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Blood, Vol. 95 No. 1 (January 1), 2000:
pp. 263-269
IMMUNOBIOLOGY
From the Department of Medicine, University of California, San
Diego; and the Laboratory of Immunology and Vascular
Biology, La Jolla Institute for Experimental Medicine, La
Jolla, CA.
To determine the relative in vivo importance of IL-1 release after
allergen challenge to the subsequent endothelial adhesion and
recruitment of eosinophils, the authors used ovalbumin sensitization and inhalation challenge to induce airway eosinophilia in IL-1 receptor
type 1-deficient and control wild-type mice. Bronchoalveolar lavage
(BAL) eosinophil recruitment in IL-1 receptor type 1-deficient mice
challenged with ovalbumin (24.3% ± 6.3% BAL eosinophils) was
significantly reduced compared with wild-type mice (63.7% ± 2.5%
BAL eosinophils). To determine whether the inhibition of eosinophil
adhesion to vascular endothelium contributed to the inhibition of
eosinophil recruitment in IL-1 receptor type 1-deficient mice, the
authors used intravital microscopy to visualize the rolling and firm
adhesion of fluorescence-labeled mouse eosinophils in the
microvasculature of the allergen-challenged mouse mesentery. Eosinophil
rolling, eosinophil firm adhesion to endothelium, and transmigration
across endothelium (peritoneal eosinophils) were significantly
inhibited in allergen-challenged IL-1 receptor type 1-deficient mice
compared with wild-type mice. Overall, these studies demonstrate that
cytokines such as IL-1, released after allergen challenge, are
important in the induction of endothelial cell adhesiveness, a
prerequisite for the recruitment of circulating eosinophils. (Blood.
2000;95:263-269)
The recruitment of eosinophils from the bone marrow,
where they are produced across inflamed postcapillary venules to tissue sites, is a multistep process.1-3 Bone marrow-derived
eosinophils circulate intravascularly until they are exposed to
inflamed endothelium, as noted at sites of allergic
inflammation.4 Several cytokines (IL-1, tumor necrosis
factor (TNF), IL-4)5-8 and mediators
(histamine)9 released at sites of allergic inflammation are
important upregulators of adhesion molecule expression by the
endothelium. In vitro cytokines such as IL-1 and TNF induce human
umbilical vein endothelial cells to express several adhesion molecules,
including VCAM-1, ICAM-1, E-selectin, and P-selectin.5-7,10
In contrast, cytokines such as IL-4 (induces VCAM-1 but not ICAM-1 or
E-selectin)7,8 and mediators such as histamine (induces
P-selectin)9 induce the expression of a more restricted
profile of endothelial cell adhesion molecules. In vivo specific
endothelium-expressed adhesion molecules, such as
P-selectin11,12 and VCAM-1,11,13 are important
to the initial eosinophil rolling on inflamed endothelium, whereas
endothelium-expressed adhesion molecules, such as
ICAM-111,14,15 and VCAM-1,13,15 are important
to the subsequent eosinophil firm adhesion to endothelium.
We have, therefore, sought to determine the relative importance of an
individual cytokine, IL-1, to eosinophil adhesion to endothelium and to
the subsequent recruitment of eosinophils in a mouse model using IL-1
receptor type 1-deficient mice challenged with allergen. The potential
importance of IL-1 to eosinophilic inflammation and asthma has been
suggested by previous studies16 demonstrating the increased
expression of IL-1 Two forms of IL-1, IL-1 IL-1 R type 1-deficient mice
Mouse model of eosinophilic pulmonary inflammation
Bronchoalveolar lavage cells Bronchoalveolar lavage (BAL) cells from wild-type and IL-1 R type 1-deficient mice were recovered by lavage with 1 mL phosphate-buffered saline (PBS) through a tracheal catheter. The resultant BAL cells were immediately separated from BAL fluid by centrifugation (700g for 5 minutes). An appropriate PBS dilution of the recovered BAL cells was added to trypan blue, and the viability and total number of BAL white blood cells were counted with a hemocytometer. Differential leukocyte counts were performed after brief acetone fixation and staining of the BAL cells with May-Grünwald-Giemsa stains. Eosinophil, neutrophil, and mononuclear cell percentages on each slide were assessed by counting at least 300 cells in random high-power fields using a light microscope (magnification × 40) to display the slide image on a TV monitor (Videometric 150 image analysis program; American Innovision, San Diego, CA).Quantitation of lung eosinophils The number of eosinophils in lung tissue was determined using a sensitive method dependent on the presence of a cyanide-resistant eosinophil peroxidase.36,37 Excised lungs from ovalbumin or PBS-challenged wild-type or IL-1 R type 1-deficient mice were placed in Tissue Tek OCT compound (Sakura Finetek USA, Torrance, CA), snap-frozen in liquid nitrogen, and stored at 70°C. Cryosections (5-µm thick) of lung tissue were cut
onto microscope slides and fixed for 5 minutes in acetone. Slides were
rehydrated in PBS for 5 minutes. The lung sections were incubated at
room temperature for 1 minute in the presence of cyanide buffer (10 mmol/L potassium cyanide, pH 6). Slides were then rinsed
in PBS and incubated for 10 minutes with the peroxidase substrate DAB
(3, 31-diaminobenzine) (Vector Laboratories, Burlingame,
CA). Tissue sections were subsequently washed in PBS before
counterstaining with hematoxylin. Cells that stained dark brown, which
is characteristic of the eosinophil cyanide-resistant
peroxidase,36,37 were counted in 4 random high-power fields
(magnification × 40) in each lung section. Results were
expressed as the number of eosinophils per high-power field (hpf) of
lung tissue.
Immediate hypersensitivity skin test Wild-type and IL-1R type 1-deficient mice were sensitized to ovalbumin as described above. On day 32, 50 µL ovalbumin antigen or diluent control was injected into the shaved backs of the different groups of mice. Immediately after antigen administration, 200 µL 1% Evans blue dye was injected into the tail veins of the mice.38 Bluing size of the skin (measured as the largest transverse diameter in millimeters) at the challenged site was assessed 15 minutes later.Mouse model of peritoneal eosinophilic inflammation: ragweed allergen immunization and peritoneal allergen challenge Techniques used for ragweed immunization and challenge were similar to those previously described in this and other laboratories.11,39,40 Mice were immunized by a series of 5 injections of a 1:1000 dilution of a ragweed pollen extract (Miles, Spokane, WA). On days 0 and 1, 0.1 mL was injected subcutaneously, and on days 6, 8, and 14, 0.2 mL was injected subcutaneously. A control group of ragweed-immunized mice (challenged with PBS diluent) and nonimmunized mice (prepared by subcutaneous injections of isotonic saline instead of the ragweed pollen extract) was kept on the same immunization schedule. Each group of mice studied consisted of 3 to 5 mice. Mice were challenged on day 20 by the intraperitoneal injection of 0.2 mL ragweed allergen (or control PBS diluent).Assessment of eosinophils in the peritoneal cavity At time points before (day 0) and after immunization, and before and 48 hours after intraperitoneal allergen challenge (day 22), the mice were killed by cervical dislocation. Two mL PBS containing 6 U/mL heparin was injected intraperitoneally, the abdomen was massaged, and the peritoneal infusion was collected after the peritoneum was opened. An appropriate PBS dilution of the recovered peritoneal fluid was added to trypan blue, and the viability and total number of white blood cells were assessed and counted with a hemocytometer. Differential leukocyte counts were taken after brief acetone fixation and staining of the peritoneal cells with May-Grünwald-Giemsa stains. Eosinophil percentage on each slide was assessed by counting at least 300 cells in random high-power fields using a light microscope (magnification × 40) to display the slide image on a TV monitor (Videometric 150 image analysis program; American Innovision, San Diego, CA).Isolation of murine eosinophils from IL-5 transgenic mice for fluorescent labeling Mouse eosinophils of 85% to 95% purity and >98% viability were purified from IL-5 transgenic mice (kindly provided by Dr Colin Sanderson)41 using a Percoll gradient as previously described.11 IL-5 transgenic mice (aged 10 weeks) had peripheral blood leukocyte differential cell counts exhibiting about 40% to 60% eosinophils. The contaminating white blood cells comprised about 30% to 40% T lymphocytes, about 2% mononuclear cells, and about 10% neutrophils. Eosinophils with at least 98% viability and >90% purity were selected and labeled with carboxy fluorescein diacetate (CFDA; Molecular Probes, Eugene, OR) as previously described in our laboratory for labeling of murine and human eosinophils.1,11 CFDA-labeled eosinophils were resuspended at a concentration of 0.5 × 107 cells/200 µL PBS containing 0.01% glucose and were kept at room temperature in the dark until used.FACS analysis of mouse eosinophil expression of L-selectin and VLA-4 Expression of L-selectin and VLA-4 integrins on purified
populations of murine eosinophils derived from IL-5 transgenic mice was
determined on a FACSstar flow cytometer (Becton Dickinson, Mountain
View, CA).42 Eosinophils were incubated with the primary monoclonal antibodies (mAb) MEL-14 (a rat antimouse L-selectin IgG2a mAb), PS/2 (a rat antimouse 4 integrin
IgG2b mAb), or species- and isotype-matched mAb on ice for
30 minutes, washed, and incubated with goat-antirat-fluorescein
isothiocyanate IgG (Sigma, St. Louis, MO) for an additional 30 minutes.
Surface expression was determined after gating for eosinophils by
characteristic forward and side light scatter.
Preparation of mice for detection of eosinophil rolling in the peritoneal microcirculation Ragweed-sensitized IL-1R type 1-deficient or control wild-type mice (25-35 g body weight) were prepared for intravital microscopy 24 hours after the final peritoneal ragweed or PBS challenge. We previously reported11 that this 24-hour time point after allergen challenge is optimal for visualizing allergen-induced intravascular eosinophil rolling and adhesion in this mouse model. It was chosen because it slightly precedes peak eosinophil tissue recruitment, which peaks 24 to 48 hours after allergen challenge.11,38-40 Mice were anesthetized with subcutaneous injections of saline solution containing a cocktail of ketamine hydrochloride and xylazine (7.5 mg and 2.5 mg, respectively, per 100 mg body weight). Mice were then placed on a heating pad maintained at 37°C. A midline incision was made, and the mesentery was gently exteriorized and spread on a heated glass window (37.5°C) of the stage of a Leitz intravital microscope. The exteriorized portion of mouse mesentery was kept continuously moist with endotoxin-free isotonic saline solution (pH 7.4). Other parts of the intestine that were exposed but not microscopically observed were kept moist with isotonic saline-soaked cotton pads, and the mesentery was covered with plastic wrap. To minimize endotoxin contamination, the plastic wrap was presoaked with 1% E-Toxa-Clean (Sigma) overnight and then rinsed in 70% ethanol and endotoxin-free distilled water and given a final wash with sterile isotonic saline solution.Visualization of eosinophils in the mouse mesentery Fluorescent CFDA-labeled eosinophils were injected into the tail veins of mice previously sensitized with ragweed allergen and challenged with either ragweed or saline 24 hours before intravital fluorescence microscopy. All studies were conducted 0 to 2 hours after exteriorization of the mouse mesentery. Rolling of mouse eosinophils in mesenteric venules was made visible by stroboscopic epi-illumination using a video-triggered xenon lamp and a Leitz Ploemopak epi-illuminator (Leitz, Wetzlar, Germany) using an I2 filter block. All images were recorded through a silicon-intensified tube camera (SIT68; Dage MTI, Michigan City, IN) using a × 10 or a × 20 water immersion objective (Nikon, Melville, NY) as described previously.11 The rolling fraction (Rf) of CFDA-labeled mouse eosinophils in ragweed-challenged mice (wild-type control and IL-1 R type 1-deficient mice) was determined by frame-by-frame analysis as previously described.11 Rolling eosinophils were quantitated by counting the number of eosinophils interacting with the vessel wall in 1 minute in a plane perpendicular to a vessel axis, whereas cells that were stationary for at least 1 minute were considered adherent eosinophils.Statistics The numbers of eosinophils in lung, BAL fluid, and peritoneal cavity were compared by Student's t-test using a statistical software package (InStat, San Diego, CA). Rolling fractions of injected eosinophils were compared by multiple comparisons of paired data by Student's t-test using a statistical software package (SigmaStat; Jandel Scientific, San Rafael, CA). P < .05 was considered statistically significant. All results are given as mean ± SEM.
Mouse model of eosinophilic lung inflammation Broncho-alveolar lavage. As previously described,36 sensitization and ovalbumin allergen challenge of wild-type mice (n = 3 experiments) induce significant BAL eosinophilia (63.7% ± 2.5% BAL eosinophils) compared with mice that were not sensitized or challenged with ovalbumin (1.1% ± 0.2% BAL eosinophils) (P = .004) or compared with mice immunized with ovalbumin and challenged with PBS diluent (1.9% ± 0.2% BAL eosinophils) (P = .0001). Neutrophils comprised <2% of BAL cells before or after allergen challenge and after diluent challenge. Mononuclear cells comprised the remainder of the BAL cells.
Lung.
Ovalbumin sensitization and challenge also induced significant lung
tissue eosinophilia (97.8 ± 31.3 lung eosinophils/hpf) (n = 3
experiments) compared with mice that were not sensitized or challenged
with ovalbumin (2.5 ± 0.3 lung eosinophils/hpf) (P = .05) or compared with mice immunized with ovalbumin and
challenged with PBS diluent (3.0 ± 0.9 lung eosinophils/hpf)
(P = .002) (Figure 2). Analysis
of lung sections of IL-1 R type 1-deficient mice immunized and
challenged with ovalbumin also demonstrated a significant reduction in
lung eosinophils (IL-1 R type 1-deficient mice 10.5 ± 2.3 lung
eosinophils/hpf vs. wild-type mice 97.8 ± 31.3 lung eosinophils/hpf) (n = 3 experiments) (P = .01) (Figure 2).
There was no significant difference in the number of lung eosinophils in wild-type mice compared with IL-1 R type 1-deficient mice not immunized or challenged with ovalbumin (2.5 ± 0.3 lung
eosinophils/hpf in wild-type vs. 3.1 ± 0.8 lung
eosinophils/hpf in IL-1 R type 1-deficient mice).
Mouse model of eosinophilic peritonitis in IL-1R type
1-deficient mice
Expression of L-selectin and VLA-4 by mouse eosinophils
Intravital microscopy and eosinophil rolling and adhesion in IL-1 R type 1-deficient mice The passage of the fluorescence-labeled eosinophils in the allergen-challenged mesenteric circulation was made visible by stroboscopic epi-illumination (Figure 4). We previously demonstrated36 that peritoneal ragweed challenge induces a significant increase in eosinophil rolling in the mesenteric venules of wild-type mice challenged with ragweed compared with wild-type mice challenged with PBS diluent. Eosinophil rolling in venules of ragweed-challenged IL-1 R type 1-deficient mice (eosinophil rolling fraction 8.2% ± 2.8%) was significantly reduced than it was in ragweed-challenged wild-type mice (eosinophil rolling fraction 16.5% ± 3.9%) (P = .05) (Figure 5A).
In this study we demonstrated that IL-1 R type 1-deficient mice exhibited reduced BAL and lung eosinophil recruitment compared with wild-type mice when challenged by inhaled allergen. This suggested that IL-1 released at sites of allergic inflammation in the lung might have contributed to the recruitment of eosinophils during episodes of allergen-induced asthma. The mechanism by which IL-1 induced eosinophil recruitment was most likely not a direct effect on eosinophil chemotaxis but was more likely an indirect effect on eosinophils mediated by IL-1 upregulation of endothelial cell adhesion molecules that bind circulating eosinophils. This hypothesis is supported by our intravital videomicroscopy studies demonstrating that eosinophils exhibited reduced rolling and firm adhesion to allergen-challenged endothelium in IL-1 R type 1-deficient mice in vivo. IL-1, by binding to the IL-1 R type 1 on endothelial cells, induces endothelial cells to express adhesion receptors capable of supporting eosinophil rolling (P-selectin, VCAM-1)10,11,13 and of supporting eosinophil firm adhesion (ICAM-1, VCAM-1)11,14 in vivo. The absence of IL-1 R type 1 on endothelial cells in IL-1 R type 1-deficient mice could therefore have resulted in reduced expression of these adhesion molecules and the reduced eosinophil rolling and adhesion we noted. An additional consequence of the reduced eosinophil rolling and endothelial cell adhesion could be the reduced eosinophil recruitment we noted in the lung and in the peritoneal cavity of IL-1 R type 1-deficient mice after allergen challenge.
The authors thank Dr J. Peschon (Immunex, Seattle, WA) for providing IL-1 R type 1-deficient mice and Dr Colin Sanderson (Perth, Australia) for providing IL-5 transgenic mice, Greg Hughes and Mark Santoz for technical assistance, and Lanesha Hill for expert secretarial support during the preparation of the manuscript.
Submitted April 9, 1999; accepted September 2, 1999.
Supported by National Institutes of Health grants AI 33977 and AI 38425 (DHB) and AI 35796 and California Tobacco-Related Disease Research program grant 7RT0197 (PS).
Reprints: David H. Broide, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0635; e-mail: dbroide{at}ucsd.edu.
The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked "advertisement" in accordance with 18 U.S.C. section 1734.
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 N. W. Lukacs, A. John, A. Berlin, D. C. Bullard, R. Knibbs, and L. M. Stoolman E- and P-Selectins Are Essential for the Development of Cockroach Allergen-Induced Airway Responses J. Immunol., August 15, 2002; 169(4): 2120 - 2125. [Abstract] [Full Text] [PDF]
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 D. H. Broide, M. Miller, D. Castaneda, J. Nayar, J. Y. Cho, M. Roman, L. G. Ellies, and P. Sriramarao Core 2 oligosaccharides mediate eosinophil and neutrophil peritoneal but not lung recruitment Am J Physiol Lung Cell Mol Physiol, February 1, 2002; 282(2): L259 - L266. [Abstract] [Full Text] [PDF]
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D. H. Broide, G. Stachnick, D. Castaneda, J. Nayar, and P. Sriramarao Inhibition of Eosinophilic Inflammation in Allergen-Challenged TNF Receptor p55/p75- and TNF Receptor p55-Deficient Mice Am. J. Respir. Cell Mol. Biol., March 1, 2001; 24(3): 304 - 311. [Abstract] [Full Text] [PDF]
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L. H. K. Lim, B. S. Bochner, and E. M. Wagner Leukocyte recruitment in the airways: an intravital microscopic study of rat tracheal microcirculation Am J Physiol Lung Cell Mol Physiol, May 1, 2002; 282(5): L959 - L967. [Abstract] [Full Text] [PDF]
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Abstract
Introduction
mRNA and protein in the airway of patients with
symptomatic asthma compared with those with asymptomatic asthma. In
addition, increased nocturnal levels of IL-1
