Airway Eosinophils, T Cells, Th2-Type Cytokine mRNA, and Hyperreactivity in Response to Aerosol Challenge of Allergic Mice with Previously Established Pulmonary Inflammation

Garlisi, Charles G.; Falcone, A.; Hey, John A.; Paster, T.; Fernandez, Xiomara; Rizzo, Charles A.; Minnicozzi, Michael; Jones, Howard; Billah, M. Motasim; Egan, Robert W.; Umland, Shelby P.

doi:10.1165/ajrcmb.17.5.2866

Cited by 43 publications

(29 citation statements)

References 46 publications

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“…Considering the high expression of Thy-1 on murine TCs [29], [14] and the pathogenic role of TCs in OVA-induced lung inflammation [21], we excluded that the reduced lung inflammation in Thy-1 À/À mice was dependent of the different Thy-1 expression levels on TCs. In Thy-1 BM chimera, the Thy-1-expression was detectable on 70% of TCs.…”

Section: Discussionmentioning

confidence: 99%

“…Considering the high expression of Thy-1 on murine TCs and the pathogenic role of TCs in OVA-induced lung inflammation [20,21], we tested whether the differences observed in Thy-1 À/À mice, compared to WT mice, were merely due to the lack of Thy-1 on TCs. Because Thy-1 is expressed only by TCs and not by other haematopoietic cells, we focused on the expression of Thy-1 on TCs.…”

Section: Tcs Are Not Involved In Decreased Influx Of Inflammatory Celmentioning

confidence: 99%

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Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

et al. 2011

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Human Thy-1 (CD90) has been shown to mediate adhesion of inflammatory cells to activated microvascular endothelial cells via interaction with Mac-1 (CD11b/CD18) in vitro. Since there are no data showing the physiological relevance of Thy-1 for the recruitment of inflammatory cells in vivo, different inflammation models were investigated in Thy-1-deficient mice and littermate controls. In thioglycollate-induced peritonitis, the number of neutrophils and monocytes was significantly diminished in Thy-1-deficient mice. During acute lung inflammation, the extravasation of eosinophils and monocytes into the lung was significantly reduced in Thy-1-deficient mice. Moreover, during chronic lung inflammation, the influx of eosinophils and monocytes was also strongly decreased. These effects were independent of Thy-1 expression on T cells, as shown by the transplantation of WT BM into the Thy-1-deficient mice. In spite of the strong Thy-1 expression on T cells in the chimeric mice, the extravasation of the inflammatory cells in these mice was significantly diminished, compared to control mice. Finally, the altered number and composition of infiltrating leukocytes in Thy-1-deficient mice modified the chemokine/cytokine and protease expression at the site of inflammation. In conclusion, Thy-1 is involved in the control of inflammatory cell recruitment and, thus, also in conditioning the inflammatory microenvironment.Key words: Extravasation . Inflammation . Thy-1 Supporting Information available online IntroductionThe recruitment of inflammatory cells to sites of inflammation plays an important role in the pathogenesis of several inflammatory diseases. Leukocyte adhesion to endothelial cells (ECs) follows a multistep process, including the capture of free leukocytes out of the blood stream, rolling, firm adhesion, and transendothelial diapedesis. The importance of several adhesion molecules in this series of events has been described previously [1]. In ICAM-1-deficient mice, neutrophil recruitment was significantly reduced, but it was not completely blocked in a chemical peritonitis model or in a lipopolysaccharide 645(LPS)-induced airway inflammation model, indicating the involvement of additional adhesion molecules [2,3]. Furthermore, leukocyte recruitment in experimental colitis was not affected by blocking ICAM-1 or MadCAM, whereas the blocking of VCAM-1 resulted in a significant attenuation of colitis [4]. Thus, under specific inflammatory conditions, certain adhesion molecules mediate adhesion and transmigration of leukocytes into the perivascular tissue.Recently, human Thy-1 expressed on ECs was identified as an adhesion molecule mediating the binding of neutrophils and monocytes to activated microvascular ECs [5]. Thy-1 is a highly glycosylated GPI-anchored surface protein and a member of the immunoglobulin superfamily [6,7,8]. In humans, Thy-1 is expressed on ECs at sites of inflammation or in tumours whereas ECs do not express Thy-1 in healthy tissue [5,9]. Thy-1 is also expressed on fibroblasts, neurons, and a su...

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Section: Discussionmentioning

confidence: 99%

Section: Tcs Are Not Involved In Decreased Influx Of Inflammatory Celmentioning

confidence: 99%

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

et al. 2011

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“…It has recently been reported that in mice primarily sensitized with OVA and subsequently challenged with the same Ag through the airways, a reexposure to OVA 1 wk after the first airway challenge results in an augmented allergic response (41). Although various factors could contribute to the augmented response, considering our finding that IgE persists in the airways for Ͼ2 wk after last Ag exposure, it is possible that IgE immune complexes, which are formed in the airways when the mice are reexposed to the Ag, contribute to the potentiated secondary response.…”

Section: Discussionmentioning

confidence: 99%

Role for IgE in Airway Secretions: IgE Immune Complexes Are More Potent Inducers Than Antigen Alone of Airway Inflammation in a Murine Model

Zuberi

Apgar

Chen

et al. 2000

The Journal of Immunology

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IgE is present in airway secretions from human patients with allergic rhinitis and bronchial asthma. However, the contribution of IgE present locally to the overall airway inflammation is not well understood. We hypothesize that Ag-specific IgE can capture airborne Ags and form immune complexes. These immune complexes may function as potent inducers of immune responses in the lung, contributing to the perpetuation of airway inflammation. BALB/c mice were first sensitized with OVA in alum systemically and then challenged with nebulized OVA. Bronchoalveolar lavage (BAL) fluid from these mice contained significant amounts of IgE, of which >50% was Ag specific. The IgE levels in airway secretions remained elevated for more than 15 days after the termination of Ag exposure. Significant amounts of IgE-OVA immune complexes were detected in BAL fluid from the OVA-challenged mice. For comparison of IgE immune complexes vs Ag alone, we treated OVA-immunized mice with intranasal administration of trinitrophenyl-OVA or trinitrophenyl-OVA-anti-DNP IgE. Those treated with the immune complexes showed significantly higher levels of IL-4 and more pronounced eosinophilia in BAL fluid than did those receiving the Ag alone. The IgE immune complexes did not augment the inflammatory response in high affinity IgE receptor (FcεRI)-deficient mice. We conclude that IgE present in the airways can capture the Ag and that the immune complexes thus formed may augment allergic airway response in an FcεRI-dependent manner. Thus, IgE present in airway secretions may facilitate Ag-mediated allergic airway inflammation.

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“…Pulmonary eosinophilia in response to OVA was generated in mice as described previously (25,26). In this experience we modified this model.…”

Section: Induction Of Murine Asthma Modelmentioning

confidence: 99%

Intervention of Thymus and Activation-Regulated Chemokine Attenuates the Development of Allergic Airway Inflammation and Hyperresponsiveness in Mice

Kawasaki

Takizawa²,

Yoneyama

et al. 2001

The Journal of Immunology

245

168

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Thymus- and activation-regulated chemokine (TARC; CCL17) is a lymphocyte-directed CC chemokine that specifically chemoattracts CC chemokine receptor 4-positive (CCR4+) Th2 cells. To establish the pathophysiological roles of TARC in vivo, we investigated here whether an mAb against TARC could inhibit the induction of asthmatic reaction in mice elicited by OVA. TARC was constitutively expressed in the lung and was up-regulated in allergic inflammation. The specific Ab against TARC attenuated OVA-induced airway eosinophilia and diminished the degree of airway hyperresponsiveness with a concomitant decrease in Th2 cytokine levels. Our results for the first time indicate that TARC is a pivotal chemokine for the development of Th2-dominated experimental allergen-induced asthma with eosinophilia and AHR. This study also represents the first success in controlling Th2 cytokine production in vivo by targeting a chemokine.

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Airway Eosinophils, T Cells, Th2-Type Cytokine mRNA, and Hyperreactivity in Response to Aerosol Challenge of Allergic Mice with Previously Established Pulmonary Inflammation

Cited by 43 publications

References 46 publications

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

Role for IgE in Airway Secretions: IgE Immune Complexes Are More Potent Inducers Than Antigen Alone of Airway Inflammation in a Murine Model

Intervention of Thymus and Activation-Regulated Chemokine Attenuates the Development of Allergic Airway Inflammation and Hyperresponsiveness in Mice

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