Alton Lee Melton

Latex Hypersensitivity in Emergency Medical Service Providers

BACKGROUND Emergency medical service providers have a high degree of exposure to latex products. Patients utilizing emergency medical services can be allergic to latex products used during rescue efforts. OBJECTIVE To determine the prevalence of latex hypersensitivity among emergency medical service providers. METHODS Study questionnaires were distributed to a group of emergency medical service providers. Skin prick testing was performed using latex, common aeroallergens, and food extracts. Patch testing was done using latex and individual rubber additives. Serum latex-specific IgE was also measured. RESULTS A total of 93 completed surveys were collected. Average exposure to latex in the work environment was 8.2 years. Eighty-four (90%) used latex gloves routinely at work. Of those, thirteen (14%) gave history of reaction to latex gloves. Sixty-two percent were not aware of the possibility of latex allergy in themselves or their patients. Forty-one (44%) had skin testing. Of those, four (10%) had positive prick tests for at least one of the four latex preparations used. Five had positive skin tests to avocado extract without supporting clinical history. Two had positive skin tests to banana, one with supporting clinical history for banana allergy. No food cross-reactivity with latex was demonstrated. Latex-specific serum correlated with prick skin test results. No positive reactions were noted with patch testing. CONCLUSIONS A significant percentage of emergency medical service providers were not aware of the occupational risk of latex allergy or the potential risk in their patients. A positive prick skin test for latex was present in 4 of 41 (10%), representing one-third of those who reported symptoms from latex exposure.

Differential regulation of human blood monocyte and alveolar macrophage inflammatory cytokine production by nitric oxide

BACKGROUND Nitric oxide (NO) has been associated with airway inflammation in asthma. Our previous work suggests that NO functions in an anti-inflammatory capacity through downregulation of stimulated cytokine secretion by normal human alveolar macrophages. Functional differences between alveolar macrophages and blood monocytes are thought to be related to maturation. OBJECTIVE The purpose of this study was to determine the effect of NO on stimulated cytokine production by monocytes from asthmatics and normal healthy controls. METHODS Monocytes and alveolar macrophages were obtained from normal volunteers (n = 13) and asthmatics with atopy (n = 7). Monocyte and alveolar macrophage cultures were stimulated with 0.5 microgram/mL lipopolysaccharide +/- 1.0 mM DETA NONOate (releases NO in culture with t1/2 = 20 hours at 37 degrees C) and incubated for 24 hours. Cell-free supernatants were collected and assayed by ELISA for tumor necrosis factor-alpha (TNF) and granulocyte macrophage colony stimulating factor (GM-CSF). RESULTS Nitric oxide did not inhibit TNF production in monocytes of asthmatics and normals (mean +/- SEM % TNF stimulation = 19.6 +/- 9.7). Similar to previous results, NO did inhibit alveolar macrophages (% TNF suppression = 60.6 +/- 4.4). To determine whether this differential effect of NO on the two cell populations was related to maturation, monocytes were matured by culture for 7 days. The in vitro matured monocytes demonstrated 51.7 +/- 7.9% suppression of TNF. For each cell population, the responses of the asthmatics and healthy controls were not different. The differential effect is not cytokine specific since similar results were obtained with GM-CSF. CONCLUSION These results demonstrate a differential effect of NO on monocyte and alveolar macrophages cytokine regulation and this effect may be related to the state of maturation.

Nitric oxide blocks inflammatory cytokine secretion triggered by CD23 in monocytes from allergic, asthmatic patients and healthy controls.

BACKGROUND In allergic asthma, monocytes/macrophages may be activated to produce inflammatory cytokines through triggering of the low-affinity IgE receptor (CD23). Elevated airway levels of nitric oxide (NO) are associated with asthmatic exacerbations. Our previous work suggested that NO may function in an anti-inflammatory capacity by downregulating endotoxin-stimulated cytokine production by alveolar macrophages and matured monocytes. OBJECTIVE The purpose of this study was to determine the effect of NO on CD23-triggered cytokine production by monocytes from asthmatic patients and healthy controls. METHODS Monocytes were obtained from normal volunteers (n = 13) and asthmatic patients with atopy (n = 8). Monocyte cultures were treated with interleukin-4 (IL-4) and granulocyte macrophage colony-stimulating factor (GM-CSF) for 24 hours to upregulate CD23 expression. Cultures were stimulated by anti-CD23 and treated with DETA NONOate [2,2-(hydroxynitrosohydrazonon)-bis-ethanamine] releases NO in culture with t(1/2) of 20 hours at 37 degrees C for 24 hours. Cell free culture supernatants were collected and assayed by enzyme-linked immunoadsorbent assay for macrophage inflammatory protein-1-alpha (MIP-1) and IL-6. RESULTS NO inhibits MIP-1 secretion triggered by CD23 activation of IL-4- and GM-CSF-matured monocytes (percentage of MIP-1 suppression = 52 +/- 11 of monocytes from asthmatic patients; percentage = 55 +/- 8 healthy controls). The inhibitory effect of NO was not cytokine-specific, as similar results were obtained with IL-6 (50 +/- 9% IL-6 suppression, asthmatic patients; 66 +/- 20%, healthy controls). CONCLUSIONS The results demonstrate for the first time an inhibitory effect of NO on cytokine production stimulated by CD23 receptor activation. We suggest that NO may be upregulated as a potent anti-inflammatory agent in the asthmatic lung.