Decreases Airway Eosinophilia, and Enhances Mucus Production in Allergic Airway Disease

Wu¹,

Puddington²,

Whiteley

et al. 2001

The Journal of Immunology

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Concomitant infection of murine CMV (MCMV), an opportunistic respiratory pathogen, altered Th1/Th2 cytokine expression, decreased bronchoalveolar lavage (BAL) fluid eosinophilia, and increased mucus production in a murine model of OVA-induced allergic airway disease. Although no change in the total number of leukocytes infiltrating the lung was observed between challenged and MCMV/challenged mice, the cellular profile differed dramatically. After 10 days of OVA-aerosol challenge, eosinophils comprised 64% of the total leukocyte population in BAL fluid from challenged mice compared with 11% in MCMV/challenged mice. Lymphocytes increased from 11% in challenged mice to 30% in MCMV/challenged mice, and this increase corresponded with an increase in the ratio of CD8+ to CD4+TCRαβ lymphocytes. The decline in BAL fluid eosinophilia was associated with a change in local Th1/Th2 cytokine profiles. Enhanced levels of IL-4, IL-5, IL-10, and IL-13 were detected in lung tissue from challenged mice by RNase protection assays. In contrast, MCMV/challenged mice transiently expressed elevated levels of IFN-γ and IL-10 mRNAs, as well as decreased levels of IL-4, IL-5, and IL-13 mRNAs. Elevated levels of IFN-γ and reduced levels of IL-5 were also demonstrated in BAL fluid from MCMV/challenged mice. Histological evaluation of lung sections revealed extensive mucus plugging and epithelial cell hypertrophy/hyperplasia only in MCMV/challenged mice. Interestingly, the development of airway hyperresponsiveness was observed in challenged mice, not MCMV/challenged mice. Thus, MCMV infection can modulate allergic airway inflammation, and these findings suggest that enhanced mucus production may occur independently of BAL fluid eosinophilia.

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Virus-induced Airway Hyperresponsiveness and Asthma

Cited by 253 publications

References 160 publications

p38 Mitogen-Activated Protein Kinase and c-Jun-NH2-Terminal Kinase Regulate RANTES Production by Influenza Virus-Infected Human Bronchial Epithelial Cells

p38 Mitogen-Activated Protein Kinase and c-Jun-NH2-Terminal Kinase Regulate RANTES Production by Influenza Virus-Infected Human Bronchial Epithelial Cells

A model of viral wheeze in nonasthmatic adults: symptoms and physiology

Murine Cytomegalovirus Infection Alters Th1/Th2 Cytokine Expression, Decreases Airway Eosinophilia, and Enhances Mucus Production in Allergic Airway Disease

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