Increase In Chemiluminescence Response Research Articles

Neutrophil activation by Campylobacter concisus

BackgroundCampylobacter concisus is an emerging enteric pathogen associated with prolonged diarrhoea and possibly inflammatory bowel disease in children as well as adults, but the interaction with cells of the innate immune system is unclear. The magnitude of systemic immunoglobulin response in acute infection is unknown.MethodsNeutrophils from healthy volunteers were activated with five faecal isolates of C. concisus from patients with gastroenteritis as well as the oral reference strain C. concisus ATCC33237. Neutrophils were tested for the expression of adherence molecule CD11b by immunoflourescence and for oxidative burst response by chemiluminescence. The opsonic activity in a chemiluminescence assay was assessed with heat treated serum from patients with C. concisus infection.ResultsA strong and dose-dependent activation of neutrophil adherence molecule CD11b and oxidative burst response was demonstrated with all six C. concisus isolates. Bacteria opsonised in heat treated serum induced an increased chemiluminescence response. Heat treated serum from patients with C. concisus infection did not have a higher opsonic activity than heat treated serum from healthy volunteers.ConclusionC. concisus has the capability to activate the innate immune system by stimulating neutrophil cells to increased adherence molecule expression and oxidative burst response, both crucial for acute inflammation. In a chemiluminescence assay the opsonic activity of heat treated serum from patients was not increased compared to heat treated control serum suggesting a weak systemic IgG response to infection.

Chemiluminescence determination of sulphite using a cyclometalated iridium complex as chemiluminescence reagent

A simple, fast and accurate chemiluminescence (CL) method for the determination of sulphite has been developed, based on its sensitizing effect on the CL reaction between a novel water-soluble iridium complex, [(dpci)2Ir(bvbbi)](PF6) (dpci = 3,4-diphenylcinnoline; bvbbi = N,N'-bivinylester-(1)H,(1')H-[2,2'] bibenzimidazole) and cerium(IV). Under the optimal experimental conditions, the increased CL response was linear, with the concentration of sulphite over the range 5.0 × 10(-7)-5.0 × 10(-4) mol/L. The detection limit of the method was 1.6 × 10(-7) mol/L, with a relative standard deviation (RSD) of 2.7% for nine repetitive determination of 1.0 × 10(-4) mol/L sulphite. The method was successfully applied to the quantitative analysis of sulphite in sugar samples. The possible reaction mechanism of sulphite on the [(dpci)2Ir(bvbbi)](PF6)-cerium(IV) system is also briefly discussed.

Comparison of the responses of peritoneal macrophages from Japanese flounder ( Paralichthys olivaceus) against high virulent and low virulent strains of Edwardsiella tarda

In vivo infection studies in Japanese flounder ( Paralichthys olivaceus) demonstrated that the number of viable cells of the virulent strain (NUF251) of Edwardsiella tarda increased gradually in kidney and hepato-pancreas after intraperitoneal injection, but the low virulent strain (NUF194) did not. To gain insight into the virulence factors of E. tarda, in vitro responses of Japanese flounder ( P. olivaceus) peritoneal macrophages to these strains were compared in terms of phagocytosis, bactericidal activity, and reactive oxygen species (ROS) generation as measured by chemiluminescence (CL) responses. Microscopic observation revealed that these two strains of E. tarda were phagocytosed by the peritoneal macrophages, and there was no significant difference in the mean numbers of ingested bacteria per macrophage between these strains. A gradual increase in the number of viable cells of the highly virulent strain within macrophages was observed during 9 h post-phagocytosis, whereas no significant replication of the low virulent strain within macrophages was detected. These results suggest that the virulent strain of E. tarda has an ability to survive and replicate within macrophages, while the low virulent strain has no such ability. When the peritoneal macrophages were exposed to the opsonized low virulent E. tarda strain, a rapid increase in CL response was induced. However, the highly virulent strain caused only background level of CL response. By the subsequent stimulation with phorbol myristate acetate, the macrophages exposed to the virulent E. tarda strain showed extremely higher CL response than that of the one exposed to the low virulent E. tarda strain. These results suggest that the virulent E. tarda prevents the activation of ROS generation system during phagocytosis, though the system is still capable of responding to other stimulation. The virulent strain significantly reduced the CL response induced by xanthine/xanthine oxidase system, while the low virulent strain had almost no effect. Furthermore, the virulent strain showed greater resistance to H 2O 2 than the low virulent strain. Our results suggest that the virulent strain of E. tarda is highly resistant to ROS, and such ability might allow the organism to survive and multiply within phagocytes, and may serve to disseminate E. tarda throughout the host during in vivo infection.

Evaluation of ambrein and epicoprostanol for their antioxidant properties: Protection against adriamycin-induced free radical toxicity

Ambrein and epicoprostanol were evaluated for their antioxidant potential in vitro by chemiluminescence (CL), as well as in vivo using lipid peroxides and glutathione levels as indicators in liver tissue of rats treated with adriamycin (doxorubicin) a well known free radicals producing drug. In the in vitro test, the inhibition in CL by ambrein was dose dependent. Both the high concentrations of ambrein (20–40 μg/ml) inhibited CL response significantly ( P < 0.05 and P < 0.01, respectively) when compared to control. Similarly two low concentrations (5–20 μg/ml) of epicoprostanol inhibited CL significantly ( P < 0.001 and P < 0.01, respectively) in comparison of DMSO control. The high concentration (40 μg/ml) of epicoprostanol behaved exceptionally and caused an increase in CL response that was more than control and significantly ( P < 0.001) higher than both the low concentrations. In the in vivo studies adriamycin treatment significantly ( P < 0.05) increased malondialdehyde (MDA) and decreased non-protein sulfhydryl (NP-SH) contents in the liver tissue of mice after 5 days treatment. Ambrein (25 and 50 mg/kg) treatment as a solo therapy at both the dose levels significantly ( P < 0.001) decreased MDA contents in the liver tissue. On the other hand, in the combined treatment the high dose effectively prevented any rise in MDA contents and it remained around the levels of ambrein alone. In the same experiment, adriamycin declined NP-SH contents significantly ( P < 0.001). Ambrein alone at both the dose levels caused a decline ( P < 0.01) in NP-SH contents when compared to adriamycin group. But in the combined treatment this decline in NP-SH was significantly ( P < 0.05) different from adriamycin alone. In the experiments dealing with epicoprostanol, adriamycin treatment increased MDA contents significantly ( P < 0.05) that declined significantly ( P < 0.001) with epicoprostanol (10- or 20 mg/kg) treatment. In the same experiment co-treatment with adriamycin prevented any rise in MDA contents significantly ( P < 0.001) as it was observed in adriamycin alone group. Although, this treatment failed to prevent any decline in NP-SH contents either alone or in combination with adriamycin. Epicoprostanol itself had the comparative declining effect on the contents of NP-SH as seen in adriamycin group. From the results of our experiments it seems that ambrein at all concentrations behaves like antioxidant in in vitro studies but the same time it decreased NP-SH contents in vivo accompanied by a decline in MDA contents. Whereas, epicoprostanol at two low concentrations had a decline in CL indicating a possible antioxidant potential but the high concentration increased CL showing a tendency towards oxidant prospective. However, in animal studies it has shown a clear protection against adriamycin induced free radical damage.

Cyclosporin-A Augments Respiratory Burst of Whole Blood Phagocytes in Pregnant Rats

Both pregnancy and cyclosporin A (CsA) are known to inhibit T-cell mediated immune response and to activate phagocytes against microbial infections as a compensatory mechanism. Pregnant women, either with organ transplantation or suffering from autoimmune diseases, are commonly managed with CsA therapy. This investigation was aimed to study effect of CsA on phagocytic activity of whole blood polymorphonuclear leukocytes (PMNs) in pregnant rats. Both pregnant and non-pregnant Sprague–Dawley rats (4 animals per group) were treated with CsA (40 mg/kg, oral) for 7 days starting from gestation day 7. Respective control groups of non-pregnant and pregnant rats received vehicle only. Luminol-dependent chemiluminescence (CL) was used to measure the generation of reactive oxygen species (ROS) in respiratory burst of whole blood PMNs stimulated by zymosan. The results showed a moderate and insignificant increase in CL response in non-pregnant rats with CsA treatment or pregnant rats without CsA treatment. Whereas the CL response of whole blood PMNs was significantly higher (ANOVA F = 35.66, P < 0.001) in pregnant rats treated with CsA. In conclusion, this preliminary study demonstrates synergistic effects of pregnancy and CsA on activation of PMNs resulting in massive and sustained generation of ROS that could be deleterious to both host and fetus.

Impaired phagocytosis and opsonisation towards group B streptococci in preterm neonates

AIMSTo study the chemiluminescence response in polymorphonuclear leucocytes (PMNL) at different stages of maturity and the opsonic capacity of sera with defined titres of anti-capsular type III antibodies, after exposure...

Influence of heat inactivation of human serum on the opsonization of Streptococcus mutans.

Phagocytosis of bacteria, such as Streptococcus mutans, is important to host defense. One mechanism by which phagocytosis can be enhanced is by antibody or complement-mediated opsonization of bacteria. Many studies utilize opsonization of bacteria to enhance a cellular response, but little information has been found examining methodology or validity of the opsonization process following the denaturization of the serum. Human serum was inactivated by heat in order to disrupt the classical and alternative pathways of the complement cascade. S. mutans isolated from human subjects were opsonized with heat-inactivated human serum before exposing them to viable neutrophils in vitro. Luminol-dependent chemiluminescence (CL) was used to measure neutrophil activation. Human serum used to opsonize the bacteria was denatured by incubation at 57 degrees C for intervals of 30 and 60 min to inactivate complement. The results from the opsonization data indicated that there was significantly increased CL with 60-min inactivation of the serum (34% increase in mean integration mV.min; p < or = 0.05) over the nonopsonized control. This indicated a successful opsonization of the bacteria. In addition, the data demonstrate that the inactivation of serum requires a minimum of 60 min at 57 degrees C to disrupt the complement cascade, while 30- and 15-min inactivations produced no significant increase in CL activity over the control. Standard sandwich ELISA assays, detecting complement binding to S. mutans, confirmed successful heat inactivation of serum showing a significant decrease (p < or = 0.001) in complement binding to S. mutans after 30 min, but could not explain the increased CL response after 60-min heat deactivation of the serum.

Leukocytes in a Plasmodium falciparum-infected blood meal reduce transmission of malaria to Anopheles mosquitoes

Mosquitoes are infected with Plasmodium falciparum by taking a blood meal from a gametocyte carrier. Since a mosquito takes a volume of 1 to 2 microl, a blood meal may contain 1 x 10(4) to 3 x 10(4) leukocytes (WBC). The majority of WBC are composed of neutrophils which may phagocytose and kill developing gametes inside the mosquito midgut. Phagocytosis was measured in vitro by a luminol-dependent chemiluminescence (CL) assay. In the presence of P. falciparum gametes, sera from areas of endemicity had an increased CL response compared to controls. In mosquito membrane feeding experiments some such sera showed a transmission reduction which was related to the presence of viable WBC. The results of this study suggest that phagocytosis of opsonized gametes inside the mosquito midgut occurs and can contribute to a reduction in the transmission of P. falciparum parasites.

Effect of serotonin on the chemiluminescence response of rat peripheral blood leucocytes

Serotonin (5-HT) has been shown to exert various immunomodulatory effects. In this study, the effects of 5-HT, 5-hydroxy-DL-tryptophan (5-HTP) and dl- p-chlorophenylalanine (PCPA) on the chemiluminescence (CL) responses of rat peripheral blood leucocytes (PBL) activated by phorbol myristate acetate (PMA), opsonized zymosan or latex beads were assessed. The CL responses were measured following in vitro treatment with 0.01-100 μM 5-HT, and either 1 h after the last i.p. administration of 5-HT (0.05, 0.5, 1, 2.5, 5 or 10 mg/kg for 4 days), 5-HTP (25 or 100 mg/kg for 4 days) or PCPA (200 mg/kg for 4 days, n = 5), or 48 h after a single 200 mg/kg PCPA injection. A concentration-dependent decrease in CL responses was noted following in vitro 5-HT treatment. In vivo treatment of rats with 5-HT produced a reverse bell-curve inhibiting effects on the CL response with a maximal inhibition in rats receiving 1 mg/kg/day 5-HT and a weaker response of PMA-activated PBL. In vivo treatment with high-dose 5-HTP increased CL response of opsonized zymosan-activated PBL, while low-dose 5-HTP decreased CL response of opsonized zymosan and latex beads-activated PBL. No effect was observed in PMA-activated PBL from rats treated with 5-HTP. By contrast, in vivo treatment with PCPA increased CL responses induced by PMA or latex beads, whereas CL responses using opsonized zymosan were not significantly affected. These results suggest that 5-HT modulates the CL response of rat leucocytes to particulate stimuli.

Impaired neutrophil function in the cutaneous form of anthrax.

Spontaneous and Bacillus anthracis induced luminol-dependent chemiluminescence of neutrophils was studied in six patients with the cutaneous form of anthrax. Spontaneous chemiluminescence in anthrax was decreased compared to the healthy controls (p < 0.05). B. anthracis, opsonized by complement-containing sera from patients, induced chemiluminescence in neutrophils from control donors but not from patients. B. anthracis, opsonized by complement-free sera from the patients, did not cause an increase in chemiluminescence response in either the patient or the control neutrophils. Also, B. anthracis, opsonized with normal sera and nonopsonized, did not induce chemiluminescence in either patient or control neutrophils. It was concluded that oxidative metabolism by neutrophils is impaired in anthrax, whereas the functional capacity of antibodies seems to be unaffected.

Subcutaneously Administered Recombinant Interferon-γ in Humans

A Phase I trial was conducted to investigate the clinical toxicity, pharmacokinetics, and chemiluminescence (CL) responses of alveolar macrophages (AMs), peripheral blood neutrophils, and monocytes after subcutaneous injection of recombinant interferon-gamma (rIFN-gamma). Six patients with lung cancer received rIFN-gamma subcutaneously as single doses of 0.2, 0.6, and 1.8 mg. Bronchoalveolar lavage was performed three times: 21 h before as well as 6-7 and 27 h after injection. Serum samples were taken five times during the 27-h follow-up. IFN concentrations were measured from alveolar epithelial lining fluid (ELF) and serum by using an antiviral bioassay. IFN-gamma was not detectable in ELF after subcutaneous injection. AMs did not effect an increase in CL responses to N-formyl-methionyl-leucyl-phenylalanine or to phosphate-buffered saline. Circulating IFN-gamma was detectable at 3-12 h after an injection of 1.8 mg of rIFN-gamma, the highest dose given. CL responses of peripheral blood monocytes increased in all patients after injection, whereas the responses of neutrophils were less clear-cut. All patients developed systemic side effects such as transient fever, nausea, headaches, and flu-like symptoms. The findings suggest that rIFN-gamma passes poorly from the blood to the pulmonary alveoli. On the basis of this and our previous findings of increased CL responses in AMs and measurable IFN concentrations in ELF after inhalation of rIFN-gamma, we recommend inhalation rather than the parenteral route of IFN-gamma for the treatment of respiratory diseases.

Effect of growth factors on Escherichia coli alpha-hemolysin-induced mediator release from human inflammatory cells: involvement of the signal transduction pathway.

Previously, we have shown that Escherichia coli alpha-hemolysin represents a potent stimulus for inflammatory mediator release (O2- release, beta-glucuronidase release, and leukotriene generation) from human polymorphonuclear granulocytes (PMN) as well as for histamine release from a human lymphocyte-monocyte-basophil cell suspension (LMB). In contrast, the E. coli alpha-hemolysin leads to a downregulation of cytokine release (interleukin 6 [IL-6], tumor necrosis factor alpha, and IL-1 beta) from human LMB. This study was undertaken (i) to analyze the priming efficacy of growth factors (granulocyte-macrophage colony-stimulating factor [GM-CSF] and granulocyte CSF [G-CSF]) on inflammatory mediator release from human PMN and LMB challenged with hemolysin-producing E. coli bacteria as well as with cell-free E. coli alpha-hemolysin and (ii) to identify major components involved in GM-CSF and G-CSF priming. GM-CSF pretreatment led to an increased chemiluminescence response from human PMN by up to 100%, leukotriene B4 generation was enhanced up to fivefold, and histamine release from human LMB increased from 45% +/- 15% to 75% +/- 5% (mean +/- standard distribution) of the total histamine content. G-CSF priming induced an increase in the chemiluminescence response by up to 50% +/- 5% from human PMN and an increase in histamine release from human LMB by 20% +/- 5%. The growth factors, GM-CSF and G-CSF, modulated neither beta-glucuronidase release from human PMN nor IL-8 release from human PMN and LMB challenged with the E. coli alpha-hemolysin. GM-CSF and G-CSF pretreatment increased the fluoride (NaF)-induced chemiluminescence response by up to 10-fold; the serine/threonine phosphatase inhibitor okadaic acid inhibited GM-CSF- and G-CSF-induced priming. NaF-induced histamine release was enhanced up to 60 and 30% by GM-CSF and G-CSF priming, respectively. GM-CSF and G-CSF pretreatment did not modulate phorbol 12-myristate 13-acetate-induced chemiluminescence response or histamine release. GM-CSF by itself induced an increase in 5-lipoxygenase-specific mRNA expression within 5 min. Our results indicate that (i) GM-CSF and G-CSF interact with inflammatory cells via distinct cellular signalling, (ii) the signal transduction pathway is dependent on the cellular mediator, and (iii) the use of growth factors may be a potent tool to influence the clinical outcome in infectious diseases.

Increased chemiluminescence response of neutrophils from the peripheral blood of patients with senile dementia of the Alzheimer's type

The metabolic activity of circulating neutrophils from patients with senile dementia of the Alzheimer's type (SDAT) was investigated by a chemiluminescence assay and compared with that of old and young healthy controls. Neutrophils from demented patients showed a higher and faster chemiluminescence emission than those of controls when activated in vitro by autologous or heterologous sera. Granulocytes from patients with Parkinson's disease did not show an increased chemiluminescence activity. Moreover, serum from patients with SDAT depressed the chemiluminescence emission of granulocytes from young donors. Serum levels of α 1-antichymotrypsin ( α 1-ACT) were also determined and were found to be higher in demented subjects than in old and young controls. These data suggest that peripheral and systemic indexes of inflammation are present in the disease and might be associated with mental deterioration.

Lucigenin-dependent chemiluminescence in articular chondrocytes

We were recently able to measure intracellular levels of hydrogen peroxide within normal articular chondrocytes using the trapped indicator 2′,7′-dichlorofluorescein diacetate. Further studies have shown that stimulated chondrocytes produce luminol-dependent chemiluminescence, suggesting that these cells produce hydrogen peroxide and singletoxygen. In the present study, we have investigated the lucigenin-dependent chemiluminescence response in normal articular chondrocytes. Chondrocytes either in suspension or adhered to cover slips showed lucigenin-dependent chemiluminescence. There was a dose-dependent increase in chemiluminescence response when chondrocytes were incubated with soluble stimuli like phorbolmyristate-acetate, concanavalin A, and f-met-leu-phe. Catalase and the metabolic inhibitor, sodium azide, which inhibits the enzyme myeloperoxidase, had no inhibitory effect on lucigenin-dependent chemiluminescence production. Only the antioxidant, superoxide dismutase, prevented lucigenin-dependent chemiluminescence, indicating that this assay measures the production of superoxide anions by chondrocytes. We confirmed that chondrocytes release superoxide radicals using the biochemical assay of ferricytochrome c reduction. Since cartilage tissue is semitransparent, we were able to measure chemiluminescence response in live cartilage tissue, showing that chondrocytes which are embedded within the matrix can also generate superoxide anion radicals. Reactive oxygen intermediates have been shown to play a significant role in the degradation of matrix in arthritis. Our previous and present studies suggest that oxygen radiccals produced by chondrocytes may be an important mechanism by which chondrocytes induce cartilage matrix degradation.

Interleukin-5-induced granulocyte activation in atopic patients

The effect of recombinant human and murine interleukin-5 (IL-5) on granulocytes was investigated in patients with atopic dermatitis (AD) and allergic rhinitis and compared with those from patients with plaque psoriasis and normal non-atopic controls. Granulocyte activation was measured as lucigenin-dependent chemiluminescence (CL) and release of eosinophil cationic protein (ECP) as well as by scanning- and transmission-electron microscopy (EM) and the ultrastructural detection of production of H2O2. A significant direct effect of both human and murine IL-5 on granulocyte oxidative metabolism could only be detected in those patients with AD and allergic rhinitis. Also, as compared to normal controls, significantly increased CL responses were observed in these patients with stimulation with other granulocyte-activating cytokines, particularly GM-CSF. In patients with psoriasis there was no significant increase in response to stimulation with TNF alpha, TNF beta or GM-CSF, but IL-5 induced slight but significant CL responses in the granulocytes. None of the cytokines tested significantly stimulated the release of ECP in any of the groups. Ultrastructural studies showed that stimulation with human as well as murine IL-5 produced significant morphological changes in both eosinophils and polymorphonuclear neutrophilic granulocytes from the patients with AD. Production of H2O2 was visualized at the luminal part of the intracytoplasmic vesicles of the granulocytes and at the points of contact between the cells. On morphometric analysis, almost all the polymorphonuclear neutrophils in the patients with AD appeared to be activated, whereas only some of these cells in the normal controls showed signs of activation.

Priming of Rabbit Alveolar Macrophages for Enhanced Oxidative Responses by Herpes Simplex Virus Type 2 Infection

The effect of herpes simplex virus type 2 (HSV-2) infection on the oxidative response in infant and adult rabbit alveolar macrophages (AM) was studied using either phorbol myristate acetate (0.5 microgram PMA/ml) or latex (250 micrograms/ml) as eliciting agents in a chemiluminescence (CL) assay. Results indicated that uninfected infant AM responded to a latex-elicited but not PMA-elicited CL response. HSV-2 infection (moi = 1.0) of infant AM for 2 hr at 37 degrees C did not alter the PMA or latex-elicited CL responses. In contrast, uninfected adult AM exhibited a markedly increased CL response when elicited with either PMA or latex. HSV-2 infection (moi = 1) of adult AM for 2 hr further increased both PMA- and latex-elicited CL responses. Increasing the moi to 10 inhibited both PMA- and latex-elicited CL responses. Incubation of uninfected control and HSV-2 infected adult AM for 18 hr at 37 degrees C resulted in spontaneous priming of the cells for increased CL responses. In the absence of PMA HSV-2 alone failed to elicit a CL response in adult AM. Infection with heat-inactivated HSV-2 (moi = 1.0 before heat inactivation) did not prime adult AM for enhanced CL responses. AM from BCG immunized adult rabbit produced a considerably higher level CL response that nonimmunized AM; however, HSV-2 infection of these cells did not further enhance the response. In summary, these data indicate that adult AM but not infant AM can be primed by active HSV-2 infection for an increased CL response elicited by either PMA or latex.

Increased whole blood chemiluminescence in patients with Shwachman syndrome: therapy trial with thiamine and α-tocopherol

Neutrophils purified from peripheral blood of patients with the Shwachman syndrome show enhanced chemiluminescence (CL) and depressed chemotaxis. Here we present data showing that the increased CL response can be demonstrated by using a whole blood CL assay. This assay is well-suited for studies in infants, because the blood sample volumes needed are small. Increase in CL was most distinct in the initial (1 min) activation induced by N-formyl-methionyl-leucyl-phenylalanine. The 1-min response is considered to derive from extracellular production of oxygen radicals. Such an extracellular oxygen radical production may render the patients susceptible to undue oxidant stress. We therefore treated the patients with two antioxidants, thiamine and alpha-tocopherol, for 3 months. This supplementation, however, failed to exert any significant effect on either whole blood CL or migration of the patients' neutrophils under agarose.

Influence of gluten‐derived fractions on chemiluminescence production by human neutrophils

The effects of gliadin and glyc-gli on leukocyte chemiluminescence response were assessed in vitro. A dose-dependent increase in chemiluminescence response of neutrophils stimulated by zymosan was observed by using gliadin at concentrations ranging between 1 and 20 micrograms. By increasing glyc-gli concentration, a bimodal response was observed with an enhancement up to 50 micrograms/ml, followed by suppressive effects, which were again dose-dependent. The possible implications of these findings in human pathology are discussed.

Activation of phagocyte oxidative metabolism by opsonized Plasmodium falciparum merozoites

A luminol-dependent chemiluminescence (CL) method was used to measure the oxidative burst of phagocytes triggered by antimalarial antibodies and Plasmodium falciparum merozoites. A specific antibody-dependent increase in chemiluminescence response was obtained using both polymorphonuclear leukocytes and monocytes as effector cells. Using various sera from malaria infected subjects it was observed that antibodies involved in the increased chemiluminescence responses were encountered at higher levels in sera from protected subjects than in those susceptible to clinical manifestations. In the conditions used the assay shows substantial intertest variation but appears of interest to assess the protective status of groups of exposed individuals.

Relationship between intracellularly and extracellularly generated oxygen metabolites from primed polymorphonuclear leukocytes differs from that obtained from nonprimed cells

The ability of primed human polymorphonuclear leukocytes (PMNLs) to respond metabolically to stimulation with formylmethionyl-leucyl-phenylalanine (FMLP) was investigated. Cells isolated from an aseptic inflammatory reaction and from patients with a severe bacterial infection as well as cells that had been treated with a bacterial lipopolysaccharide were investigated. When these cells were compared to peripheral blood cells isolated from healthy controls, they were found to be metabolically primed, i.e., the cells gave rise to an increased chemiluminescence response to subsequent stimulation with the peptide. It was also shown that proportionally more of the activity generated from the primed PMNL was of an intracellular origin compared with that obtained from nonprimed cells. The biological effects induced by radicals produced extracellularly and intracellularly are discussed.