Pulmonary responses to bronchoconstrictor agonists in the mouse

Martin, Thomas R.; Gerard, Norma P.; Galli, Stephen J.; Drazen, J. M.

doi:10.1152/jappl.1988.64.6.2318

Cited by 227 publications

(194 citation statements)

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“…Airway responsiveness was assessed as a change in airway function after challenge with aerosolized methacholine (MCh) via the airways. Anesthetized, tracheostomized mice were mechanically ventilated and lung function was assessed as a modification to described procedures (5,14,15). Lung resistance (R L ) and dynamic compliance (C dyn ) were continuously computed (LABVIEW, National Instruments, Austin, TX) by fitting flow, volume, and pressure to an equation of motion.…”

Section: Methodsmentioning

confidence: 99%

“…injection with anti-TCR-␦ mAbs were exposed to aerosolized OVA on 3 consecutive days. Forty-eight hours later, airway responsiveness was assessed as changes in R L and C dyn in response to inhaled MCh (14,15). In both-genetically deficient and Abdepleted mice-airway responsiveness was similarly increased, ruling out as a cause for increased airway reactivity long-term developmental changes caused by the absence of ␥␦ T cells.…”

Section: Airway Responsiveness Is Regulated By Pulmonary ␥␦ T Cellsmentioning

confidence: 99%

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MHC class I-dependent Vγ4⁺pulmonary T cells regulate αβ T cell-independent airway responsiveness

Lahn

Kanehiro

Takeda

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

110

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Section: Methodsmentioning

confidence: 99%

Section: Airway Responsiveness Is Regulated By Pulmonary ␥␦ T Cellsmentioning

confidence: 99%

MHC class I-dependent Vγ4⁺pulmonary T cells regulate αβ T cell-independent airway responsiveness

Lahn

Kanehiro

Takeda

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

110

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“…In some mice, airway responses to graded doses of methacholine were assessed 24 hours after the last intranasal challenge, either by a noninvasive approach (as described in Williams and Galli, 19 with results reported as enhanced respiratory pause [Pen]) or by an invasive approach. 20 Briefly, mice were deeply anesthetized with ketamine intramuscularly, and surgically intubated. Intubated mice were connected to plethysmograph chambers (PLY3111; Buxco Research Systems, Wilmington, NC) with a ventilator (type 845; Hugo Sachs Elektronik-Harvard Apparatus, March-Hugstetten, Germany) and mechanically ventilated.…”

Section: Induction Of Neutrophilic Airway Inflammationmentioning

confidence: 99%

Mast cell–derived TNF can promote Th17 cell–dependent neutrophil recruitment in ovalbumin-challenged OTII mice

Nakae

Suto

Berry

et al. 2006

Blood

144

124

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IntroductionSeveral proinflammatory cytokines, including TNF, IL-1, and IL-17, can directly induce neutrophil recruitment. For example, inhalation of recombinant TNF, IL-1, or IL-17 can provoke neutrophil infiltration into the airways. [1][2][3] These cytokines can also play important roles in the pulmonary neutrophilia induced by infection with the Gram-negative bacteria Klebsiella pneumoniae, and can contribute to bacterial clearance. [4][5][6] However, both the roles of these proinflammatory cytokines, and the most important cellular sources of their production, can vary according to the models of inflammation analyzed. For example, in mice, mast cell-derived TNF has been reported to contribute importantly to neutrophil recruitment and host defense against K. pneumoniae. 7 By contrast, it has been reported that 8,9 but neither TNF nor IL-1, 10 is important for the pulmonary neutrophilia induced by LPS, a component of Gram-negative bacteria.To date, no reports have investigated the possible role of mast cells in the development of T helper 17 (Th17) cell-dependent, neutrophil-rich inflammatory responses, either in the airways or in other anatomical sites. To address this question, we decided to use a model of protein antigen (Ag) (ovalbumin [OVA])-induced neutrophil-predominant airway inflammation in OVA-specific T-cell receptor (TCR)-expressing mice. We took this approach because of reports indicating that OVA challenge can induce neutrophil-rich airway inflammation in OVA-specific TCR-expressing BALB/c-DO11.10 mice, 11,12 and that IL-17 is required for the induction of airway hyperreactivity (AHR) in this model. 13 However, we elected to use OVA-specific TCR-expressing C57BL/6-OTII mice, 14 instead of BALB/c-DO11.10 mice, for the work reported herein. C57BL/6-OTII mice are on the same strain background as mice that are either profoundly deficient in mast cells, lack the FcR␥ chain (that is required for the activation of mast cells via either the Fc⑀RI or Fc␥RIII that are expressed on their surface 15,16 ), or lack IL-17 or any of several other specific cytokines or cytokine receptors. Therefore, by working with C57BL/6-OTII mice, we were able to use a genetic approach to investigate in detail the importance of each of these candidate elements in the airway neutrophil infiltration elicited by OVA challenge in this model. Materials and methods Experimental approachWe first established and characterized a model of OVA-induced neutrophilrich airway inflammation in OVA-specific TCR-expressing C57BL/6-OTII mice. We then used a combination of pharmacologic and genetic approaches to investigate the potential roles of individual mediators, cytokines, and chemoattractants in the development of the neutrophil-rich airway inflammation induced by Ag challenge in this model. Finally, we used a genetic approach to investigate the roles of FcR␥, mast cells, and mast cell-derived TNF in this model of Ag-and Th17 cell-dependent, neutrophil-rich airway inflammation. The online version of this article contains a data supplement...

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“…Flow was calculated by differentiation of the volume signal, transpulmonary pressure was measured as the difference of tracheal cannula and box pressure, and lung resistance was calculated as reported previously. 43 Lung resistance (R L ) was measured before and after each dose (26 to 34 l volume) of intravenous methacholine (MCh). Percent baseline R L was calculated by dividing the greatest R L value obtained after MCh injection by the baseline value obtained immediately before and multiplying the result by 100.…”

Section: Measurement Of Airway Responsivenessmentioning

confidence: 99%

Critical Role for Galectin-3 in Airway Inflammation and Bronchial Hyperresponsiveness in a Murine Model of Asthma

Zuberi

Hsu

Kalaycı

et al. 2004

The American Journal of Pathology

160

154

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Galectin-3 is a member of a ␤-galactoside-binding animal lectin family. Previous in vitro studies have demonstrated that galectin-3 is involved in a number of activities; however, the roles of this lectin in physiological and pathological processes in vivo remain to be elucidated. Herein, we show, in a murine model of ovalbumin (OVA)-induced asthma that 1) peribronchial inflammatory cells expressed large amounts of galectin-3; 2) bronchoalveolar lavage fluid from OVAchallenged mice contained significantly higher levels of galectin-3 compared to control mice; and 3) macrophages in bronchoalveolar lavage fluid were the major cell type that contained galectin-3. We investigated the role of galectin-3 in the allergic airway response by comparing galectin-3-deficient (gal3 ؊/؊ ) mice and wild-type (gal3 ؉/؉ ) mice. OVA-sensitized gal3 ؊/؊ mice developed fewer eosinophils and lower goblet cell metaplasia, after airway OVA challenge compared to similarly treated gal3 ؉/؉ mice. In addition, the OVA-sensitized gal3 ؊/؊ mice developed significantly less airway hyperresponsiveness after airway OVA challenge compared to gal3 ؉/؉ mice. Finally, gal3 ؊/؊ mice developed a lower Th2 response, but a higher Th1 response, suggesting that galectin-3 regulates the Th1/Th2 response. We conclude that galectin-3 may play an important role in the pathogenesis of asthma and inhibitors of this lectin may prove useful for treatment of this disease.

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Pulmonary responses to bronchoconstrictor agonists in the mouse

Cited by 227 publications

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MHC class I-dependent Vγ4⁺pulmonary T cells regulate αβ T cell-independent airway responsiveness

MHC class I-dependent Vγ4⁺pulmonary T cells regulate αβ T cell-independent airway responsiveness

Mast cell–derived TNF can promote Th17 cell–dependent neutrophil recruitment in ovalbumin-challenged OTII mice

Critical Role for Galectin-3 in Airway Inflammation and Bronchial Hyperresponsiveness in a Murine Model of Asthma

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Pulmonary responses to bronchoconstrictor agonists in the mouse

Cited by 227 publications

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MHC class I-dependent Vγ4+pulmonary T cells regulate αβ T cell-independent airway responsiveness

MHC class I-dependent Vγ4+pulmonary T cells regulate αβ T cell-independent airway responsiveness

Mast cell–derived TNF can promote Th17 cell–dependent neutrophil recruitment in ovalbumin-challenged OTII mice

Critical Role for Galectin-3 in Airway Inflammation and Bronchial Hyperresponsiveness in a Murine Model of Asthma

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MHC class I-dependent Vγ4⁺pulmonary T cells regulate αβ T cell-independent airway responsiveness

MHC class I-dependent Vγ4⁺pulmonary T cells regulate αβ T cell-independent airway responsiveness