Interleukin‐6, interleukin‐8, interleukin‐11, and interferon‐γ levels in nasopharyngeal aspirates from wheezing children with respiratory syncytial virus or influenza A virus infection

Oh, Jae‐Won; Lee, Ha-Baik; Park, Il‐Kyu; Kang, Jung-Oak

doi:10.1034/j.1399-3038.2002.02018.x

Cited by 40 publications

(32 citation statements)

References 35 publications

(30 reference statements)

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“…IL-6 plays a major role in triggering and sustaining the allergic inflammatory response. Elevated levels of IL-6 have been reported to occur in the bronchoalveolar lavage fluid of patients with asthma (Oh et al, 2002). In the present study, TOS remarkably inhibited the production of TNF-α and IL-6.…”

Section: Discussionsupporting

confidence: 55%

Typha orientalis inhibits inflammatory cytokine expression through suppression of ERK phosphorylation in HMC-1 cells

Choi¹,

Na²,

Um³

et al. 2010

Oriental Pharmacy and Experimental Medicine

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SUMMARYTypha orientalis' stem (TOS) is traditionally used as an herbal medicine for difficulty in urination, galactophoritis purulenta, whooping cough, and allergic dermatitis. However, its effect in experimental models remains unknown. Here, we report the effect of TOS on the phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187-induced inflammatory cytokine production and extracellular signal-regulated kinase (ERK) activation in the human mast cell line, HMC-1. TOS inhibited PMA plus A23187-induced cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6. Maximal inhibition rate of TNF-α and IL-6 production by TOS (1 mg/ml) was about 44.02%, and 45.20%, respectively (P < 0.05). In addition, TOS inhibited the expression of TNF-α and IL-6 mRNA under the same condition. Moreover, TOS partially blocked PMA plus A23187-induced ERK phosphorylation. These results suggested TOS could inhibit the cytokine production through blocking of ERK activity.

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Section: Discussionsupporting

confidence: 55%

Typha orientalis inhibits inflammatory cytokine expression through suppression of ERK phosphorylation in HMC-1 cells

Choi¹,

Na²,

Um³

et al. 2010

Oriental Pharmacy and Experimental Medicine

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“…We also show that RSV infection of human eosinophils results in the replication-dependent release of IL-6, a cytokine localized to specific granules 50 and released in response to mast cell chymase, IL-23, and various TLR ligands. [51][52][53] Although the precise role of IL-6 in the overall clinical picture of RSV disease has not been discerned, Bennett et al 54 and Oh et al 55 independently evaluated intranasal samples from patients with RSV and other virus infections and found elevated levels of proinflammatory cytokines, including IL-6.…”

Section: Discussionmentioning

confidence: 99%

Pneumoviruses infect eosinophils and elicit MyD88-dependent release of chemoattractant cytokines and interleukin-6

Dyer

Percopo

Fischer³

et al. 2009

Blood

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Eosinophils are recruited to the lung in response to infection with pneumovirus pathogens and have been associated with both the pathophysiologic sequelae of infection and, more recently, with accelerated virus clearance. Here, we demonstrate that the pneumovirus pathogens, respiratory syncytial virus (RSV) and pneumonia virus of mice (PVM), can infect human and mouse eosinophils, respectively, and that virus infection of eosinophils elicits the release of diseaserelated proinflammatory mediators from eosinophils. RSV replication in human eosinophils results in the release of infectious virions and in the release of the proinflammatory mediator, interleukin-6 (IL-6). PVM replication in cultured bone marrow eosinophils (bmEos) likewise results in release of infectious virions and the proinflammatory mediators IL-6, IP-10, CCL2, and CCL3. In contrast to the findings reported in lung tissue of RSVchallenged mice, PVM replication is accelerated in MyD88 gene-deleted bmEos, whereas release of cytokines is dimin- IntroductionEosinophils are unique proinflammatory leukocytes that are easily recognized but poorly understood. Although eosinophil expansion in the bone marrow and recruitment from the bloodstream to peripheral tissues are prominent findings that are clearly associated with asthma, allergic diseases, and infection with helminthes, there is no full consensus about the physiologic or pathophysiologic roles played by eosinophils in any of these disease states. [1][2][3] Interestingly, among the many points that have emerged from the clinical studies featuring therapeutic administration of antiinterleukin 5 (IL-5) monoclonal antibody (mepolizumab), 4-7 it has become evident that we have a very limited understanding of the subtleties of eosinophil recruitment and function; this limited understanding may relate to a long-standing focus on numbers of eosinophils recruited rather than on the nature, quality, and extent of eosinophil activation.With this in mind, we have focused our studies on the role of eosinophils and of eosinophil activation in acute respiratory virus infections, 8 specifically, infections with respiratory syncytial virus (RSV) and pneumonia virus of mice (PVM), a mouse pneumovirus pathogen that replicates the sequelae of the more severe forms of RSV infection in inbred strains of mice. 9,10 Several converging lines of evidence suggest that eosinophils recruited to the lungs in response to pneumovirus infection may have a direct effect on the outcome of disease. Among these findings, several groups have detected immunoreactive eosinophil degranulation products in bronchial washings of patients with the most severe forms of RSV infection, 11,12 and we and others have reported direct recruitment of eosinophils to the lungs of PVM-infected mice. 13-15 RSV and PVM infections of their respective target cells result in the production of numerous proinflammatory cytokines, including the eosinophil chemoattractants RANTES and macrophage inflammatory protein-1␣/CCL3, [16][17][18][19] and RSV-infected tar...

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“…Several large clinical studies have led to the consistent conclusion that RSV-induced severe lower respiratory tract infection in the first year of life is associated with subsequent allergic airway inflammation, recurrent wheeze or asthma from infancy to childhood [69][70][71]. Although the mechanisms remain poorly understood, many studies have implicated the important role of immune response factors [50,[72][73][74][75][76][77].…”

Section: The Role Of Cytokines and Chemokines In Rsv-associated Asthmamentioning

confidence: 99%

The role of cytokines and chemokines in severe respiratory syncytial virus infection and subsequent asthma

Zeng

et al. 2011

Cytokine

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Interleukin‐6, interleukin‐8, interleukin‐11, and interferon‐γ levels in nasopharyngeal aspirates from wheezing children with respiratory syncytial virus or influenza A virus infection

Cited by 40 publications

References 35 publications

Typha orientalis inhibits inflammatory cytokine expression through suppression of ERK phosphorylation in HMC-1 cells

Typha orientalis inhibits inflammatory cytokine expression through suppression of ERK phosphorylation in HMC-1 cells

Pneumoviruses infect eosinophils and elicit MyD88-dependent release of chemoattractant cytokines and interleukin-6

The role of cytokines and chemokines in severe respiratory syncytial virus infection and subsequent asthma

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