Intratracheal Instillation Method for Mouse Lungs

Ho, William L.; Furst, Arthur

doi:10.1159/000224748

Cited by 73 publications

(42 citation statements)

References 3 publications

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“…injection of Avertin (4.4 mM 2,2,2-tribromoethanol, 2.5% 2-methyl-2-butanol, in distilled water) using 200 l/10 g body weight. The instillation was performed using a nonsurgical, intratracheal instillation method adapted from Ho and Furst (37). Briefly, the anesthetized mouse was placed with its upper teeth hooked over a wire at the top of a support frame with its jaw held open and a spring pushing the thorax forward to position the pharynx, larynx, and trachea in a vertical straight line.…”

Section: Measurement Of Ll-37-induced Chemokine Production In the Resmentioning

confidence: 99%

The Human Antimicrobial Peptide LL-37 Is a Multifunctional Modulator of Innate Immune Responses

Scott

Davidson

Gold

et al. 2002

The Journal of Immunology

613

581

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The role of LL-37, a human cationic antimicrobial peptide, in the immune system is not yet clearly understood. It is a widely expressed peptide that can be up-regulated during an immune response. In this report, we demonstrate that LL-37 is a potent antisepsis agent with the ability to inhibit macrophage stimulation by bacterial components such as LPS, lipoteichoic acid, and noncapped lipoarabinomannan. We also demonstrate that LL-37 protects mice against lethal endotoxemia. In addition to preventing macrophage activation by bacterial components, we hypothesized the LL-37 may also have direct effects on macrophage function. We therefore used gene expression profiling to identify macrophage functions that might be modulated by LL-37. These studies revealed that LL-37 directly up-regulates 29 genes and down-regulated another 20 genes. Among the genes predicted to be up-regulated by LL-37 were those encoding chemokines and chemokine receptors. Consistent with this, LL-37 up-regulated the expression of chemokines in macrophages and the mouse lung (monocyte chemoattractant protein 1), human A549 epithelial cells (IL-8), and whole human blood (monocyte chemoattractant protein 1 and IL-8), without stimulating the proinflammatory cytokine, TNFα. LL-37 also up-regulated the chemokine receptors CXCR-4, CCR2, and IL-8RB. These findings indicate that LL-37 may contribute to the immune response by limiting the damage caused by bacterial products and by recruiting immune cells to the site of infection so that they can clear the infection.

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Section: Measurement Of Ll-37-induced Chemokine Production In the Resmentioning

confidence: 99%

The Human Antimicrobial Peptide LL-37 Is a Multifunctional Modulator of Innate Immune Responses

Scott

Davidson

Gold

et al. 2002

The Journal of Immunology

613

581

View full text Add to dashboard Cite

show abstract

“…PBS (80 l) containing either DTx (catalog 150; List Biological Laboratories), LPS (Escherichia coli 055:B5; Sigma-Aldrich catalog L4005), or OVA (Sigma-Aldrich; catalog A5503) was applied to mouse tracheae, as previously described, with modifications (29). Briefly, mice were lightly anesthetized using isoflurane and placed vertically, and their tongues were pulled out.…”

Section: Intratracheal (It) Instillationmentioning

confidence: 99%

Distinct Differentiation Potential of Blood Monocyte Subsets in the Lung

Landsman

Varol

Jung

2007

The Journal of Immunology

274

270

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Peripheral blood monocytes are a population of circulating mononuclear phagocytes that harbor potential to differentiate into macrophages and dendritic cells. As in humans, monocytes in the mouse comprise two phenotypically distinct subsets that are Gr1 high CX 3 CR1 int and Gr1 low CX 3 CR1 high , respectively. The question remains whether these populations contribute differentially to the generation of peripheral mononuclear phagocytes. In this study, we track the fate of adoptively transferred, fractionated monocyte subsets in the lung of recipient mice. We show that under inflammatory and noninflammatory conditions, both monocyte subsets give rise to pulmonary dendritic cells. In contrast, under the conditions studied, only Gr1 low CX 3 CR1 high monocytes, but not Gr1 high CX 3 CR1 int cells, had the potential to differentiate into lung macrophages. However, Gr1 high CX 3 CR1 int monocytes could acquire this potential upon conversion into Gr1 low CX 3 CR1 high cells. Our results therefore indicate an intrinsic dichotomy in the differentiation potential of the two main blood monocyte subsets.

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“…injections with OVA (Grade V; Sigma Chem., St. Louis, MO, USA) adsorbed to Al(OH) 3 , which was made according to our previously reported method (13), at a dose of 50 μg OVA adsorbed to 2 mg Al(OH) 3 /0.5 ml PBS per animal on days 0, 14, and 28. The sensitized mice were challenged on days 35, 36, 37, and 40 under inhalation anesthesia with isoflurane (Abbott Japan, Tokyo) with 2% OVA at a volume of 25 μl by intratracheal administration, as reported previously (19). As a negative control group, mice were sensitized with OVA + Al(OH) 3 , i.p.…”

Section: Sensitization and Challengementioning

confidence: 99%

Complete Dependence on CD4+ Cells in Late Asthmatic Response, but Limited Contribution of the Cells to Airway Remodeling in Sensitized Mice

Nabe¹,

Morishita²,

Matsuya³

et al. 2011

J Pharmacol Sci

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Abstract. It is known that the late asthmatic response (LAR), a characteristic feature of asthma, is closely associated with CD4 + Th2 cell-mediated allergic inflammation. Airway remodeling is also a pathogenesis of asthma, but literature reporting roles of CD4 + cells in the remodeling is controversial. There has been no study that simultaneously assessed the roles of CD4 + cells in both LAR and airway remodeling. Sensitized mice were intratracheally challenged with ovalbumin 4 times. Treatment with an anti-CD4 monoclonal antibody (mAb) before the 1st challenge almost completely abolished increase in CD4 + cells in the tissues after the 4th challenge. The late phase increase in airway resistance after the 4th challenge was also completely inhibited by anti-CD4 mAb. Parameters of airway remodeling, subepithelial fibrosis and epithelial thickening were attenuated by treatment, whereas the inhibition was only 30% -40%. Bronchial smooth muscle thickening was not affected. Because interleukin (IL)-5 production as well as eosinophilia was effectively suppressed by anti-CD4 mAb, the effect of anti-IL-5 mAb was also examined, resulting in no inhibition of airway remodeling. Collectively, although the LAR was completely dependent on CD4 + cell activation, airway remodeling was only partially dependent on the cell.

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Intratracheal Instillation Method for Mouse Lungs

Cited by 73 publications

References 3 publications

The Human Antimicrobial Peptide LL-37 Is a Multifunctional Modulator of Innate Immune Responses

The Human Antimicrobial Peptide LL-37 Is a Multifunctional Modulator of Innate Immune Responses

Distinct Differentiation Potential of Blood Monocyte Subsets in the Lung

Complete Dependence on CD4+ Cells in Late Asthmatic Response, but Limited Contribution of the Cells to Airway Remodeling in Sensitized Mice

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