Bronchoalveolar lavage cytokine profiles in acute asthma and acute bronchiolitis

Kim, Chang Keun; Kim, Sang Woo; Park, Choon-Sik; Kim, Beyong Il; Kang, Hee Joon; Koh, Young Yull

doi:10.1067/mai.2003.1618

Cited by 93 publications

(87 citation statements)

References 38 publications

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“…More importantly, CCL11, but not CCL5, mediated most of the eosinophil chemotactic activity in the culture supernatant of the poly(I:C)/IL-4-stimulated BSMC. These observations suggest that, in the Th2-dominant microenvironment, respiratory virus infections can exacerbate the eosinophilic inflammation of the airways via the production of CCL11, as observed in a proportion of patients with RSV infections (5).…”

Section: Discussionmentioning

confidence: 92%

“…The number of eosinophils and the concentration of eosinophil cationic protein in induced sputum have been correlated with an increase in bronchial responsiveness during experimental rhinovirus infections in adult asthmatics (3). A marked eosinophilic inflammation of the airways was observed in a substantial proportion of children with RSV bronchiolitis (4,5), and the pathologic changes in the airways of mice with RSV infection mimicked eosinophilic bronchiolitis in humans, especially in allergen-sensitized and exposed animals (6,7).…”

Section: Tlr3-mediated Synthesis and Release Of Eotaxin-1/ccl11 From mentioning

confidence: 99%

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TLR3-Mediated Synthesis and Release of Eotaxin-1/CCL11 from Human Bronchial Smooth Muscle Cells Stimulated with Double-Stranded RNA

Niimi

Asano

Shiraishi

et al. 2007

The Journal of Immunology

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Respiratory infections with RNA viruses, such as rhinovirus or respiratory syncytial virus, are a major cause of asthma exacerbation, accompanied by enhanced neutrophilic and/or eosinophilic inflammation of the airways. We studied the effects of dsRNA synthesized during RNA virus replication, and of its receptor, TLR3, on the synthesis of eosinophilic chemokines in bronchial smooth muscle cells (BSMC). Synthetic dsRNA, polyinosinic-cystidic acid (poly(I:C)), induced the synthesis of eosinophilic chemokines, eotaxin-1/CCL11 and RANTES/CCL5, from primary cultures of human BSMC, and IL-4 increased synergistically the synthesis of poly(I:C)-induced CCL11. A robust eosinophil chemotactic activity was released from BSMC stimulated with poly(I:C) and IL-4, which was mostly inhibited by preincubation with an anti-CCL11, but not with an anti-CCL5 Ab. Although the immunoreactivity of TLR3 was detectable on the cellular surface of BSMC by flow cytometric analysis, pretreatment with an anti-TLR3-neutralizing Ab failed to block the poly(I:C)-induced synthesis of CCL11. We have determined by confocal laser-scanning microscopy that the immunoreactivity of TLR3 was aggregated intracellularly in poly(I:C)-stimulated BSMC, colocalizing with fluorescein-labeled poly(I:C). The synthesis of CCL11 was prominently inhibited by the transfection of TLR3-specific small interfering RNA or by bafilomycin A1, an endosomal acidification inhibitor, further supporting the essential role played by intracellular TLR3 in the synthesis of poly(I:C)-induced CCL11 in BSMC. In conclusion, these observations suggest that, by activating intracellular TLR3 in BSMC, respiratory RNA virus infections stimulate the production of CCL11 and enhance eosinophilic inflammation of the airways in the Th2-dominant microenvironment.

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Section: Discussionmentioning

confidence: 92%

Section: Tlr3-mediated Synthesis and Release Of Eotaxin-1/ccl11 From mentioning

confidence: 99%

TLR3-Mediated Synthesis and Release of Eotaxin-1/CCL11 from Human Bronchial Smooth Muscle Cells Stimulated with Double-Stranded RNA

Niimi

Asano

Shiraishi

et al. 2007

The Journal of Immunology

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“…Interferon-gamma (IFNγ), is one of the primary cytokines produced by Th1 cells, and has been implicated as part of the disease-sparing Th1 response to RSV infection [42]. IFNγ is also produced by T cells, NK cells and activated macrophages, and is detected in nasal washings and bronchoalveolar lavage fluids from patients with acute HRSV infection [43][44][45], and IFNγ gene polymorphisms have been associated with the severity of lower respiratory tract infection [46]. The role of IFNγ has also been explored in the HRSV mouse challenge model [47][48][49] and has been detected in lung tissue in response to acute infection with virulent PVM J3666 [50; Table 3].…”

Section: Discussionmentioning

confidence: 99%

Mucosal inoculation with an attenuated mouse pneumovirus strain protects against virulent challenge in wild type and interferon-gamma receptor deficient mice

Ellis

Martin

Waldner

et al. 2007

Vaccine

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Protective mechanisms underlying the responses to mucosal vaccination are not yet clearly defined. Using the natural mouse pneumovirus pathogen, pneumonia virus of mice (PVM), we explore responses of wild type and interferon-gamma (IFNγ) receptor gene-deleted mice to virulent challenge after mucosal vaccination with an attenuated virus strain. Serum neutralizing antibodies develop after intranasal inoculation with 30 pfu of attenuated, replication-competent PVM strain 15, which correlate with diminished gross and microscopic pulmonary pathology and protection from weight loss in response to subsequent challenge with the virulent parent PVM strain J3666. Virus replication in response to challenge was blunted in PVM strain 15 vaccinated mice, as was local production of secretory mediators IFNγ, TNF-α, MIP-1α, and MIP-2. Interestingly, responses of vaccinated IFNγ receptor gene-deleted mice were indistinguishable from those of the wild type, suggesting that IFNγ signaling may not be crucial for the generation of adaptive responses to pneumovirus infection in vivo. (150 words).

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“…Such virus-induced M2R dysfunction is seen in nonatopic humans (38), which may be secondary to increased interferon (IFN)-c. The IFN-c is higher in nonallergen virus-infected animals (49) and humans (50), it positively correlates with AHR in humans (51), and it decreases M2R expression in nerve cell culture (52).…”

Section: Tissue Localization and Activation Status Of The Eosinophil mentioning

confidence: 99%

The rise of the phoenix: the expanding role of the eosinophil in health and disease

Adamko

Odemuyiwa

Vethanayagam

et al. 2004

Allergy

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We have entered a new phase in the evolution of our understanding of the role of the eosinophil with a greater appreciation of novel potential functions that may be ascribed to this enigmatic cell type. This review not only provides an update to our current understanding of the various immunobiological roles for the eosinophil, but also attracts attention to some novel observations predicting functions beyond its putative effector role. These observations include the intriguing possibility that the eosinophil may posses the capacity to regulate the immune and inflammatory responses in diseases such as asthma.

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Bronchoalveolar lavage cytokine profiles in acute asthma and acute bronchiolitis

Cited by 93 publications

References 38 publications

TLR3-Mediated Synthesis and Release of Eotaxin-1/CCL11 from Human Bronchial Smooth Muscle Cells Stimulated with Double-Stranded RNA

TLR3-Mediated Synthesis and Release of Eotaxin-1/CCL11 from Human Bronchial Smooth Muscle Cells Stimulated with Double-Stranded RNA

Mucosal inoculation with an attenuated mouse pneumovirus strain protects against virulent challenge in wild type and interferon-gamma receptor deficient mice

The rise of the phoenix: the expanding role of the eosinophil in health and disease

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