Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “INFLAMMATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,207 records · Page 67Linked to original sources
PubMed1994

[Application of inflammation markers in the "essential laboratory tests" to new outpatients and analysis for the efficacious selection of these items].

We have re-evaluated the usefulness of the inflammation markers in the "essential laboratory tests" advocated by Japan Society of Clinical Pathology and analyzed for efficacious selection of these items by applying these tests to 349 new outpatients visited Comprehensive Medicine, National Defense Medical College. Among the patients with "tentative initial diagnoses" of infectious or inflammation-related diseases (133 cases), the diagnoses were confirmed in 102 patients by positive inflammation marker(s), whereas additional 22 cases with the diagnoses other than inflammation-related diseases were found to be in the inflammatory status by these tests. Elevated C-reactive protein (CRP) levels were not correlated with the leukocyte number, however, neutrophilia (neutro. > 70%) and/or left shift of the neutrophils (stab > 15%) were demonstrated in approximately 50% of the patients with elevated serum CRP levels. Increases of serum sialic acid highly accompanied with increases of CRP, alpha 1 or alpha 2 fraction of serum protein and elevation of erythrocyte sedimentation rate (ESR), indicating that serum sialic acid levels reflected more strictly inflammatory status than ESR. There is a relatively good correlation (r = 0.813) between serum sialic acid values and the total amounts of alpha 1 and alpha 2 protein fraction, while poor correlations were shown between CRP and sialic acid values (r = 0.606), or ESR and sialic acid values (r = 0.671). These results indicate that (1) simultaneous measurements of CRP, leukocyte number and leukocyte differential fraction are useful for the confirmation of early stage of inflammation and evaluation of the nature of infectious diseases; (2) measurement of serum sialic acid levels is more desirable for the evaluation of inflammatory status than ESR; and (3) serum protein profile can be substituted by sialic acid for the evaluation of acute inflammatory status alone.

Adolescent↗
PubMed1996

Cluster headache presenting with orbital inflammation.

Acute, noninfectious orbital inflammations often defy a specific diagnosis despite a thorough medical evaluation and are grouped in the nonspecific diagnostic category of idiopathic inflammation of the orbit (pseudotumor). An atypical case of cluster headache presenting with intermittent migratory facial swelling and orbital inflammation, and 3 mm of exophthalmos simulating idiopathic orbital inflammation is presented. Although periobital pain is a frequent finding in patients suffering from cluster headaches, to the authors' knowledge this is the first reported case of orbital inflammation with cluster headache. After unsuccessful treatment directed at potential infectious and inflammatory causes, the patient responded well to methysergide, an established treatment for cluster headaches. A review of the known mechanism for this disorder, peripheral and central nervous system mechanisms of pain, and migratory angioedema reveals overlapping pathophysiology, clinical findings, and associated symptoms.

Adult↗
PubMedDate not supplied

Dual effect of the serotonin agonist, sumatriptan, on peripheral neurogenic inflammation.

BACKGROUND AND OBJECTIVES: Sumatriptan is a novel drug for migraine headache pain, which, on the basis of its mechanism of action, may have therapeutic potential in other pain states. Sumatriptan inhibits neurogenic inflammation in dural vessels by activating the 5-HTIB and 5-HTID inhibitory serotonin (5-hydroxytryptamine [5-HT]) receptor subtypes on terminals of trigeminal neurons. This study was designed to determine the role of sumatriptan in peripheral pain mechanisms by detecting whether 5-HTIB and 5-HTID receptors and the recently cloned excitatory 5-HT7 receptor, for which sumatriptan displays moderate binding affinity, are present in peripheral sensory neurons, and by determining the effect of sumatriptan on peripheral neurogenic inflammation. METHODS: A polymerase chain reaction (PCR) technique was used to detect mRNA for 5-HT receptors in rat lumbar dorsal root ganglia. Rat knee joint plasma extravasation was used to determine the effect of sumatriptan on peripheral neurogenic inflammation. RESULTS: The mRNA for the sumatriptan-activated receptors 5-HTIB, 5-HTID, and 5-HT7, was detected in lumbar dorsal root ganglia. In rat knee joint, capsaicin-activated C-fibers stimulated plasma extravasation to 273 +/- 62% of baseline. Low-concentration sumatriptan (50 nM) significantly inhibited capsaicin-induced plasma extravasation to 106 +/- 6% of baseline. High-concentration sumatriptan (1 microM) significantly enhanced capsaicin-induced plasma extravasation to 572 +/- 55% of baseline. CONCLUSIONS: Sumatriptan inhibits peripheral neurogenic inflammation, probably via 5-HT1B/1D receptors, and may be a novel therapy for inflammatory pain states. However, high concentrations (> 200 nM) may enhance neurogenic inflammation, possibly by activation of 5-HT7 receptors, which may explain lack of migraine relief and excessive injection site pain in 20-30% of patients treated with sumatriptan.

Animals↗
PubMed1996

Effects of ozone and airway inflammation on glutathione status and iron homeostasis in the lungs of horses.

OBJECTIVE: To investigate the effects of ozone and airway inflammation on indices of oxidant injury in horses. ANIMALS: 5 clinically normal horses and 25 horses referred for poor performance. PROCEDURE: Blood, tracheal wash, and bronchoalveolar lavage fluid samples were collected before and after ozone exposure (n = 5) or from clinical cases (n = 25), and were analyzed for reduced glutathione (GSH), glutathione disulfide (GSSG), and free and total iron (Fe) values. A scoring system (0 to 5) was used to assess airway inflammation on the basis of clinical signs and cytologic analysis of the tracheal wash and bronchoalveolar lavage fluid samples. RESULTS: Ozone induced significant (P < 0.05) increases in GSH (195.4 +/- 68.5 microM), GSSG (19.4 +/- 6.4 microM), and free (25.5 +/- 16.1 microM) and total (93.1 +/- 13.4 microM) Fe values in the pulmonary epithelial lining fluid, compared with preozone samples (49.2 +/- 18.6, 2.4 +/- 1.2, 0.0, and 33.1 +/- 5.9 microM, respectively). The presence of airway inflammation (19/25) was associated with high GSSG and free and total Fe, but not GSH, values in epithelial lining fluid, compared with values for clinically normal horses (6/25). There were no differences in the systemic values of GSH, GSSG, and free and total Fe between any of the groups. A strong correlation (r = 0.84; P < 0.001) existed between inflammation score and the glutathione redox ratio (GSSG/[GSH + GSSG]) in the 25 horses admitted for clinical examination. CONCLUSIONS: Oxidant injury in the lung will induce changes in the glutathione status and Fe homeostasis that could affect pathogenesis of the disease. CLINICAL RELEVANCE: Measurement of indices of oxidant injury may be useful in the diagnosis of airway inflammation and the response to inhaled oxidants.

Animals↗
PubMed1996

Nitric oxide in exhaled air is a new marker of airway inflammation.

The measurement of exhaled NO has excited considerable interest, as it may provide a simple noninvasive means of measuring airways inflammation. There is now persuasive evidence that levels of NO are increased in association with airway inflammation and are decreased with anti-inflammatory treatment. Correlation of exhaled NO with more direct measurements of inflammation in the airways, such as induced sputum, bronchoalveolar lavage and bronchial biopsies, is needed. The great advantage of exhaled NO is that the measurement is completely noninvasive. It can, therefore, be performed repeatedly, and also in children and patients with severe airflow obstruction, where more invasive techniques are not possible. However, the measurement is not specific, and exhaled NO is increased in inflammation due to asthma, bronchiectasis, and respiratory tract infections. This means that absolute values are less important than serial measurements in individual patients. The value of this approach has been demonstrated in asthmatic patients, where the dose of inhaled steroid is changed, resulting in increased levels when the dose is reduced and lower levels when the dose is increased. Because exhaled NO is reduced by anti-inflammatory treatments, it may be of use in monitoring whether therapy is adequate. The technique may also have application in the monitoring of the anti-inflammatory effects of new antiasthma drugs, such as selective phosphodiesterase inhibitors, leukotriene antagonists and synthesis inhibitors, and immunomodulators. Because the measurement is precise and reasonably reproducible, it may facilitate the measurement of dose-response effects with anti-inflammatory treatments, which is difficult at present. The analysers for exhaled NO that are currently available are expensive, but in the future it is likely that technological advances will make it possible to miniaturize these analysers, so that they are portable and may even be used at home in conjunction with peak flow meters. -his may lead to their application in epidemiological research, which may be a useful screening measurement for community studies. Although we have discussed exhaled nitric oxide, other volatile substances may also be detected in exhaled air. Thus, ethane and pentane, which are volatile products of lipid peroxidation, and hydrogen peroxide, may be used to detect oxidant stress in the respiratory tract and may also be useful as markers of inflammation. There is little doubt that this is a rapidly expanding area of research.

Biomarkers↗
PubMed1997

The codependence of angiogenesis and chronic inflammation.

Angiogenesis is the growth of new blood vessels from existing ones. It is an important aspect of new tissue development, growth, and tissue repair. It is also a component of many diseases including cancer, blindness, and chronic inflammation such as rheumatoid arthritis (RA) and psoriasis. There is considerable evidence to suggest that angiogenesis and chronic inflammation are codependent; recent studies have begun to reveal the nature of this link, which involves both augmentation of cellular infiltration and proliferation and overlapping roles of regulatory growth factors and cytokines. Through these studies, we have begun to understand the codependence of chronic inflammation and angiogenesis, the potential benefits of targeting angiogenesis in the treatment of chronic inflammation, and of targeting chronic inflammation to affect angiogenesis.

Animals↗
PubMed1997

Inflammation increases the distribution of dorsal horn neurons that internalize the neurokinin-1 receptor in response to noxious and non-noxious stimulation.

Although the neurokinin-1 (NK-1)/substance P (SP) receptor is expressed by neurons throughout the spinal dorsal horn, noxious chemical stimulation in the normal rat only induces internalization of the receptor in cell bodies and dendrites of lamina I. Here we compared the effects of mechanical and thermal stimulation in normal rats and in rats with persistent hindpaw inflammation. Electron microscopic analysis confirmed the upregulation of receptor that occurs with inflammation and demonstrated that in the absence of superimposed stimulation, the increased receptor was, as in normal rats, concentrated on the plasma membrane. In general, noxious mechanical was more effective than noxious thermal stimulation in inducing NK-1 receptor internalization, and this was increased in the setting of inflammation. Although a 5 sec noxious mechanical stimulus only induced internalization in 22% of lamina I neurons in normal rats, after inflammation, it evoked near-maximal (98%) internalization in lamina I, produced significant changes in laminae III-VI, and expanded the rostrocaudal distribution of neurons with internalized receptor. Even non-noxious (brush) stimulation of the inflamed hindpaw induced internalization in large numbers of superficial and deep neurons. For thermal stimulation, the percentage of cells with internalized receptor increased linearly at >45 degrees C, but in normal rats, these were restricted to lamina I. After inflammation, however, the 52 degrees C stimulus also induced internalization in 25% of laminae III-IV cells. These studies provide a new perspective on the reorganization of dorsal horn circuits in the setting of persistent injury and demonstrate a critical contribution of SP.

Animals↗
PubMed1995

Expression of murine VCAM-1 in vitro and in different models of inflammation in vivo: correlation with immigration of monocytes.

VCAM-1 (vascular cell adhesion molecule-1) is a cytokine-inducible adhesion molecule which is known to mediate adhesion of mononuclear cells to endothelial cells in vitro via binding to the integrin VLA-4 (very late antigen-4). To further elucidate the role and regulation of VCAM-1 in vitro, we compared in vitro and in vivo expression of VCAM-1 in response to cytokines and investigated immunohistochemically the expression of VCAM-1 in three murine models of experimental inflammation. These models differed with regard to the pathogenetic mechanism, and the subsesquent infiltrate: allergic contact dermatitis (ACD) to DNFB as a T cell-controlled, DTH type of inflammation, cutaneous infection with Leishmania major as a chronic granulomatous inflammation and the cauterized cornea as a model for acute inflammation. VCAM-1 was found to be markedly enhanced on vascular endothelia in all types of inflammation and after subcutaneous administration of LPS and TNF-alpha. Administration of IL-4, however, failed to induce VCAM-1 both in vivo and in vitro. The increased VCAM-1 expression in the inflammatory models correlated with the appearance of infiltrating monocytes/macrophages. A concomitant influx of CD4-positive/CD8-positive lymphocytes was only observed in ACD and Leishmaniasis.

Animals↗
PubMedDate not supplied

Role of pro- and anti-inflammatory cytokines during inflammation: experimental and clinical findings.

There is an emerging concept that the net biological response of pro and anti-inflammatory cytokines affects the outcome of certain diseases. In inflammatory diseases, interleukin-1 (IL-1) and tumor necrosis factor (TNF) are produced and function primarily as pro-inflammatory cytokines. In addition, other cytokines such as IFN gamma, IL-12 and IL-18 are also produced and affect the production and cellular response to IL-1 and TNF. Biologically, IL-1 and TNF are closely related, although the respective structures and the specific receptors for IL-1 and TNF are clearly distinct. IL-1 and TNF are truly pleiotropic cytokines and are active in the low pM and fM range. Because of their multiple pro-inflammatory properties, these cytokines contribute to disease. Most of our knowledge on IL-1 and TNF are derived from experiments in which either humans or animals have been injected with the cytokine or added to cells in vitro. However, in models of inflammation where several cytokines are produced, specific blockade of either IL-1 or TNF or both results is a reduction in the severity of the inflammation. These latter data therefore implicate IL-1 and TNF as primary cytokines involved with inflammation. Moreover, IL-1 and TNF act synergistically in nearly every in vitro and in vivo model of inflammation. This review will focus on IL-1 and TNF as cytokines of strategic importance to the initiation and progression of inflammation. In addition, this review examines the effects of anti-inflammatory cytokines which non-specifically reduce the production and activity of IL-1 and TNF.

Animals↗
PubMed1998

Differential activities of secreted lymphotoxin-alpha3 and membrane lymphotoxin-alpha1beta2 in lymphotoxin-induced inflammation: critical role of TNF receptor 1 signaling.

Lymphotoxin (LT, LT alpha, TNF beta) is a member of the immediate TNF family that also includes TNF-alpha and lymphotoxin-beta (LT beta). LT is produced by activated lymphocytes and functions as either a secreted homotrimer or a membrane-associated heterotrimer that includes the transmembrane protein LT beta. Secreted LT alpha3 can bind to two cell surface receptors, TNFR1 and TNFR2, while the membrane-bound heterotrimer LT alpha1beta2 has been shown to interact with a distinct receptor, LT betaR. LT alpha induces inflammation at the sites of expression of a rat insulin promoter-driven lymphotoxin (RIPLT) transgene in the pancreas and kidney. To determine the role of the various ligands and their receptors in LT-induced inflammation, mice deficient in either TNFR1, TNFR2, or LT beta were crossed to RIPLT-transgenic mice. Our results indicate that LT alpha-induced inflammation is dependent on the interaction of LT alpha3 with TNFR1, and there is no obvious role for TNFR2, since in its absence, LT alpha-induced inflammation is quantitatively and qualitatively similar to that seen in the wild type. However, the absence of LT beta results in accentuated infiltration of the kidney with an increase in the proportion of memory cells in the infiltrate. These data show a crucial role for the secreted LT alpha3 signaling via TNFR1 in LT alpha-induced inflammation, and a separate and distinct role for the membrane LT alpha1beta2 form in this inflammatory process.

Animals↗
PubMed1998

[Detection and treatment of iron deficiency anaemia coexisting with inflammation prevalent in aged individuals].

As the author found that serum ferritin is decreased below 12 ng/ml in iron deficiency anemia (IDA) even then it is coexisting with anaemia other than IDA, an attempt was made to detect and treat IDA coexisting with anaemia other than IDA. When surveyed in a general hospital admitting 222 patients, anaemias were detected in 95 out of 190 patients aged above 60:82 inflammation anaemia, 9 IDA including 6 cases with inflammation and 4 other anaemias. According to the above results, aged patients above 60 with IDA only and IDA coexisting with inflammation were treated by injecting iron intravenously. By the treatment, haemoglobin (Hb) was increased from 9.0 to 13.8 g/dl and the ratio of Hb increase was 0.59 in 4 patients with IDA only, and Hb was increased from 7.7 to 11.5 g/dl and the ratio of Hb increase was 0.63 in 18 patients with IDA coexisting with inflammation. After the treatment, general disease states were improved in many cases. Thus, the treatment of aged patients with IDA coexisting with inflammation seems to be comparably effective as for IDA only.

Anemia, Hypochromic↗
PubMedDate not supplied

How to measure airway inflammation: bronchoalveolar lavage and airway biopsies.

Airway inflammation is a characteristic feature of asthma. Bronchoscopy with bronchoalveolar lavage (BAL) and/or mucosal airway biopsies has provided invaluable information about the nature of asthmatic inflammation. A common finding in all BAL studies in asthma is increased numbers or proportions of eosinophils even in subjects with mild disease. BAL cells in asthmatics demonstrate a cytokine profile consistent with a T helper2-like phenotype, with increased expression of interleukin (IL)-4 and IL-5. Endobronchial mucosal biopsies show loss of surface epithelium, thickening of the reticular layer of the basement membrane and an increased cellular infiltrate of mainly eosinophils, mast cells and T lymphocytes, and up-regulation of a number of cytokines. Recently, peripheral airways from asthmatics have been investigated, and even more intense inflammation has been described. However, in severe steroid-dependent asthmatics, intriguing differences in the type of inflammation have been described. The term 'airway remodelling' indicates structural changes seen in long standing asthma, where myofibroblasts might be of particular importance. BAL and mucosal biopsies are important tools in the investigation of airway inflammation in asthma.

Asthma↗
PubMedDate not supplied

[The role of eosinophilic leukocytes in allergic inflammation].

Eosinophilic leukocytes are tissue cells of granulocytic structure and secretory nature. They are produced in the bone marrow and transported to the targeted tissue via the blood where they are present in concentrations hundred times higher than in peripheral circulation. Eosinophilic leukocytes are the essential effector of allergic inflammation, which is a pathophysiological basis of allergic diseases. These diseases are characterized by disturbed distribution of eosinophilic leukocytes, i.e., peripheral eosinophilia and/or infiltration of the affected organs. Migration of these cells from the peripheral circulation into the targeted tissues, i.e., affected with the allergic inflammation, is influenced by helper T2 cells-dependent cytokines, and other mediators of inflammation. Subsequent to their activation, eosinophilic leukocytes release numerous made and newly produced mediators of inflammation and also present antigens which define their effector function in allergic inflammation. In this way, eosinophilic leukocytes participate in numerous pathological and pathophysiological disorders characteristic of allergic diseases which clearly confirm the active role of these cells in their production.

Eosinophils↗
PubMed1984

Steroidal and nonsteroidal anti-inflammatory agents. Effect on postsurgical inflammation and blood-aqueous humor barrier breakdown.

Two hundred and eighty-three patients scheduled to undergo extracapsular cataract extraction with intraocular lens implantation were randomized into four treatment groups that received 1% topical indomethacin and 0.1% topical dexamethasone sodium phosphate, either drug and the other drug's placebo, or two placebos. Inflammation was assessed by clinical grading, and the breakdown of the blood-aqueous barrier was evaluated by slit-lamp anterior segment fluorophotometry. Patients who used either or both anti-inflammatory agents had significantly less inflammation or blood-aqueous barrier breakdown than did those who used neither agent. Also, the use of both topical indomethacin and dexamethasone resulted in less fluorescein leakage during the second postoperative week than did the use of dexamethasone alone. Since this difference could not be detected by clinical measurement, we believe that fluorophotometry is a more sensitive quantitative measure. Clinical assessment of inflammation did correlate with fluorophotometric measurements, as patients with clinically unacceptable inflammation had 3.7 times more fluorescein leakage in the surgically treated eye than did patients with clinically acceptable inflammation.

Administration, Topical↗
PubMed1989

Effect of dichloroacetate on plasma and hepatic amino acids in sterile inflammation and sepsis.

The effect of sterile inflammation and chronic sepsis on the plasma and hepatic free amino acid concentrations was determined. Relative to control animals, only minor alterations in the plasma amino acid concentrations were observed in sterile inflammation and sepsis. In liver, concentrations of alanine, serine, threonine, asparagine, proline, and glycine were significantly increased to the same extent in sterile inflammation and sepsis, while hepatic glutamine concentrations were significantly decreased. Compared with sterile inflammation, the branched-chain amino acid concentrations were depressed in the liver of septic animals. Following administration of dichloroacetate, hepatic alanine concentrations were significantly reduced more than threefold in each of the conditions examined; in contrast, significant increases in hepatic concentrations of threonine, glycine, glutamine, glutamate, histidine, and proline were observed. Also following administration of dichloroacetate, the branched-chain amino acid concentrations were all significantly elevated in each of the conditions examined, and plasma alanine concentrations were significantly decreased, while those of glutamine and glycine were significantly increased. These results demonstrate that there is a disassociation between the plasma and hepatic concentration of free amino acids in sterile inflammation and sepsis. Furthermore, the results demonstrate that some of the alterations in hepatic amino acid metabolism may be reversed pharmacologically by dichloroacetate.

Abscess↗
PubMed1997

Association of coronary plaque rupture and atherosclerotic inflammation.

Coronary plaque inflammation may promote plaque rupture and thrombosis. To test this hypothesis, 351 coronary plaques from 83 patients were formalin-fixed and stained with haematoxylin and eosin. There were six groups: (1) ruptured plaques; (2) intact plaques from recently infarcted hearts; (3) plaques from hearts with severe coronary atherosclerosis without identifiable thrombosis; (4) native explanted hearts with severe coronary atherosclerosis; (5) cardiac transplant atherosclerosis; and (6) fatalities unrelated to coronary atherosclerosis. Selected arteries were immunostained for leukocyte markers and serially sectioned to identify plaque rupture. There were infiltrates of CD68-positive macrophages and CD3- and CD8-positive T cells adjacent to all plaque ruptures. Labelling with HLA-DR and CD30 indicated inflammatory cell activation. Plaque rupture was strongly statistically associated with the severity and frequency of superficial plaque inflammation but not that of deep plaque inflammation. Although atherosclerotic inflammation has been identified adjacent to rupture, this is its first comparison with control plaques. These results support the concept that inflammation in the fibrous cap is particularly associated with plaque rupture.

Arteritis↗
PubMed2000

Deep intralobular extension of human hepatic 'progenitor cells' correlates with parenchymal inflammation in chronic viral hepatitis: can 'progenitor cells' migrate?

Ductular reaction and putative progenitor cells (or 'progenitor cells'), which are presumed to be the human counterpart of the oval cells in rat liver, have been discerned in various human liver diseases, including chronic viral hepatitis. Since in experimental models of chronic hepatitis the activation of oval cells is correlated with the inflammatory infiltrate, this study investigated whether there is a correlation in chronic viral hepatitis between the number of 'progenitor cells' extending into the lobule and the severity of parenchymal inflammation, on the one hand, and the extent of ductular reaction and the severity of interface hepatitis, on the other hand. Liver biopsies of 55 patients with chronic hepatitis B and/or C were used. The severity of parenchymal inflammation and of interface hepatitis was semiquantitatively graded on a haematoxylin and eosin-stained paraffin section, while the number of 'progenitor cells' and the extent of the ductular reaction were assessed on a serial section stained for cytokeratin (CK) 7. In addition, more extensive phenotyping of 'progenitor cells' was performed on sections from frozen material from five patients, using antibodies against CK7, CK8, CK18, CK19, chromogranin-A, and the rat oval cell marker OV-6. The number of more centrally located 'progenitor cells' correlated significantly with the severity of the parenchymal inflammation, while the extent of the ductular reaction correlated significantly with the severity of interface hepatitis. These findings suggest that in chronic viral hepatitis, inflammation plays a role in 'progenitor cell' activation and its topography. In cases with moderate and severe lobular inflammation, 'progenitor cells' were strikingly scattered throughout the parenchyma and surrounded by intermediate hepatocyte-like cells, suggesting their migration into the parenchyma and their differentiation towards the hepatocytic lineage.

Antibodies, Monoclonal↗
PubMed2002

Costimulatory molecule OX40L is critical for both Th1 and Th2 responses in allergic inflammation.

T cell activation and cytokine secretion are important mediators of inflammation in allergic asthma. The costimulatory pathway CD28/CD80/CD86 has been shown to play an important role in T cell activation in allergic asthma, but less is known about the effect of other costimulatory molecules in allergy. The costimulatory molecule OX40 ligand (OX40L), a member of the tumor necrosis factor superfamily, has been shown to be important in T cell priming and cytokine production. We investigated the role of OX40L in a murine model of allergic inflammation using OX40L(-/-) mice. In this model, following OVA sensitization and challenge, mice develop features of allergic inflammation including elevated levels of total serum IgE, pulmonary eosinophils, cytokines, and pulmonary inflammation. In the absence of OX40L, total serum IgE, pulmonary eosinophils, cytokines, and pulmonary inflammation were all significantly reduced compared to wild-type controls. Levels of eotaxin mRNA, an eosinophil-specific chemoattractant, were also markedly reduced, paralleling the significant reduction in pulmonary eosinophils. Levels of allergen-induced Th1 as well as Th2 cytokines were also significantly reduced. Together, the data support a critical role for OX40L signals in allergic responses.

Animals↗