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PubMed1997

Bronchial and bronchoalveolar inflammation in single early and dual responders after allergen inhalation challenge.

To characterize the cellular inflammation at the bronchial and bronchoalveolar levels, we evaluated 43 patients with asthma who were sensitized to house dust mites. On 2 consecutive days patients underwent methacholine challenge and allergen bronchial challenge. In addition, 6, 24, or 72 h after allergen challenge, fiberoptic bronchoscopy with bronchial lavage (BL) and bronchoalveolar lavage (BAL) was performed. Patients belonging to the 6-h, 24-h, or 72-h group were divided further into two subgroups: those with isolated early response to allergen (LAR-), and those with dual response to allergen (LAR+). The percentage of eosinophils and of epithelial cells in BAL fluid was significantly higher in LAR+ than in LAR- patients in the 6-h group (p < 0.05, each comparison), but not 24 or 72 h after (p > 0.05, each comparison). Similarly, the proportion of BL eosinophils was also higher in LAR+ than in LAR- patients, both in the 6-h and in the 24-h group (p < 0.05, each comparison). In addition, increased proportions of BL neutrophils were present in the LAR+ patients belonging to the 24-h group (p < 0.05). Comparing "proximal" = BL vs "distal" = BAL data, we found a significantly higher proportion of epithelial cells in BL compared with BAL, in both LAR- and LAR+ subjects, either 6, or 24, or 72 h after challenge (p < 0.01, each comparison) and increased percentages of BL neutrophils and eosinophils in LAR+ patients (p < 0.05, each comparison), but not in LAR- patients, in the 24-h group. The percentages of BL or BAL macrophages and lymphocytes did not differ significantly among the different patient groups. These data indicate that the development of LAR after allergen inhalation challenge is associated with an early recruitment of eosinophils and with epithelial desquamation in the airways. In addition, after allergen challenge epithelial desquamation is more pronounced in the proximal than in the distal airways, independently of the type of bronchial response.

Adolescent↗

PubMed2006

Role of matrix metalloproteinases in the inflammatory response in human airway cell-based assays and in rodent models of airway disease.

Since the discovery of the first matrix metalloproteinase (MMP), this ever-growing family of proteinases has been the subject of intense research. Although it was initially believed that MMPs were solely involved in matrix turnover and degradation, there are now data suggesting MMPs are actively involved in the inflammatory process. In previous studies, we have demonstrated an increase in MMP expression in human cell-based assays and in preclinical rat models of airway inflammation. Therefore, the aim of this study was to characterize the role of MMPs in these models by profiling the impact of a broad-spectrum MMP inhibitor. In lipopolysaccharide (LPS)-stimulated THP-1 cells and primary human lung tissue macrophages, the MMP inhibitor had no significant effect on the release of tumor necrosis factor-alpha, interleukin (IL)-8, IL-1 beta, growth-regulated oncogene-alpha, macrophage inflammatory protein-1 alpha, or IL-6 whereas dexamethasone has a significant impact on all cytokines from both cell types. Similarly, in the more biologically complex LPS-driven rat model of airway inflammation, the MMP inhibitor did not have an impact on mediator release and cellular burden. The compound did, however, significantly reduce levels of lung MMP-9. Furthermore, in a "disease" model, the compound did not affect cellular inflammation but did significantly reduce elastase-induced experimental emphysema. In summary, these data demonstrate for the first time that MMPs do not play a role in the increase in inflammatory mediators or cellular burden observed in these preclinical models. However, they do appear to be involved in the elastase-driven breakdown of airway structure, which is not due to a direct effect of the stimulus.

Animals↗

PubMed1990

Cellular immune response to Ia induction by intraocular gamma-interferon.

BALB/c mice and Lewis rats were injected intraocularly with recombinant gamma-interferon (IFN-gamma). The distribution of Ia antigens and cellular infiltrates was studied over a 21-day time course. In mice, Ia antigens were induced on cells in the corneal stroma, corneal endothelium, iris, ciliary body, retinal pigment epithelium and cells in the retina. No detectable cellular infiltrate accompanied class II major histocompatibility (MHC) antigen induction in mice. In rats, cells in all of the intraocular tissues mentioned above were induced to express Ia antigens. However, in distinct contrast to mice, the induction of Ia antigens on intraocular structures in rats was accompanied by intense cellular inflammation composed predominantly of polymorphonuclear cells. These findings demonstrate that aberrant Ia expression on intraocular tissues by IFN-gamma is not sufficient to elicit a cellular autoimmune response in mice. The observed species-related differences in cellular immune response to class II MHC antigen induction on intraocular tissues parallels the susceptibility of mice and rats to experimental autoimmune uveitis.

Animals↗

PubMed1992

Effects of prazosin on the blood-brain barrier during experimental autoimmune encephalomyelitis.

Alterations in normal function of the blood-brain barrier (BBB) are important in the pathophysiology of multiple sclerosis and its laboratory counterpart, experimental autoimmune encephalomyelitis (EAE). As part of studies on drugs that affect vascular tone in rats with EAE, we have shown previously that the specific alpha 1-adrenoreceptor antagonist, prazosin, suppressed clinical and pathologic disease. In the present study we used quantitative morphometric analysis of capillary endothelium and the tracer horseradish peroxidase (HRP) to define effects of this drug on vascular events associated with central nervous system edema. In prazosin-treated and saline-treated EAE rats, protein extravasation in the spinal cord correlated with clinical presentation. Consistent with our previous data, the results showed that increased edema was associated with increased vesicular content of capillary endothelium. In prazosin-treated rats with no clinical signs, vesicular content was comparable to that found in normal animals. With increasing severity of disease, vesicular content increased and mitochondrial content decreased. In both prazosin- and saline-treated rats, mitochondrial content was reduced even when clinical signs were slight, and sharply declined when clinical signs increased. These results suggest that damage to mitochondria may be associated with early pathological events. In prazosin-treated animals, HRP accumulated in pericytes, suggesting that these cells were a target for the action of prazosin and may restrict the extravasation of fluid into the perivascular parenchyma. Our results underscore the presence of capillary changes associated with inflammation of the central nervous system, in addition to the well-recognized cellular inflammation that is targeted to the venular bed. The extent of capillary changes was closely associated with extent of tracer leakage in the spinal cord and support the conclusion that transcytotic vesicles are involved in transport of edema fluid during EAE, and that high mitochondrial levels are important for the normal function of BBB endothelium.

Animals↗

PubMed2006

Tapered progesterone withdrawal promotes long-term recovery following brain trauma.

We previously demonstrated that after traumatic brain injury (TBI), acute progesterone withdrawal (AW) causes an increase in anxiety behaviors and cerebro-cellular inflammation compared to tapered progesterone withdrawal (TW). Our current study investigates the behavioral and cellular effects of AW two weeks after termination of treatments to determine the longer-term influence of withdrawal after injury. Adult, male Sprague-Dawley rats received either bilateral frontal cortex contusion (L) or sham (S) surgery. Rats were injected at 1 and 6 h post-injury, then every 24 h for six days. Vehicle (V)-treated rats were given 9 injections of 22.5% cyclodextrin, whereas AW rats received 9 injections of 16 mg/kg progesterone and TW rats received 7 injections of P at 16 mg/kg, followed by one at 8 mg/kg and one at 4 mg/kg. On day 8, sensory neglect and locomotor activity tests were initiated. Animals were killed 22 days post-TBI and the brains prepared for either molecular or histological analysis. Western blotting revealed increased brain-derived neurotrophic factor (BDNF) and heat shock protein 70 (HSP70) in TW vs. AW animals. P53 was increased in VL animals, whereas all progesterone-treated groups were equivalent to shams. TW animals had markedly decreased sensory neglect compared to AW animals and increased center time in locomotor activity assays. In addition, lesion reconstruction revealed a decreased lesion size for TWL over AWL over VL animals. Glial fibrillary acidic protein (GFAP) immunofluorescent staining followed this pattern as well. In conclusion, after TBI, AW affects select behaviors and molecular markers in the chronic recovery period.

Anesthetics↗

PubMed1999

Role of bronchoscopy in asthma research.

Over the past 15 years, much has been learned about the presence of airway inflammation in asthma through the use of investigative bronchoscopy. It has become quite clear that inflammation is present even in mild asthma. In addition to the eosinophils, T-lymphocytes and a variety of cytokines have been identified to play a prominent role in asthmatic inflammation. The concept of delayed asthmatic response after allergen exposure and its relationship to cellular inflammation and airway hyper-reactivity has become more clearly established. Our understanding of asthmatic airway inflammation, however, is incomplete. As interesting as the database has been so far, investigative FB has not defined a unique profile for patients with asthma. Specifically, lavage or endobronchial biopsy has not identified parameters that help in the diagnosis, assessment of disease severity, prognosis, or likelihood to respond to specific therapies. Also, the exact relationship between parameters in lavage compared with mucosal biopsy and how these are related to airway hyper-reactivity and the clinical syndrome of asthma remains poorly understood. In this regard, it must be confessed that currently FB with lavage and biopsy in asthmatics needs to be considered as a research tool for specimen retrieval to help characterize and express inflammation. Although these techniques have contributed immensely to our understanding of asthma pathogenesis, presently these techniques do not have any practical role or clinical usefulness.

Asthma↗

PubMed2005

Testosterone augments endotoxin-mediated cerebrovascular inflammation in male rats.

Activation of inflammatory mechanisms contributes to cerebrovascular pathophysiology. Male gender is associated with increased stroke risk, yet little is known about the effects of testosterone in the cerebral circulation. Therefore, we explored the impact of testosterone treatment on cerebrovascular inflammation with both in vivo and in vitro models of inflammation. We hypothesized that testosterone would augment the expression of two vascular markers of cellular inflammation, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). Using four groups of male rats [intact, orchiectomized (ORX), and ORX treated with either testosterone (ORXT) or the testosterone metabolite 17beta-estradiol (ORXE)], we determined effects of the sex hormones on cerebrovascular inflammation after intraperitoneal LPS injection. Western blot analysis showed that induction of inflammatory markers was increased in cerebral blood vessels from ORXT rats compared with intact or ORX rats. In contrast, in cerebral blood vessels from ORXE rats, there was a significant decrease in endotoxin-induced COX-2 and iNOS protein levels. Confocal microscopy of cerebral blood vessels from ORXT rats showed increased COX-2 and iNOS immunoreactivity in both endothelial and smooth muscle cells after LPS treatment. In vitro incubation with LPS also induced COX-2 in pial vessels isolated from the four animal treatment groups, with the greatest induction observed in ORXT vessels compared with the ORX and ORXE groups. Production of PGE2, a principal COX-2-derived prostaglandin end product, was also greatest in cerebral vessels isolated from ORXT rats. In conclusion, testosterone increases cerebrovascular inflammation; this effect may contribute to stroke differences between men and women.

Animals↗

PubMed1994

Ultrastructural studies of the blood-retina barrier after exposure to interleukin-1 beta or tumor necrosis factor-alpha.

BACKGROUND: During inflammatory conditions of the central nervous system (CNS), the protective function of the blood-brain barrier (BBB) may be compromised, resulting in CNS edema. However, it is not well understood how inflammatory cells may increase BBB permeability, since increased transendothelial transport of serum proteins is observed in CNS capillaries that are not directly in contact with inflammatory cells. One possible explanation may be that soluble inflammatory factors may cause BBB changes, since pathologic conditions that increase circulating cytokines produce detectable increases in BBB permeability. EXPERIMENTAL DESIGN: To investigate the role of inflammatory cytokines in induction of endothelial cell changes and inflammation in the CNS, we utilized the rabbit retinal system as a model. This system shows vascularization similar to the BBB, and is termed the blood-retina barrier (BRB). The rabbit visual system allows injection of cytokines, causing minimal trauma, and the contralateral eye serves as an intra-animal control. RESULTS: Ultrastructural morphometric analysis of vesicular content in BRB endothelium showed significant increase at 3 hours postintravitreal injection of interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha (TNF-alpha). Increased transport did not correlate with increased vitreal protein. However, intravascular tracer (horseradish peroxidase) revealed that pericytes, Müller cells, and perivascular microglia accumulate serum proteins, thus acting as sinks for extravasated proteins after BRB disruption. The IL-1 beta-induced inflammatory response was characterized by polymorphonuclear and mononuclear cells, whereas the TNF-alpha-induced response was less intense and comprised monocytes and occasional eosinophils. At the height of inflammation, IL-1 beta produced large gaps between endothelial cells that allowed for extensive cellular inflammation and hemorrhage. TNF-alpha induced necrotic changes on endothelial cells, being most severe at 3 hours postintravitreal injection, revascularization was noted at 24 hours postintravitreal injection. CONCLUSIONS: These results demonstrate that proinflammatory effects of IL-1 beta and TNF-alpha in the BRB initiate many of the changes associated with inflammation of the CNS vasculature, such as those induced during experimental autoimmune encephalitis and multiple sclerosis. Once the permeability of the BRB endothelium is increased, perivascular phagocytic cells such as perivascular, microglia and Müller cells may act as secondary barriers to extravasated proteins.

Animals↗

PubMed2004

Relationship of small airway chymase-positive mast cells and lung function in severe asthma.

Distal lung inflammation may be important in asthma pathophysiology. The goal of this study was to measure cellular inflammation in the large airway and four distal lung regions (small airway inner and outer wall, alveolar attachments, and peripheral alveolar tissue) and to correlate the specific inflammatory cells with several lung function parameters. Sections of concurrently obtained endobronchial and transbronchial/surgical biopsy tissue from 20 individuals with severe asthma were immunostained for T-lymphocyte, eosinophil, monocyte/macrophage, neutrophil, and two mast cell markers (tryptase and chymase). Specific cell distributions were determined and correlated with lung function measures. The number of inflammatory cells generally increased toward the periphery, but the percentage of T-lymphocytes, eosinophils, monocytes/macrophages, and neutrophils remained similar or decreased from large to small airways. In contrast, mast cell number, percentage, and the chymase-positive phenotype increased in small airway regions. After the analysis was adjusted for multiple comparisons, only chymase-positive mast cells significantly and positively correlated with lung function. Such a relationship was seen only in the small airway/alveolar attachments lung region (r(s) = 0.61-0.89; p </= 0.001 for all correlations). These data suggest that induction of chymase-positive mast cells, particularly in the small airway outer wall/alveolar attachments region, may be protective for lung function in severe asthma.

Adult↗

PubMed1993

Clinical relevance of cellular mediators of inflammation in workers exposed to asbestos.

To identify the clinical relevance of cellular mediators of inflammation in workers exposed to asbestos, we investigated the relationship between inflammatory products primarily released by alveolar macrophages and the clinical expression of asbestos-induced interstitial fibrosis. Our study population consisted of 93 white men who had been occupationally exposed to asbestos and were on average 60 yr of age. Pulmonary function tests, chest radiographs, high-resolution CT scans, and bronchoalveolar lavage (BAL) were performed on almost all study subjects; 11 (11.8%) had restrictive lung function, 22 (23.7%) had abnormal gas exchange, 30 (32.3%) had interstitial fibrosis on chest x-ray, and 24 (25.8%) had interstitial changes on high-resolution CT scan. The cellular markers of parenchymal inflammation that we examined included fibronectin in BAL fluid and alveolar macrophage release of prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta), and tumor necrosis factor (TNF-alpha) under unstimulated and endotoxin (LPS)-stimulated culture conditions. Significantly higher concentrations of fibronectin in BAL fluid were observed among those with restrictive lung function. In addition, higher concentrations of PGE2, released from cultured but otherwise unstimulated alveolar macrophages, were associated with restrictive lung function. However, the inverse relationship with PGE2 was observed among subjects with abnormal gas exchange. Interestingly, no consistent changes in these inflammatory mediators were observed in those with interstitial changes identified on either the chest radiograph or the high-resolution CT scan.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

Infection and inflammation in skeletal muscle from nonhuman primates infected with different genospecies of the Lyme disease spirochete Borrelia burgdorferi.

Lyme borreliosis is a multisystemic disease caused by various genospecies of the spirochete Borrelia burgdorferi. To investigate muscle involvement in the nonhuman primate (NHP) model of Lyme disease, 16 adult Macaca mulatta animals inoculated with strain N40 of B. burgdorferi sensu strictu by syringe or by tick bite or with strain Pbi of B. burgdorferi genospecies garinii by syringe were studied. Animals were necropsied while immunosuppressed on day 50 (two animals each inoculated with B. burgdorferi N40 by syringe and with B. garinii Pbi by syringe) or on day 90, 40 days after immunosuppression had been discontinued (four animals each inoculated with strain N40 by syringe, with strain N40 by tick bite, and with strain Pbi by syringe). Skeletal muscles removed at necropsy were studied by (i) microscopic examination of hematoxylin-eosin-stained sections for inflammation and tissue injury; (ii) immunohistochemical and digital image analyses for antibody and complement deposition and cellular inflammation; (iii) Western blot densitometry for the presence of antibodies; and (iv) reverse transcription-PCR for measurement of the spirochetal load or C1q (the first component of the complement cascade) synthesis. The results showed that N40 was more infectious for NHPs than Pbi. NHPs inoculated with N40 but not with Pbi developed myositis. The inflammation in skeletal muscle was more severe in NHPs inoculated with N40 by syringe than in those inoculated by tick bite. The predominant cells in the inflammatory infiltrate were T cells and plasma cells. The deposition of antibody and complement in inflamed muscles from N40-inoculated NHPs was significantly higher than that in Pbi-inoculated NHPs. The spirochetal load was very high in the two N40-inoculated NHPs examined while they were immunosuppressed but decreased to minimal levels in the NHPs when immunocompetence was restored. We conclude that myositis can be a prominent feature of Lyme borreliosis depending on the infecting organism and host immune status.

Animals↗

PubMed2004

Review: Pharmacological treatment of airway remodeling: inhaled corticosteroids or antileukotrienes?

Chronic stable asthma is characterized by inflammation of the airway wall, with abnormal accumulation of basophils, eosinophils, lymphocytes, mast cells, macrophages, dendritic cells, and myofibroblasts. Airway inflammation is not limited to severe asthma, but is also found in mild and moderate asthma. This inflammation results in a peculiar type of lymphocytic infiltration whereby Th2 lymphocytes secrete cytokines that orchestrate cellular inflammation and promote airway hyper-responsiveness. The term "airway remodeling" in bronchial asthma refers to structural changes that occur in conjunction with, or because of, chronic airway inflammation. Airway remodeling results in alterations in the airway epithelium, lamina propria, and submucosa, leading to thickening of the airway wall. Consequences of airway remodeling in asthma include incompletely reversible airway narrowing, bronchial hyper-responsiveness, airway edema, and mucus hypersecretion; these effects may predispose subjects with asthma to exacerbations and even death due to airway obstruction. To avoid this progression, it is important to follow an adequate treatment aimed at interacting and modifying the inflammatory process. Inhaled corticosteroids remain the cornerstone of asthma management. Altough several drugs, such as ketotifen, sodium cromoglycate, sodium nedocromil, and theophylline have anti-inflammatory properties, they are less effective than corticosteroids. Antileukotrienes are a new class of anti-inflammatory drugs that interfere directly with leukotriene receptors. The aim of this brief review is to delineate the effects of inhaled corticosteroids and antileukotriene drugs on inflammation and remodeling.

Administration, Inhalation↗

PubMed2000

Increased phosphorylated extracellular signal-regulated kinase immunoreactivity associated with proliferative and morphologic lung alterations after chrysotile asbestos inhalation in mice.

Activation of extracellular signal-regulated kinases (ERK) has been associated with the advent of asbestos-associated apoptosis and proliferation in mesothelial and alveolar epithelial cells and may be linked to the development of pulmonary fibrosis. The objective of studies here was to characterize the development of inflammation, cellular proliferation, and fibrosis in asbestos-exposed C57Bl/6 mice in relationship to patterns of ERK phosphorylation. Inflammation occurred after 10 and 20 days of asbestos exposure as evidenced by increases in total protein and neutrophils in bronchoalveolar lavage fluid. Increases in cell proliferation were observed at 30 days in bronchiolar epithelia and at 4, 14, and 30 days in the alveolar compartment of the lung. Trichrome-positive focal lesions of pulmonary fibrosis developed at 30 days in the absence of elevations in lung hydroxyproline or procollagen mRNA levels. Striking increases in ERK phosphorylation were observed within pulmonary epithelial cells at sites of developing fibrotic lesions after 14 and 30 days of inhalation. In addition to characterizing a murine inhalation model of asbestosis, we provide the first evidence showing activation of ERK signaling within lung epithelium in vivo, following inhalation of asbestos fibers.

Administration, Inhalation↗

PubMed1978

Observations on the pathology of canine microsporidiosis.

The available literature on canine microsporidiosis indicates that this disease, primarily of young dogs, is a distinct clinicopathological entity. It has been confused with canine distemper and rabies, and must be differentiated from toxoplasmosis. Information available on the spectrum of pathological change associated with this disease is incomplete but a distinct pattern emerges from a study of the reports. The aetiological agent appears to have a predilection for the central nervous system and kidneys, but other tissues and organs, and especially the liver, may also be infected. Vasculitis and perivasculitis, which may include fibrinoid necrosis, seem to be a basic lesion. Cellular inflammation ranges from polymorphonuclear leukocyte infiltration in areas of necrosis to focal granulomas. There may be no cellular reaction to compact groups of organisms. Histopathological and ultrastructural studies of this case augment our knowledge of the pathological changes seen with canine microsporidiosis.

Animals↗

PubMed1992

Activity-dependent neuronal plasticity following tissue injury and inflammation.

Increases in neuronal activity in response to tissue injury lead to changes in gene expression and prolonged changes in the nervous system. These functional changes appear to contribute to the hyperalgesia and spontaneous pain associated with tissue injury. This activity-dependent plasticity involves neuropeptides, such as dynorphin, substance P and calcitonin gene-related peptide, and excitatory amino acids, such as NMDA, which are chemical mediators involved in nociceptive processing. Unilateral inflammation in the hindpaw of the rat results in an increase in the expression of preprodynorphin and preproenkephalin mRNA in the spinal cord, which parallels the behavioral hyperalgesia associated with the inflammation. Cellular intermediate-early genes, such as c-fos, are also expressed in spinal cord neurons following inflammation and activation of nociceptors. Peripheral inflammation results in an enlargement of the receptive fields of many of these neurons. Dynorphin applied to the spinal cord also induces an enlargement of receptive fields. NMDA antagonists block the hyperexcitability produced by inflammation. A model has been proposed in which dynorphin, substance P and calcitonin gene-related peptide enhance excitability at NMDA receptor sites, leading first to dorsal horn hyperexcitability and then to excessive depolarization and excitotoxicity.

Animals↗

PubMed1998

Sputum eosinophilia is more closely associated with airway responsiveness to bradykinin than methacholine in asthma.

Hyperresponsiveness of the airways to various spasmogenic stimuli is a characteristic feature of bronchial asthma. However, the association between the different stimuli to which asthmatic airways are hyperresponsive and airways inflammation is not completely understood. We have investigated the relationship between airway inflammation and airway hyperresponsiveness in asthma, as assessed by bronchoprovocation tests to methacholine and bradykinin, two well defined bronchoconstrictor agonists. Sputum induction by hypertonic saline and methacholine and bradykinin challenges were performed in 14 nonsmoking subjects with mild-to-moderate asthma. Airway responsiveness to either agonist did not correlate with sputum neutrophils, lymphocytes, and macrophages. Whilst the absolute number of eosinophilia failed to be significantly related to methacholine responsiveness (r=-0.47; p=0.09), it correlated markedly and significantly with provocative concentration of methacholine causing a 20% fall in forced expiratory volume in one second (r=0.72; p<0.01). When expressed as % of total cell counts, sputum eosinophils correlated with both types of responsiveness (r=-056; p=0.04 and r=-0.76, p<0.001, respectively). Although the concentration of eosinophil cationic protein (ECP) in the sputum correlated with the absolute numbers of eosinophils (r=0.62; p<0.02), no correlation was found between ECP levels and the airway responsiveness to any of the agonists tested. In subjects with mild-to-moderate asthma, airway responsiveness to bradykinin is more strongly associated with the magnitude of eosinophilic inflammation in the airways than methacholine. This finding underlines the selectivity of diverse agonists in assessing airway hyperresponsiveness and cellular inflammation in asthma.

Adolescent↗

PubMed2001

Effects of macrophage-CSF on pulmonary-macrophage repopulation after bone marrow transplantation.

Pulmonary infections are important causes of morbidity and mortality in immunosuppressed patients after transplantation. After experimental irradiation and syngeneic bone marrow transplantation in mice, macrophages show reduced repopulation in the lung compared with that in other tissues. Macrophages are major microbicidal immune effector cells in host pulmonary defense. Therefore, we examined the role of locally applied cytokines for macrophage repopulation in the lung. An accelerated repopulation of macrophages in the lung was observed after intranasal application of macrophage-colony stimulating factor (M-CSF), but this effect was not enhanced by a combination of M-CSF with interleukin (IL)-3. Local proliferation contributed to this effect. Macrophages in the lung tissue of M-CSF-treated mice displayed greater secretion of IL-6, whereas M-CSF treatment did not enhance the gene expression of other macrophage-specific chemokines. The role of M-CSF treatment was determined in pulmonary murine cytomegalovirus infection using an irradiation/reconstitution model. The M-CSF treatment had no effect on virus load in the lung tissue. However, phosphate-buffered saline-treated mice seemed to develop stronger inflammation after viral infection than M-CSF-treated mice. We conclude that local M-CSF treatment modulates cellular inflammation in the lung during immunosuppression.

Administration, Intranasal↗

PubMed2000

Bronchoalveolar lavage cellular composition in acute asthma and acute bronchiolitis.

OBJECTIVE: To compare cellular inflammation in the airways between acute bronchiolitis and asthma. STUDY DESIGN: Using a bronchoalveolar lavage with flexible bronchoscopy procedure, we investigated the cellular constituents of BAL fluid in children with acute exacerbation of asthma (n = 18) and infants with acute bronchiolitis caused by respiratory syncytial virus (n = 20). These results were compared with those of healthy control subjects (n = 14). RESULTS: Total lavage fluid recovered was similar in all groups. The total cell numbers were highest in the bronchiolitis group. The BAL cellular profile in the asthma group was characterized by a higher median (interquartile range) ratio of eosinophils (2.4% [1.6%-9.5%]; P <.01) than in the bronchiolitis group (0% [0%-0%]) or the control group (0% [0%-0%]). Neutrophil ratio was higher in the bronchiolitis group (40.0% [26.5%-50.0%]; P <.01), with no difference found between the asthma group (3.3% [2.0%-7.9%]) and the control group (2.0% [0.8%-5.5%]). CONCLUSIONS: Asthma and acute bronchiolitis are characterized by an elevated cellular percentage of eosinophils and neutrophils, respectively, in bronchoalveolar lavage fluid.

Acute Disease↗