Related Articles

Background

Type I hypersensitivity is characterized by the overreaction of the immune system against otherwise innocuous substances. It manifests as allergic rhinitis, allergic conjunctivitis, allergic asthma or atopic dermatitis if mast cells are activated in the respective organs. In case of systemic mast cell activation, life-threatening anaphylaxis may occur. Currently, type I hypersensitivities are treated either with glucocorticoids, anti-histamines, or mast cell stabilizers. Although these drugs exert a strong anti-allergic effect, their long-term use may be problematic due to their side-effects.

Results

In the course of a routine in vitro screening process, we identified beta-escin as a potentially anti-allergic compound. Here we tested beta-escin in two mouse models to confirm this anti-allergic effect in vivo. In a model of the early phase of allergic reactions, the murine passive cutaneous anaphylaxis model, beta-escin inhibited the effects of mast cell activation and degranulation in the skin and dose-dependently prevented the extravasation of fluids into the tissue. Beta-escin also significantly inhibited the late response after antigen challenge in a lung allergy model with ovalbumin-sensitized mice. Allergic airway inflammation was suppressed, which was exemplified by the reduction of leucocytes, eosinophils, IL-5 and IL-13 in the bronchoalveolar lavage fluid. Histopathological examinations further confirmed the reduced inflammation of the lung tissue. In both models, the inhibitory effect of beta-escin was comparable to the benchmark dexamethasone.

Conclusions

We demonstrated in two independent murine models of type I hypersensitivity that beta-escin has potent anti-allergic properties. These results and the excellent safety profile of beta-escin suggest a therapeutic potential of this compound for a novel treatment of allergic diseases.

A female in her early 50s presented with a long-standing history of episodic urticaria and angioedema. She also reported urticarial reactions after ingestion of aspirin, prednisone and multiple antibiotics. These medications were all taken during upper respiratory tract infections. An elimination diet followed by a series of open challenges to food chemicals demonstrated an urticarial eruption following the ingestion of mints, which contain high levels of salicylates. A double-blinded placebo-controlled challenge to salicylate confirmed her sensitivity and explained her reaction to aspirin. The patient informed her treating physician of her copious ingestion of mints during upper respiratory tract infections. Drug hypersensitivity to antibiotics and prednisone was excluded on the basis of negative radioallergosorbent tests (RASTs) and/or absent skin-test responses and/or tolerance to oral challenges. This patient had a salicylate intolerance that caused her episodic urticaria and angioedema, and also masqueraded as a drug allergy due to the concurrent ingestion of mints.

Menthol is a widely-used cooling and flavoring agent derived from mint leaves. In the peripheral nervous system, menthol regulates sensory transduction by activating TRPM8 channels residing specifically in primary sensory neurons. Although behavioral studies have implicated menthol actions in the brain, no direct central target of menthol has been identified. Here we show that menthol reduces the excitation of rat hippocampal neurons in culture and suppresses the epileptic activity induced by pentylenetetrazole injection and electrical kindling in vivo. We found menthol not only enhanced the currents induced by low concentrations of GABA but also directly activated GABAA receptor (GABAAR) in hippocampal neurons in culture. Furthermore, in the CA1 region of rat hippocampal slices, menthol enhanced tonic GABAergic inhibition although phasic GABAergic inhibition was unaffected. Finally, the structure-effect relationship of menthol indicated that hydroxyl plays a critical role in menthol enhancement of tonic GABAAR. Our results thus reveal a novel cellular mechanism that may underlie the ambivalent perception and psychophysical effects of menthol and underscore the importance of tonic inhibition by GABAARs in regulating neuronal activity.

The development of chronic allergic dermatitis in early life has been associated with increased onset and severity of allergic asthma later in life. However, the mechanisms linking these two diseases are poorly understood. Here, we report that the development of oxazolone-induced chronic allergic dermatitis, in a mouse model, caused enhanced ovalbumin-induced allergic asthma after resolution of the former disease. Our findings show that oxazolone-induced dermatitis caused a marked increase in tissue mast cells, which persisted long after the resolution of this disease. Subsequent ovalbumin sensitization and airway challenge of mice that had recovered from dermatitis resulted in increased allergic airway hyperreactivity. The findings demonstrate that the accumulation of mast cells during dermatitis has the detrimental effect of increasing allergic airway hypersensitivity. Importantly, our findings also show that exposure to a given allergen can modify the immune response to an unrelated allergen.

Background

Allergic contact dermatitis is a typical delayed-type hypersensitivity to sensitizing haptens mediated by T cells. Th1/Tc1 cells are currently considered to be the primary effectors in allergic contact dermatitis. There is little information concerning the role played in allergic contact dermatitis in humans by Th-17/Tc-17 cells, a recently defined subpopulation of effector T cells.

Objectives

In the present report we attempted to characterize Th-17/Tc-17 cells in the infiltrates of the skin in elicitation phase of allergic contact dermatitis.

Patients/Methods

Th-17 as well as Th1/Th2 cytokine gene expression was examined by semi-quantitative real-time polymerase chain reaction in paired samples of positive patch test biopsies and normal skins from 11 patients allergic to 9 different allergens. The in situ characterization of IL-17-producing cells was carried out using anti-RORC and anti-T cell subset antibodies by double immunofluorescence.

Results

Compared to normal paired skins, gene expression of transcription factor for human Th-17 cells, RORC, and Th-17-related cytokines IL-17A, IL-17F and IL-23, was significantly increased in positive patch test biopsies. The mRNA for IFN-γ and IL-4 was also increased. In the dermal infiltrates, about 20 % of the infiltrating cells were IL-17-producing cells as they expressed RORC, and such RORC expressing cells were detected in both CD4+ (~30%) and CD8+ (~20%) subsets.

Conclusions

This is the first demonstration of Th-17/Tc-17 cells in the elicitation phase of human allergic contact dermatitis, showing that they are a regular participant in the immunopathology of this common allergic reaction regardless of the nature of the triggering allergens.

Allergic contact dermatitis is the most frequent occupational disease in industrialized countries. It is caused by CD8+ T cell–mediated contact hypersensitivity (CHS) reactions triggered at the site of contact by a variety of chemicals, also known as weak haptens, present in fragrances, dyes, metals, preservatives, and drugs. Despite the myriad of potentially allergenic substances that can penetrate the skin, sensitization is relatively rare and immune tolerance to the substance is often induced by as yet poorly understood mechanisms. Here we show, using the innocuous chemical 2,4-dinitrothiocyanobenzene (DNTB), that cutaneous immune tolerance in mice critically depends on epidermal Langerhans cells (LCs), which capture DNTB and migrate to lymph nodes for direct presentation to CD8+ T cells. Depletion and adoptive transfer experiments revealed that LCs conferred protection from development of CHS by a mechanism involving both anergy and deletion of allergen-specific CD8+ T cells and activation of a population of T cells identified as ICOS+CD4+Foxp3+ Tregs. Our findings highlight the critical role of LCs in tolerance induction in mice to the prototype innocuous hapten DNTB and suggest that strategies targeting LCs might be valuable for prevention of cutaneous allergy.

Skin-infiltrating T-cells play a predominant role in allergic and inflammatory skin diseases such as atopic dermatitis, psoriasis and allergic contact dermatitis. These T-cells are attracted by several chemotactic factors including the chemokine CCL5/RANTES, a CC chemokine inducing both the migration and activation of specific leukocyte subsets. CCL5 has been found to be associated with various cell-mediated hypersensitive disorders such as psoriasis, atopic dermatitis and irritant contact dermatitis. We have used two antagonists, the first, Met-CCL5, a dual CCR1/CCR5 antagonist and the second, a variant in which GAG binding is abrogated, 44AANA47-CCL5, which acts as a dominant negative inhibitor of CCL5. The antagonists were tested in two models of contact skin reaction. The first, irritant contact dermatitis (ICD) is a pathological non-specific inflammatory skin condition arising from the release of pro-inflammatory cytokines by keratinocytes in response to haptens, usually chemicals. The second, contact hypersensitivity (CHS) is a T-cell dependent model, mimicking in part the T-cell-mediated skin diseases such as psoriasis. In both models, the CCL5 antagonists showed therapeutic efficacy by reducing swelling by 50% as well as the reduction of soluble mediators in homogenates derived from challenged ears. These results demonstrate that blocking the receptor or the ligand are both effective strategies to inhibit skin inflammation.

Erythema multiforme (EM) is an acute mucocutaneous hypersensitivity reaction with varying degrees of blistering and ulceration. Common causes of EM are herpes simplex virus infection, mycoplasma infection, drug hypersensitivity, vaccination and drug–virus interaction. EM induced by contact dermatitis is rare. Paraphenylene diamine, a common ingredient in many hair dyes, is well known to produce allergic contact dermatitis. We report a 35-year-old lady presenting with EM following severe contact dermatitis to hair dye. So far as we know, this is the first report from India describing EM following contact dermatitis.

Introduction

A unique case of topical food allergy is presented with unilateral swelling of the tongue with ulceration. Only one similar case has been reported in 1972.

Case presentation

76 years old female patient presented at the Emergency Department with a unilateral painful swelling and ulcerations of the tongue after eating mint chocolate. However the swelling did not compromised the airways the presentation was rather frightening for the patient. The allergic reaction responded to the parenteral steroid and oral chlorphenamine treatment and the three month follow up only revealed minimal scar formations.

Conclusion

Unilateral hemiglossitis is a rare form of allergic reactions which is usually self-limiting with full recovery of which takes an unusually long time.

Contact dermatitis is produced by external skin exposure to an allergen, but sometimes a systemically administered allergen may reach the skin and remain concentrated there with the aid of the circulatory system, leading to the production of systemic contact dermatitis (SCD). Metals such as nickel, cobalt, chromium, and zinc are ubiquitous in our environment. Metal allergy may result in allergic contact dermatitis and also SCD. Systemic reactions, such as hand dermatitis or generalized eczematous reactions, can occur due to dietary nickel or cobalt ingestion. Zinc-containing dental fillings can induce oral lichen planus, palmoplantar pustulosis, and maculopapular rash. A diagnosis of sensitivity to metal is established by epicutaneous patch testing and oral metal challenge with metals such as nickel, cobalt, chromium, and zinc. In vitro tests, such as the lymphocyte stimulating test (LST), have some advantages over patch testing to diagnose allergic contact dermatitis. Additionally, the determination of the production of several cytokines by primary peripheral blood mononuclear cell cultures is a potentially promising in vitro method for the discrimination of metal allergies, including SCD, as compared with the LST.

Allergic contact dermatitis differs from most other immune reactions by its strict dose dependence during the elicitation phase. Moreover, almost all known contact allergens can also induce dose-dependent irritative dermatitis and in general only elicit allergic contact dermatitis in sensitized individuals when applied within a narrow dose range. Therefore, we hypothesized that elicitation of contact hypersensitivity (CHS) may require two signals, antigen-specific effector cell activation and a non-antigen-specific proinflammatory signal, both of which are provided by application of a sufficient dose of hapten. To dissociate these putative two signals, oxazolone-sensitized mice were ear challenged with a dose of the specific hapten which was too low to elicit CHS. At the same time, an unrelated hapten was applied in a conventional concentration to the same skin site. Whereas neither treatment alone elicited a significant CHS response, application of both compounds together resulted in a strong CHS response that was indistinguishable from that elicited by the full dose of the specific hapten. Upon coadministration of the irrelevant hapten, allergic contact dermatitis could be elicited even when the dose of the specific hapten was further reduced by a factor of 10(3). In contrast, a dose reduction of the irrelevant hapten by a factor of two resulted in the loss of the CRS response. These data indicate that non-antigen-specific effects of epicutaneously applied haptens significantly contribute to the elicitation of CHS responses and that the capacity of the hapten to evoke this proinflammatory stimulus rather than its antigenicity is responsible for the strict concentration dependence.

Chlorhexidine is a widely used antiseptic and disinfectant in medical and non-medical environments. Compared to its ubiquitous use, allergic contact dermatitis from chlorhexidine has rarely been reported and so its sensitization rate seems to be low. Chlorhexidine has been used for more than 50 years but it was only in the last two decades, that reports of immediate- type reactions to chlorhexidine were seen. Reactions ranging from localized urticaria to anaphylactic shock and hypersensitivity reactions, including delayed hypersensitivity reactions such as contact dermatitis, fixed drug eruptions, and photosensitivity reactions, began to appear more frequently. However the prevalence of contact urticaria and anaphylaxis due to chlorhexidine remains to be unknown. In this case report we have reported a case of urticaria due to oral use of chlorhexidine. The adverse reaction was confirmed by a skin prick test.

Since the 1920s, menthol has been added to cigarettes and used as a characterizing flavor. The health effects of cigarette smoking are well documented, however the health effects of menthol cigarettes as compared to non-menthol cigarettes is less well studied. This review discusses menthol’s effects on 1) biomarkers of tobacco smoke exposure, 2) toxicity and cellular effects, 3) lung function and respiration, 4) pulmonary and/or vascular function, 5) allergic reactions and inflammation, and 6) tobacco-related diseases. It is concluded that menthol is a biologically active compound that has effects by itself and in conjunction with nicotine, however much of the data on the other areas of interest are inconclusive and firm conclusions cannot be drawn.

Background. Gum arabic is a potential sensitizer in food industry. Methods. We examined 11 candy factory workers referred to examinations due to respiratory and skin symptoms paying attention to exposure and sensitization to gum arabic. Skin tests, pulmonary function tests, and respiratory provocation tests were carried out as indicated by the symptoms and findings. Results. Occupational asthma, caused by gum arabic was diagnosed in 4/11 candy factory workers and two of them had also occupational contact urticaria and one had occupational rhinitis. One of them had oral symptoms associated with ingestion of products containing gum arabic. Conclusions. Airborne exposure to gum arabic may cause sensitization leading to allergic rhinitis, asthma, and urticaria.

Recent research suggests that the left inferior frontal gyrus (LIFG) plays a role in selecting semantic information from among competing alternatives. A key question remains as to whether the LIFG is engaged by the selection of semantic information only or by increased semantic competition in and of itself, especially when such competition is implicit in nature. Ambiguous words presented in a lexical context provide a means of examining whether the LIFG is recruited under conditions when contextual cues constrain selection to only the meaning appropriate to the context (e.g., coin-mint-money) or under conditions of increased competition when contextual cues do not allow for the resolution to a particular meaning (e.g., candy-mint-money). In this event-related fMRI study, an implicit task was used in which subjects made lexical (i.e., word/nonword) decisions on the third stimulus of auditorily-presented triplets in conditions where the lexical context either promoted resolution toward a particular ambiguous word meaning or enhanced the competition among ambiguous word meanings. LIFG activation was observed when the context allowed for the resolution of competition and hence the selection of one meaning (e.g., coin-mint-money) but failed to emerge when competition between the meanings of an ambiguous word was unresolved by the context (e.g., candy-mint-money). In the latter case, there was a pattern of reduced activation in frontal, temporal and parietal areas. These findings demonstrate that selection or resolution of competition as opposed to increased semantic competition alone engages the LIFG. Moreover, they extend previous work in showing that the LIFG is recruited even in cases where the selection of meaning takes place implicitly.

Abstracts

Background

Allergic disease is a consequence of exposure to normally innocuous substances that elicit the activation of mast cells. Mast-cell-mediated allergic response is involved in many diseases such as anaphylaxis, urticaria, allergic rhinitis, asthma and allergic dermatitis. The development of food products for the prevention of allergic disease is an important subject in human health. The chungkookjang (CKJ) has been reported to exhibit antiallergic inflammatory activity. Therefore, the aim of the study is to examine the effects of the CKJ to reduce histamine-induced wheal and flare skin responses.

Methods/Design

A randomized, double-blind, placebo-controlled study in 60 healthy subjects will be carried out. Sixty volunteers (aged 20-80) who gave a written consent before entering the study will be randomized in two groups of thirty subjects each. The skin prick test with histamine solution of 10 mg/ml will be performed on the ventral forearm, 10 cm from the elbow. The subjects will be instructed to take 35 g per day of either the CKJ pills or a placebo pills for a period of 3 months. Diameters of wheal and flare will be assessing 15 minutes after performing the above-mentioned skin prick test. The primary outcome is change in wheal and flare responses. Secondary outcomes will be include change in serum histamine, immunoglobulin E, cytokines (interferon-gamma, interleukin-4, -10, and tumor necrosis factor-alpha), and eosinophil cationic protein.

Discussion

This study will show the potential anti-inflammatory properties of the CKJ in their skin activity when histamine is the challenging agent as occurs in the clinical situation. And the present protocol will confirm the efficacy and safety of the CKJ for allergy symptoms, suggesting more basic knowledge to conduct further randomized controlled trials (RCT). If this study will be successfully performed, the CKJ will be an alternative dietary supplemental remedy for allergy patients.

Trial Registration

NCT01402141

The objectives of this study are 1) To review the published data and document the current knowledge on allergic manifestations to the fruit mango 2) To highlight the two distinct clinical presentations of hypersensitivity reactions caused by mango 3) To discuss the role of cross-reactivity 4) To increase awareness of potentially life threatening complications that can be caused by allergy to mango. An extensive search of the literature was performed in Medline/PubMed with the key terms "mango", "anaphylaxis", "contact dermatitis", "cross-reactivity", "food hypersensitivity", "oral allergy syndrome" and "urticaria". The bibliographies of all papers thus located were searched for further relevant articles. A total of 17 reports describing 22 patients were documented, including ten patients with immediate hypersensitivity reaction and twelve patients with delayed hypersensitivity reaction to mango. Ten of these patients (four with immediate reaction; six with delayed reaction) were from geographical areas cultivating mango, whereas twelve patients (six with immediate reaction; six with delayed reaction) were from the countries where large scale mango cultivation does not occur. The clinical features, pathogenesis and diagnostic modalities of both these presentations are highlighted. The fruit mango can cause immediate and delayed hypersensitivity reactions, as also "oral allergy syndrome". Although rare, it can even result in a life threatening event. Reactions may even occur in individuals without prior exposure to mango, owing to cross reactivity. It is imperative to recognize such a phenomenon early so as to avoid potentially severe clinical reactions in susceptible patients.

A variety of cell-mediated hypersensitivity reactions in experimental animals include a prominent infiltrate of basophilic leukocytes. This form of reactivity has been designated cutaneous basophil hypersensitivity and is favored when sensitization to several types of antigen is accomplished without the use of complete Freund's adjuvant. A similar type of hypersensitivity response was sought in man using morphologic techniques which permit identification of basophilic leukocytes. Eight individuals with allergic contact dermatitis to a variety of allergens were studied and six of these developed typical contact reactions with erythema, edema, and epidermal vesicles. The microscopic findings in 3-day biopsies from these individuals differed significantly from classic descriptions of tuberculin hypersensitivity and showed, in addition to mononuclear cells and the characteristic epidermal changes, a substantial infiltrate of basophilic leukocytes and evidence of altered vascular permeability with vascular compaction, dermal edema, and fibrin deposition. Serial biopsies from one individual permitted analysis of the microscopic pathology as it unfolded at successive intervals after patch test. The initial lesion consisted of perivascular accumulations of lymphocytes; this was followed by an influx of basophils and, subsequently, of eosinophils. These findings associate contact allergy in man with the parallel reactions of cutaneous basophil hypersensitivity in animals and provide further evidence for the heterogeneity of the cellular immune response. The data are consistent with the hypothesis that interaction between sensitized lymphocytes and antigen, at a local test site, is responsible for the attraction of basophils. They also directly implicate the clotting system in delayed-type reactions and suggest the possibility of a synergistic relationship between cellular immunity and reactions mediated by basophil-bound, homocytotrophic antibody.

Mast cells play a pivotal role in immediate hypersensitivity and chronic allergic reactions that can contribute to asthma, atopic dermatitis, and other allergic diseases. Since mast cell numbers are increased at sites of inflammation in allergic diseases, pharmacologic intervention into the proliferation, migration, and survival (or apoptosis) of mast cells could be a promising strategy for the management of allergic diseases. Mast cells differentiate from multipotent hematopoietic progenitors in the bone marrow. Stem cell factor (SCF) is a major chemotactic factor for mast cells and their progenitors. SCF also elicits cell-cell and cell-substratum adhesion, facilitates the proliferation, and sustains the survival, differentiation, and maturation, of mast cells. Therefore, many aspects of mast cell biology can be understood as interactions of mast cells and their precursors with SCF and factors that modulate their responses to SCF and its signaling pathways. Numerous factors known to have such a capacity include cytokines that are secreted from activated T cells and other immune cells including mast cells themselves. Recent studies also demonstrated that monomeric IgE binding to FcεRI can enhance mast-cell survival. In this review we discuss the factors that regulate mast cell development, migration, and survival.

Identification of pre-B-cell colony-enhancing factor (PBEF) interacting partners may reveal new molecular mechanisms of PBEF in the pathogenesis of acute lung injury (ALI). The interactions between PBEF and NADH dehydrogenase subunit 1(ND1), ferritin light chain and interferon induced transmembrane 3 (IFITM3) in human pulmonary vascular endothelial cells were identified and validated. ND1, ferritin and IFITM3 are involved in oxidative stress and inflammation. Overexpression of PBEF increased its interactions and intracellular oxidative stress, which can be attenuated by rotenone. The interaction modeling between PBEF and ND1 is consistent with the corresponding experimental finding. These interactions may underlie a novel role of PBEF in the pathogenesis of ALI.

Structured summary

MINT-6538697:

PBEF (uniprotkb:P43490) physically interacts (MI:0218) with NADH1 (uniprotkb:P03886) by two hybrid (MI:0018)

MINT-6538811, MINT-6538868:

PBEF (uniprotkb:P43490) physically interacts (MI:0218) with interferon-induced transmembra (uniprotkb:Q01628) by anti bait coimmunoprecipitation (MI:0006)

MINT-6538787, MINT-6538841:

PBEF (uniprotkb:P43490) physically interacts (MI:0218) with NADH1 (uniprotkb:P03886) by anti bait coimmunoprecipitation (MI:0006)

MINT-6538755:

PBEF (uniprotkb:P43490) physically interacts (MI:0218) with gamma-glutamil-transferase (uniprotkb:P19440) by two hybrid (MI:0018)

MINT-6538799, MINT-6538862:

PBEF (uniprotkb:P43490) physically interacts (MI:0218) with Ferritin light chain (uniprotkb:P02792) by anti bait coimmunoprecipitation (MI:0006)

MINT-6538769:

PBEF (uniprotkb:P43490) physically interacts (MI:0218) with E2L6 (uniprotkb:O14933) by two hybrid (MI:0018)

MINT-6538741:

PBEF (uniprotkb:P43490) physically interacts (MI:0218) with Adenosine A2aR (uniprotkb:P29274) by two hybrid (MI:0018)

MINT-6538727:

PBEF (uniprotkb:P43490) physically interacts (MI:0218) with interferon-induced transmembra (uniprotkb:Q01628) by two hybrid (MI:0018)

MINT-6538712:

PBEF (uniprotkb:P43490) physically interacts (MI:0218) with Ferritin light chain (uniprotkb:P02792) by two hybrid (MI:0018)

Occupational and recreational plant exposure on the skin is fairly common. Plant products and extracts are commonly used and found extensively in the environment. Adverse reactions to plants and their products are also fairly common. However, making the diagnosis of contact dermatitis from plants and plant extracts is not always simple and straightforward. Phytodermatitis refers to inflammation of the skin caused by a plant. The clinical patterns may be allergic phytodermatitis, photophytodermatitis, irritant contact dermatitis, pharmacological injury, and mechanical injury. In this article, we will focus mainly on allergy contact dermatitis from plants or allergic phytodermatitis occurring in Asia.

Background

The mint family (Lamiaceae) produces a wide variety of constituents with medicinal properties. Several family members have been reported to have antiviral activity, including lemon balm (Melissa officinalis L.), sage (Salvia spp.), peppermint (Mentha × piperita L.), hyssop (Hyssopus officinalis L.), basil (Ocimum spp.) and self-heal (Prunella vulgaris L.). To further characterize the anti-lentiviral activities of Prunella vulgaris, water and ethanol extracts were tested for their ability to inhibit HIV-1 infection.

Results

Aqueous extracts contained more anti-viral activity than did ethanol extracts, displaying potent antiviral activity against HIV-1 at sub μg/mL concentrations with little to no cellular cytotoxicity at concentrations more than 100-fold higher. Time-of-addition studies demonstrated that aqueous extracts were effective when added during the first five hours following initiation of infection, suggesting that the botanical constituents were targeting entry events. Further analysis revealed that extracts inhibited both virus/cell interactions and post-binding events. While only 40% inhibition was maximally achieved in our virus/cell interaction studies, extract effectively blocked post-binding events at concentrations similar to those that blocked infection, suggesting that it was targeting of these latter steps that was most important for mediating inhibition of virus infectivity.

Conclusions

We demonstrate that aqueous P. vulgaris extracts inhibited HIV-1 infectivity. Our studies suggest that inhibition occurs primarily by interference of early, post-virion binding events. The ability of aqueous extracts to inhibit early events within the HIV life cycle suggests that these extracts, or purified constituents responsible for the antiviral activity, are promising microbicides and/or antivirals against HIV-1.

Background

Metal-working fluids contain complex mixtures of chemicals and metal workers constitute a potential risk group for the development of allergic contact dermatitis.

Case presentation

Two metal workers developed allergic contact dermatitis on the hands and lower arms from exposure to a neat oil used in metal processing. Patch testing revealed that the relevant contact allergen was a cycloaliphatic epoxy resin, 1,2-cyclohexanedicarboxylic acid, bis(oxiranylmethyl) ester, added to the oil as a stabilizer. None of the patients had positive reactions to the bisphenol A-based epoxy resin in the standard series.

Conclusions

These cases emphasize that well-known contact allergens may show up from unexpected sources of exposure. Further, it can be a long-lasting, laborious process to detect an occupational contact allergen and cooperation from the patient and the manufacturer of the sensitizing product is essential.

Achieving satisfactory retention in online HIV prevention trials typically have proved difficult, particularly over extended timeframes. The overall aim of this study was to assess factors associated with retention in the Men’s INTernet Study II (MINTS-II), a randomized controlled trial of a sexual risk reduction intervention for men who have sex with men. Participants were recruited via e-mails and banner advertisements in December, 2007 to participate in the MINTS-II Sexpulse intervention and followed over a 12-month period. Retention across the treatment and control arms was 85.2% at 12 months. Factors associated with higher retention included: randomization to the control arm, previous participation in a study by the research team, e-mail and telephone reminders to complete a survey once it was available to take, and fewer e-mail contacts between surveys. The results provide evidence that achieving satisfactory retention is possible in online HIV prevention trials, and suggest best practices for maximizing retention.

Observation of 100 patients with atopic dermatitis due to hypersensitivity to pollen over a period of 12 years emphasized certain important diagnostic and therapeutic features. The incidence was higher in females than in males and higher in middle and old age than in the earlier years.

Pollen dermatitis may be the sole or major manifestation of allergy; 43 patients gave no history of other allergic symptoms. It may involve any or all areas of the body. The site or the distribution of lesions or the nature of the lesions gave no clue as to the diagnosis of pollen sensitivity.

The character of the eruption varied widely from patient to patient and in given patients from week to week at times.

Atopic dermatitis due to pollen sensitivity may be purely seasonal, perennial with seasonal exacerbations or perennial without seasonal variation.

Reactions to skin testing with pollens suspected as allergens may be positive, equivocal or negative. In 58 patients there were positive correlative skin reactions to pollens.

The diagnosis of atopic dermatitis due to pollen sensitivity, and the composition of the desensitizing antigen or antigens, must be based primarily on the clinical history and the area of residence.

Most patients could tolerate only very weak dilutions at the beginning of desensitization therapy. Strong dilutions caused exacerbation of the dermatitis.

Good or excellent results were obtained with perennial pollen desensitization therapy administered over long periods. In 13 patients good results took four to eight years of desensitization therapy. Fifty required less than two years. Tolerance of the patient for a given dose of antigen should determine the maximum dilution used in therapy.