儿童过敏性结膜炎与变应性鼻炎的相关性及鼻眼联合防治效果分析

目的：探讨儿童过敏性结膜炎与变应性鼻炎的相关性研究及鼻眼联合防治的临床效果。方法：回顾性分析300 例儿童过敏性 结膜炎与310 例儿童变应性鼻炎患者的临床资料,对儿童过敏性结膜炎与变应性鼻炎的相关性进行分析后将所有患儿随机均分 为对照组与观察组,对照组采用常规点眼的方法进行治疗,观察组则采用鼻朗喷鼻联合人工泪液点眼进行治疗。比较两组临床疗 效及不良反应情况。结果：（1）300 例过敏性结膜炎患儿中,50 例（16.67%）并发变应性鼻炎;310 例变应性鼻炎患儿中,59 例 （19.03%）并发过敏性结膜炎（P＞0.05）;（2）109 例同时并发两种疾病患儿中,均进行眼结膜与鼻粘膜的刮片检查嗜酸性粒细胞, 其中60 例（55.05%）结膜刮片与67 例（61.47%）鼻粘膜刮片检测到嗜酸性粒细胞（P＞0.05）;（3）两组治疗前后BUT 及角膜荧光素 染色评分、症状评分、临床总有效率比较差异明显（P＜0.05）。结论：儿童过敏性结膜炎与变应性鼻炎具有一定的相关性;鼻朗喷鼻 联合人工泪液点眼治疗儿童合并变应性鼻炎的临床疗效显著。     

Decreased sensitivity of atopic mononuclear cells to prostaglandin E2 (PGE2) and prostaglandin D2 (PGD2)

The effect of PGE2 and PGD2 on several lymphocyte functions in vitro was evaluated in nonatopic and atopic subjects. Both PGE2 and PGD2 inhibited phytohemagglutinin-induced protein synthesis ([3H] leucine uptake) by nonatopic mononuclear cells and T cells in a dose-dependent manner (10(-6) to 10(-12) M). Protein synthesis by atopic mononuclear cells was not significantly suppressed by the above concentration of PGE2. Although PGD2 effectively suppressed protein synthesis by atopic mononuclear cells and T cells at 10(-6) M, lower concentrations were ineffective. Kinetic studies revealed significant differences in the suppressive effects of PGE2 and PGD2 on atopic and nonatopic mononuclear cells at 24 and 48 h, but not at 72 or 96 hr. Protein synthesis by T helper-enriched populations (suppressor cell depletion by anti-Leu-2b + complement) obtained from nonatopics was significantly reduced by PGE2 and PGD2, suggesting that these mediators may be directly inhibiting the responding population. By contrast, protein synthesis by T suppressor-enriched populations (helper cell depletion by OKT4 + complement) obtained from nonatopics was enhanced by PGE2 and PGD2, suggesting that the PG were activating these cells. Atopic T helper and T suppressor cells exhibited decreased responsiveness to PGE2 and PGD2 compared with nonatopic cells. PGE2 and PGD2 inhibited the phytohemagglutinin-stimulated proliferative response ([3H]thymidine uptake) by both atopic and nonatopic mononuclear cells in a dose-dependent manner and to the same extent. However, although PGE2 and PGD2 generated functional suppressor activity (when using a coculture technique) in nonatopic mononuclear cells, these mediators failed to activate atopic suppressor cells. These results suggest that reduced responses by atopic T cells to signals provided by PGE2 and PGD2 are not solely restricted to suppressor cell function, and could indicate an impaired ability to regulate immune and/or inflammatory reactions.     

Nasal fungal microbiota in allergic and healthy subjects

Environmental fungi, moulds and yeasts could reach the nasal cavity with the inhaled air causing respiratory symptoms in atopic subjects, but little is known about the fungal flora of this site. In the present study samples of the nasal cavities of 135 subjects aged 18-35 years (48 allergic patients to fungi, mites and/or cat fur and from 87 normal subjects--healthy, control group) were cultured. All of them lived in the metropolitan area of Barcelona. Fungi were isolated from 41.5% of healthy people and in 14.8% of allergy patients (p = 0.011). Morphologically, 50.4% of the isolates were located within 4 genera: Cladosporium, Penicillium, Aspergillus and Alternaria, fungi which are considered the most allergenic. The most prevalent species were: Cladosporium herbarum and C. cladosporioides (23.6%). Alternaria alternata was isolated only in 8.8% of samples from the allergic group, although most subjects were sensitive to this species. There were not differences in the isolation rate between genera and smoking-no-smoking groups. The lower prevalence of nasal fungi from allergic patients could be related to the nasal insufficiency, the hypersecretion and the larger use of handkerchiefs.     

The Effect of Air Pollution on Exhaled Nitric Oxide of Atopic and Nonatopic Subjects

Levels of exhaled nitric oxide (NO) were determined in well-characterized atopic and nonatopic subjects on 4 days with a different level of outdoor air pollution. The two groups matched well regarding spirometric values, i.e., no difference with regard to FEV(1), FVC, and peak flow. On the 4 test days asymptomatic atopic subjects exhaled 1.5- to 2.4-fold higher levels of NO compared with nonatopic subjects. In both groups the increase in exhaled NO in response to air pollution was similar (2.5 times maximal increase, P < 0.01). In conclusion, atopic subjects exhale higher levels of NO compared with nonatopic subjects, but respond to a similar degree to increased levels of air pollution.     

Characterization with monoclonal antibodies of T lymphocytes bearing Fc receptors for IgE (T epsilon cells) and IgG (T gamma cells) in atopic patients

Peripheral blood T lymphocytes from nonatopic control donors, asymptomatic atopic donors, and patients with moderate to severe atopic dermatitis were analyzed for Fc receptors for IgE (T epsilon cells) and IgG (T gamma cells) by rosette assays and were characterized with monoclonal antibodies. The T cells were reacted first with monoclonal antibodies, followed by fluoresceinated F(ab')2 goat antimouse Ig; they were then rosetted, and subsequently the rosetting cells were examined for immunofluorescence. Seven nonatopic control donors had less than 0.1% T epsilon cells and a mean +/- SD of 10.5% +/- 4.1 T gamma cells. Seven asymptomatic atopic donors with low IgE levels (2 to 233 IU/ml) varied from less than 0.1 to 1.3% T epsilon cells and 7.2% +/- 3.7 T gamma cells. Six of seven patients with moderate to severe atopic dermatitis and IgE levels of 1339 to 24,261 IU/ml had less than 0.1% T epsilon cells and significantly fewer T gamma cells (3.1% +/- 2.7, p less than 0.01) than the nonatopic control donors and the atopic donors in remission. Both T epsilon and T gamma cells reacted with the pan-T cell antibody Lyt-3 (anti-sheep red cell receptor) but not with antibodies OKT3, OKT4, or OKT6. Subpopulations of both T epsilon and T gamma cells reacted with antibodies OKT8 and the antimonocyte antibody OKM1. The OKM1+ cells did not appear to be monocytes, however, because the T cells did not react with another antimonocyte antibody, BRL.2, and were negative for nonspecific esterase activity. (ABSTRACT TRUNCATED AT 250 WORDS)     

Eosinophil chemotactic chemokines (eotaxin, eotaxin-2, RANTES, monocyte chemoattractant protein-3 (MCP-3), and MCP-4), and C-C chemokine receptor 3 expression in bronchial biopsies from atopic and nonatopic (Intrinsic) asthmatics

Atopic (AA) and nonatopic (NAA) asthma are characterized by chronic inflammation and local tissue eosinophilia. Many C-C chemokines are potent eosinophil chemoattractants and act predominantly via the CCR3. We examined the expression of eotaxin, eotaxin-2, RANTES, monocyte chemoattractant protein-3 (MCP-3), MCP-4, and CCR3 in the bronchial mucosa from atopic (AA) and nonatopic (intrinsic; NAA) asthmatics and compared our findings with atopic (AC) and nonatopic nonasthmatic controls (NC). Cryostat sections were processed for immunohistochemistry (IHC), in situ hybridization (ISH), and double IHC/ISH. Compared with AC and NC, the numbers of EG2+ cells and the cells expressing mRNA for eotaxin, eotaxin-2, RANTES, MCP-3, MCP-4, and CCR3 were significantly increased in AA and NAA (p < 0.01). Nonsignificant differences in these variants were observed between AA and NAA and between AC and NC. Significant correlations between the cells expressing eotaxin or CCR3 and EG2+ eosinophils in the bronchial tissue were also observed for both AA (p < 0.01) and NAA (p = 0.01). Moreover, in the total asthmatic group (AA + NAA) there was a significant inverse correlation between the expression of eotaxin and that of the histamine PC20 (p < 0.05). Sequential IHC/ISH showed that cytokeratin+ epithelial cells, CD31+ endothelial cells, and CD68+ macrophages were the major sources of eotaxin, eotaxin-2, RANTES, MCP-3, and MCP-4. There was no significantly different distribution of cells expressing mRNA for these chemokines between atopic and nonatopic asthma. These findings suggest that multiple C-C chemokines, acting at least in part via CCR3, contribute to bronchial eosinophilia in both atopic and nonatopic asthma.     

Characteristics, clinical effect profile and tolerability of a nasal spray preparation of Artemisia abrotanum L. for allergic rhinitis.

A nasal spray formulation containing an extract of Artemisia abrotanum L. was developed for therapeutic use in patients with allergic rhinitis and other upper airway disorders. The nasal spray preparation used contains a mixture of essential oils (4 mg/ml) and flavonols (2.5 microg/ml), of which some components have been shown to possess antiinflammatory, expectorant, spasmolytic as well as antiseptic and antimicrobial activities. The most important constituents in the essential oil fraction of the preparation are 1,8-cineole, linalool and davanone, while the flavonol fraction contains centauredin, casticin and quercetin dimethyl-ethers. No trace of thujon was observed in the essential oil of the Artemisia abrotanum L. genotype "Tycho" used for the manufacture of the nasal spray preparation. In 12 patients with diagnoses of allergic rhinitis, allergic conjunctivitis and/or bronchial obstructive disease, the nasal spray was given immediately after the appearance of characteristic allergic nasal symptoms. In 10 of the 12 patients, allergic rhinitis with nasal congestion, sneezing and rhinorrhea was dominant. After administration of the nasal spray, all patients experienced a rapid and significant symptom relief of nasal symptoms, comparable to the effect of antihistamine and chromoglicate preparations which several of the patients had used previously. The effect was present within 5 minutes after the administration and lasted for several hours. In 7 of the 10 rhinitis patients with concomitant symptoms of allergic conjunctivitis, a significant subjective relief of eye symptoms was also experienced. In 3 of the 6 patients who had a history of characteristic symptoms of endogenous, exogenous or exercise induced bronchial obstructive disease, there was a bronchial symptom relief by the nasal spray preparation which was experienced as rapid and clinically significant. It is concluded from the present proof of concept study, that a nasal spray formulation containing an extract characterised by a mixture of essential oils and flavonols from the Artemisia abrotanum L. genotype "Tycho", appears to be clinically useful and suitable for the prophylactic and therapeutic management of patients with allergic rhinitis and adjuvant symptoms.     

Levocabastine eye drops are effective and well tolerated for the treatment of allergic conjunctivitis in children

This open-label, prospective, multicentre, 4-week trial was undertaken to assess the efficacy and tolerability of twice daily levocabastine eye drops (0.5 mg/ml), with sodium cromoglycate nasal spray for the relief of concurrent nasal symptoms if required, in a total of 233 children with seasonal allergic conjunctivitis. No correlation between efficacy, tolerability and age was found. Investigator assessments revealed that the total severity of ocular symptoms decreased by 84 +/- 34% in patients < 12 years and 85 +/- 30% in those >/= 12 years, with corresponding reductions in the total severity of ocular findings of 84% in both patient groups over the 4-week treatment period. Global assessments of therapeutic efficacy revealed the effect of therapy on ocular symptoms to be excellent or good in 81% of patients < 12 years and 82% of those >/= 12 years after 2 weeks of treatment, with corresponding values at the end of the trial of 88% and 82% in the two groups, respectively. Treatment tolerability was considered to be excellent or good by 94% of patients overall. Application site reactions were the most common adverse event associated with ocular levocabastine, occurring in 13% of patients < 12 years and 9% of those >/= 12 years. Twice daily levocabastine eye drops therefore appear to be effective and well tolerated for the treatment of seasonal allergic conjunctivitis in children.     

Preferential messenger RNA expression of Th1-type cells (IFN-gamma+, IL-2+) in classical delayed-type (tuberculin) hypersensitivity reactions in human skin.

We recently established that the allergen-induced late-phase cutaneous reaction in atopic subjects was associated with high mRNA expression for the cytokine gene cluster IL-3, IL-4, IL-5, and granulocyte/macrophage-CSF (GM-CSF), compared with IFN-gamma and IL-2, suggesting that allergic skin reactions contained the equivalent of murine Th2 cells. We now show that, in humans, classical delayed-type hypersensitivity is associated with cells preferentially expressing a Th1-type cytokine profile. Cryostat sections from skin biopsies from 24-h tuberculin reactions in 10 nonatopic subjects were hybridized with 35S-labeled RNA probes and processed by using in situ hybridization. On the whole, tuberculin biopsies showed preferential expression of mRNA encoding IFN-gamma and IL-2, although in some cases mRNA expression for IL-3, IL-4, IL-5, and GM-CSF was also observed. Biopsies from diluent control sites gave only occasional signals. The difference in the number of cells expressing mRNA in the diluent compared with tuberculin sites was statistically significant for IL-2 and IFN-gamma (p less than 0.01) but not for IL-3, IL-4, IL-5, and GM-CSF. These results suggest that cells infiltrating the site of the 24-h tuberculin reaction preferentially transcribe mRNA encoding IFN-gamma and IL-2, supporting the hypothesis that delayed-type hypersensitivity is associated with preferential activation of cells having a cytokine profile similar to the murine Th1 subset.     

Intrinsic ICAM-1/LFA-1 activation mediates altered responsiveness of atopic asthmatic airway smooth muscle

Cell adhesion molecules (CAMs) have been importantly implicated in the pathobiology of the airway responses in allergic asthma, including inflammatory cell recruitment into the lungs and altered bronchial responsiveness. To elucidate the mechanism of CAM-related mediation of altered airway responsiveness in the atopic asthmatic state, the expressions and actions of intercellular adhesion molecule-1 (ICAM-1) and its counterreceptor ligand lymphocyte function-associated antigen-1 (LFA-1; i.e., CD11a/CD18) were examined in isolated rabbit airway smooth muscle (ASM) tissues and cultured human ASM cells passively sensitized with sera from atopic asthmatic patients or nonatopic nonasthmatic (control) subjects. Relative to control tissues, the atopic asthmatic sensitized ASM exhibited significantly enhanced maximal contractility to acetylcholine and attenuated relaxation responses to isoproterenol. These proasthmatic changes in agonist responsiveness were ablated by pretreating the atopic sensitized tissues with a monoclonal blocking antibody (MAb) to either ICAM-1 or CD11a, whereas a MAb directed against the related beta(2)-integrin Mac-1 had no effect. Moreover, relative to control tissues, atopic asthmatic sensitized ASM cells displayed an autologously upregulated mRNA and cell surface expression of ICAM-1, whereas constitutive expression of CD11a was unaltered. Extended studies further demonstrated that 1) the enhanced expression and release of soluble ICAM-1 by atopic sensitized ASM cells was prevented when cells were pretreated with an interleukin (IL)-5-receptor-alpha blocking antibody and 2) administration of exogenous IL-5 to naive (nonsensitized) ASM cells induced a pronounced soluble ICAM-1 release from the cells. Collectively, these observations provide new evidence demonstrating that activation of the CAM counterreceptor ligands ICAM-1 and LFA-1, both of which are endogenously expressed in ASM cells, elicits autologously upregulated IL-5 release and associated changes in ICAM-1 expression and agonist responsiveness in atopic asthmatic sensitized ASM.     

Inter-Relationship between Rhinitis and Conjunctivitis in Allergic Rhinoconjunctivitis and Associated Risk Factors in Rural UK Children

Objective

Allergic conjunctivitis (AC) is a common condition, especially in childhood. The extent to which it occurs concurrently with or independently from allergic rhinitis (AR) has not been well described.

Aim

To examine the inter-relationship between rhinitis and conjunctivitis and the epidemiological risk factors for these conditions in a rural UK population.

Methods

Cross-sectional study of rural school children (aged 5–11 years). Parental questionnaires were used to diagnose allergic outcomes (including conjunctivitis, rhinitis and rhinoconjunctivitis), and to collect data on atopic history, demographic and environmental exposures. Odds ratios of allergic outcome by exposure were examined adjusted for age, sex, breastfeeding, family history of allergy, number of older and younger siblings.

Results

Prevalence of conjunctivitis was 17.5%, rhinitis 15.1% and rhinoconjunctivitis 13.0%. Seasonality of symptoms varied by condition: 64.7% of those with conjunctivitis had seasonal symptoms (April-Sept only), 46.7% of those with rhinitis and 92.2% of those with rhinoconjunctivitis. Living on a farm consistently reduced the risk of conjunctivitis (odds ratio 0.47, 95%CI 0.29–0.79, p = 0.004), rhinitis (OR 0.57, 95%CI 0.33–1.01, p = 0.05) and rhinoconjunctivitis (OR 0.57, 95%CI 0.32–1.03, p = 0.06). Exposure to farm animals (particularly in early life), current consumption of unpasteurised milk and playing in a barn or stable significantly reduced the risk of all three conditions.

Conclusion

More children had parent-reported conjunctivitis than rhinitis. The majority of children with either condition also reported symptoms with the other condition. Farmers’ children have less eye and/or nasal symptoms. A number of farming variables linked with the farm microbial environment are likely to be mediating the protective effect.     

Differentiation of the four animal and the four vegetal blastomeres of the eight-cell-stage ofTriturus alpestris

Summary The 4 animal and 4 vegetal blastomeres of the eight-cell-stage ofTriturus alpestris were isolated and cultured for up to 12 days. Because of the difficulty of obtaining intact animal and vegetal blastomeres of the same embryo, we either cut off the vegetal blastomeres or sucked off the animal blastomeres. The culture of early embryonic amphibian cells is improved by the use of 50% Leibovitz-medium with added fetal calf serum providing a stable pH and optimal osmotic pressure.Isolated animal blastomeres differentiated to irregularly shaped ciliated epidermis. 30% of the cases showed small amounts of myotomes, notochord and neuroid cells in addition to irregular epidermis. The vegetal blastomeres formed trunk and tail structures but only 6% of all cases formed nearly complete head structures in addition.From the results we conclude that the vegetal blastomeres as well as the animal blastomeres of the eight-cell-stage are already determined as to their future fate. The possibility of partial regulation and the influence of asymmetric or irregular cleavage on the further development of isolated blastomeres is discussed.     

Evidence for compartmentalization of functional subsets of CD2+ T lymphocytes in atopic patients

Lymphokine secretion profiles were studied of human allergen-specific CD4+ T lymphocyte clones (TLC). To this aim, panels of house dust mite Dermatophagoides pteronyssinus (Dp)-specific TLC were generated from two atopic Dp-allergic patients, suffering from severe atopic dermatitis (AD1) and allergic asthma (AD2), respectively, and from a non-atopic individual (NAD). From AD1 additional TLC were cloned specific for tetanus toxoid or Candida albicans, both Ag that were not relevant for the atopic state of this patient. Secretion of IL-2, IL-4, and IFN-gamma was determined after specific stimulation of these TLC, using autologous monocytes as APC. With respect to the production of IL-4 and IFN-gamma, clearly distinct profiles were observed. All Dp-specific TLC from both atopic donors produced IL-4 but not IFN-gamma, whereas the Dp-specific TLC from NAD, as well as the tetanus toxoid- and C. albicans-specific TLC from AD1, all produced IFN-gamma but not or small quantities of IL-4. Most TLC from all panels produced IL-2. These lymphokine profiles were consistent for at least 3 days and were neither dependent on the dose of allergen nor on the atopic or nonatopic state of the donor of APC. The functional consequence of these restricted lymphokine profiles was stressed by the observation that, whereas Dp-specific TLC from AD1 and AD2 supported in vitro IgE production, this support could be abrogated by a Dp-specific TLC from NAD. The present results suggest that CD4+ T lymphocytes that produce IL-4, but not IFN-gamma, occur in high frequencies in the allergen-specific T cell repertoires of atopic donors, which may have important implications for the pathomechanism of atopic disease.     

Penicillinase-producing Neisseria gonorrhoeae conjunctivitis on some Nigerian children.

During 21 month study of bacterial conjunctivitis among 121 children in two health care centres in Calabar, Nigeria, a total of 90 (74.4%) cases were culturally confirmed. Neonates had the highest age-specific attack rates with 48 (53.3%) cases. Neisseria gonorrhoeae, the predominant pathogen, was recovered from 32 (35.6%) infections; 21 (65.6%) of them from neonates. Cultures of genital swabs of consenting parents of infected neonates as well as those of three female children aged 2-12 years with concurrent vulvo-vaginitis yielded N. gonorrhoeae. Younger women, mostly primi-gravidae were more frequently found to have benefited from peri-natal health care services than older multi-gravidae. Nevertheless, such access to health care services did not appear to influence the frequency of gonococcal conjunctivitis in neonates from the two maternal groups (P < 0.01). Sexual abuse and contaminated fomites were the possible modes of gonococcal infection transmission to older children. Overall, 22 (68.8%) strains of gonococci were resistant to penicillin; 19 (59.4%) were penicillinase-producing Neisseria gonorrhoeae (PPNG), while 5 (15.6%) had chromosomally-mediated resistance. All isolates were sensitive to erythromycin. This study recommends a review of gonorrhoea surveillance in pregnancy to include routine examination of cervical swabs just before delivery.     

Echocardiographic alterations in a child with cow's milk allergy: a case report

ABSTRACT: INTRODUCTION: Cow's milk allergy is the most frequent food allergy in Europe and western countries and shows a wide spectrum of clinical features, including atopic dermatitis and gastrointestinal disease. To the best of our knowledge, this report is the first to describe Kawasaki disease-like clinical features and echocardiographic alterations which resolved after a cow's milk-free diet. CASE PRESENTATION: We report a case of a 9-month-old Caucasian girl with atopic dermatitis who developed clinical features commonly present in Kawasaki disease (erythematous skin rash, non-exudative conjunctivitis, fissured lips and neck lymph nodes), together with mild echocardiographic alterations (perivascular brightness, pericardial effusion) in the absence of fever. These features resolved within 2 weeks after the beginning of a cow's milk-free diet. CONCLUSION: Kawasaki disease has recently been considered a possible risk factor for subsequent allergic disease secondary to immune dysfunction. This case report suggests that the immune-related alterations which are commonly present in allergic patients could be similar to the antigen-related immune response in Kawasaki disease and thus could lead to similar clinical features.     

Highly Th2-skewed cytokine profile of beta-lactam-specific T cells from nonatopic subjects with adverse drug reactions.

A positive lymphocyte transformation test to beta-lactams (beta-L) was found in 12 of 29 subjects with adverse drug reaction (ADR) to beta-L, irrespective of either the type of clinical manifestation or the presence of specific serum IgE. Short-term T cell lines specific for penicillin G, amoxicillin, and ampicillin could be generated only from subjects with ADR (eight with positive and one with negative lymphocyte transformation test), while streptokinase and Dermatophagoides pteronyssinus group 1 (Der p 1)-specific T cells were obtained from all these subjects, from 7 atopic Der p-sensitive donors without history of ADR and 17 healthy nonatopic donors. Streptokinase-specific T cells from all subjects showed intracellular expression of IFN-gamma with poor or no IL-4, whereas Der p 1-specific T cells exhibited IFN-gamma but low or no IL-4 expression in nonatopics, and remarkable IL-4 expression in atopic donors. By contrast, all penicillin G-, ampicillin-, and amoxicillin-specific short-term T cell lines showed high intracellular expression of IL-4, IL-5, and IL-13, but poor or no expression of IFN-gamma, thus exhibiting a clear-cut Th2 profile. Accordingly, most penicillin G-specific T cell clones derived from two subjects with ADR released high concentrations of IL-4 alone or IL-4 and IFN-gamma. These data suggest that cytokines produced by Th2 cells play an important role in all beta-L-induced ADR, even when late clinical manifestations occur and an IgE-mediated mechanism is apparently indemonstrable.     

Respiratory fungal allergy

Fungal allergy including allergic rhinitis, conjunctivitis, bronchial asthma, and allergic bronchopulmonary mycoses results from exposure to spores. In this review we have dealt with the common allergenic fungi and allergens, immunopathogenesis, diagnostic assays, and the possible control of allergy in the future based on epitope-specific immunotherapy and vaccination.     

Anti-human IgG causes basophil histamine release by acting on IgG-IgE complexes bound to IgE receptors.

We have reexamined the ability of anti-human IgG antibodies to induce histamine release from human basophils. A panel of purified murine mAbs with International Union of Immunological Societies-documented specificity for each of the four subclasses of human IgG was used. Of the 24 allergic subjects studied, the basophils of 75% (18/24) released greater than 10% histamine to one or more anti-IgG1-4 mAb, whereas none of the 13 nonatopic donor's basophils released histamine after stimulation with optimal amounts of anti-IgG mAb. The basophils of 85% (11/13) of the nonatopic donors did respond to anti-IgE challenge, as did 92% (22/24) of the atopic donor cells. Histamine release was induced most frequently by anti-IgG3, and 10/18 anti-IgG responder cells released histamine with mAb specific for two or more different subclass specificities. The rank order for induction of histamine release was anti-IgG3 greater than anti-IgG2 greater than IgG1 greater than anti-IgG4. As in our previous study using polyclonal anti-IgG, 100- to 300-micrograms/ml quantities of the anti-IgG mAb were required for maximal histamine release, about 1000-fold higher than those for comparable release with anti-human IgE. Specificity studies using both immunoassays and inhibition studies with IgE myeloma protein indicated that anti-IgG induced histamine release was not caused by cross-reactivity with IgE. Ig receptors were opened by lactic acid treatment so that the cells could be passively sensitized. Neither IgE myeloma nor IgG myeloma (up to 15 mg/ml) proteins could restore the response to anti-IgG mAb. However, sera from individuals with leukocytes that released histamine upon challenge with anti-IgG mAb could passively sensitize acid-treated leukocytes from both anti-IgG responder and nonresponder donors for an anti-IgG response. The only anti-IgG mAb that induced release from these passively sensitized cells were those to which the serum donor was responsive. Sera from non-IgG responders could not restore an anti-IgG response. These data led to the hypothesis that the IgG specific mAb were binding to IgG-IgE complexes that were attached to the basophil through IgE bound to the IgE receptor. This was shown to be correct because passive sensitization to anti-IgG could be blocked by previous exposure of the basophils to IgE. We conclude that anti-IgG-induced release occurs as a result of binding to IgG anti-IgE antibodies and cross-linking of the IgE receptors on basophils.     

Nasal hyperreactivity and inflammation in allergic rhinitis

The history of allergic disease goes back to 1819, when Bostock described his own 'periodical affection of the eyes and chest', which he called 'summer catarrh'. Since they thought it was produced by the effluvium of new hay, this condition was also called hay fever. Later, in 1873, Blackley established that pollen played an important role in the causation of hay fever. Nowadays, the definition of allergy is 'An untoward physiologic event mediated by a variety of different immunologic reactions'. In this review, the term allergy will be restricted to the IgE-dependent reactions. The most important clinical manifestations of IgE-dependent reactions are allergic conjunctivitis, allergic rhinitis, allergic asthma and atopic dermatitis. However, this review will be restricted to allergic rhinitis. The histopathological features of allergic inflammation involve an increase in blood flow and vascular permeability, leading to plasma exudation and the formation of oedema. In addition, a cascade of events occurs which involves a variety of inflammatory cells. These inflammatory cells migrate under the influence of chemotactic agents to the site of injury and induce the process of repair. Several types of inflammatory cells have been implicated in the pathogenesis of allergic rhinitis. After specific or nonspecific stimuli, inflammatory mediators are generated from cells normally found in the nose, such as mast cells, antigen-presenting cells and epithelial cells (primary effector cells) and from cells recruited into the nose, such as basophils, eosinophils, lymphocytes, platelets and neutrophils (secondary effector cells). This review describes the identification of each of the inflammatory cells and their mediators which play a role in the perennial allergic processes in the nose of rhinitis patients.     

Effect of purified staphylococcal toxoid preparation on the in vitro production of interferon by leukocytes from patients with atopic dermatitis

The impact of purified staphylococcal toxoid (PST) on the in vitro production of interferon (IFN) by blood leukocytes was evaluated. PST was found to produce a stimulating effect on the production of alpha-IFN in patients with atopic dermatitis (AD): in 88% of cases a two-fivefold increase in IFN production was observed in AD patients in comparison with healthy donors. In addition, the incubation of leukocytes obtained from atopic and nonatopic patients with PST was shown to stimulate the production of gamma-IFN by these leukocytes fivefold, on the average. These results give theoretical basis for use of PST (as an inducer of endogenic IFN) for AD patients treatment.