leukotriene-b4 and Bacterial-Infections

Leukotriene B4 (LTB4) is an endogenous lipid mediator of inflammation derived from arachidonic acid by the sequential action of cytosolic phospholipase A2 and 5-lipoxygenase. This mediator was initially recognized for its involvement in the recruitment of neutrophils. However, in the last decade, LTB4 has been clearly demonstrated to play a significant role in the control of microbial infections through its ability to activate host innate defenses. In this review, we will focus on the modulator effects of LTB4 on the innate defenses and discuss its therapeutic potential against viral pathogens.

Topics: Animals; Bacterial Infections; Humans; Immunity, Innate; Inflammation Mediators; Leukotriene B4; Models, Immunological; Neutrophils; Toll-Like Receptors; Virus Diseases

Topics: Bacteria; Bacterial Infections; Environmental Exposure; Histamine Release; Humans; Immunoglobulin E; Leukotriene B4; Respiratory Tract Diseases

Topics: Arachidonic Acids; Bacterial Infections; Bacterial Toxins; Calcium; Fatty Acids, Unsaturated; Humans; Immunity, Cellular; Inflammation; Leukotriene B4; Lymphocyte Activation; Neutrophils; Prostaglandins E; SRS-A; Superoxides

Neutrophilic infiltration is a leading contributor to pathology in a number of pulmonary disease states, including cystic fibrosis. Hepoxilin A3 (HXA3) is a chemotactic eicosanoid shown to mediate the transepithelial passage of neutrophils in response to infection in several model systems and at multiple mucosal surfaces. Another well-known eicosanoid mediating general neutrophil chemotaxis is leukotriene B4 (LTB4). We sought to distinguish the roles of each eicosanoid in the context of infection of lung epithelial monolayers by Pseudomonas aeruginosa. Using human and mouse in vitro transwell model systems, we used a combination of biosynthetic inhibitors, receptor antagonists, as well as mutant sources of neutrophils to assess the contribution of each chemoattractant in driving neutrophil transepithelial migration. We found that following chemotaxis to epithelial-derived HXA3 signals, neutrophil-derived LTB4 is required to amplify the magnitude of neutrophil migration. LTB4 signaling is not required for migration to HXA3 signals, but LTB4 generation by migrated neutrophils plays a significant role in augmenting the initial HXA3-mediated migration. We conclude that HXA3 and LTB4 serve independent roles to collectively coordinate an effective neutrophilic transepithelial migratory response.

Topics: 8,11,14-Eicosatrienoic Acid; Animals; Bacteria; Bacterial Infections; Calcium Signaling; Cell Line; Chemotaxis, Leukocyte; Disease Models, Animal; Female; Gene Knockdown Techniques; Humans; Leukotriene B4; Mice; Neutrophil Infiltration; Neutrophils; Pseudomonas aeruginosa; Receptors, Leukotriene B4; Transendothelial and Transepithelial Migration

Chronic inflammation of the oral epithelium of bacterial origin is associated with elevated leukotriene B(4) (LTB(4)) levels. We investigated leukotriene A(4) (LTA(4))-hydrolase expression and LTB(4) levels in oral epithelium in relation to the clinical disease manifestation and immunohistopathology and LTA(4)-hydrolase expression in cultured oral keratinocytes. In 11 patients, three different types of biopsy specimens of the oral mucosa tissues were examined. Each sample was divided, and one-half was analysed using immunohistochemistry with antibodies to LTA(4)-hydrolase, CD1a, CD3, CD19, macrophages/monocytes and granulocytes. The other half of the sample was homogenised and analysed using reverse-phase high-performance liquid chromatography to determine LTB(4) levels. We found strong LTA(4)-hydrolase expression in basal cells of the oral epithelium from tissue samples that appeared clinically healthy; however, histologically a mild chronic inflammation was observed. In contrast, patients with symptoms of an inflammation of the oral mucosa showed only weak LTA(4)-hydrolase staining of the epithelial cell layers, but strong immunoreactivity in endothelial and invading inflammatory cells. LTB(4) levels were elevated in inflamed tissues compared with non-inflamed controls. Most significantly, there was a strong association between the immunohistochemical detection of the enzyme, LTB(4) levels, cellular infiltration and the clinical disease manifestations. In vitro experiments indicated that LTA(4)-hydrolase expression may be induced by bacterial contamination. This study suggests that LTA(4)-hydrolase expression and elevated LTB(4) levels in oral mucosal epithelium are integral parts of the induction and progression of chronic inflammatory reactions. Epithelial cells may participate in early stages of inflammation as a source of LTB(4).

Topics: Adult; Aged; Bacterial Infections; Chromatography, High Pressure Liquid; Chronic Disease; Epoxide Hydrolases; Humans; Immunohistochemistry; Inflammation; Leukotriene B4; Middle Aged; Mouth Mucosa

Prostaglandin E(2) (PGE(2)) production after trauma contributes to immune alterations that increase susceptibility to infections. We hypothesize that blocking PGE(2) with NS-398, a selective COX-2 inhibitor, will modulate this response and improve outcome. This study evaluated the effect of NS-398 given over 7 days on proinflammatory cytokines, intracellular signaling, and survival after a septic challenge. Balb/C mice (n = 8/group) were given 10 mg/kg NS-398 intraperitoneally over 7 days, starting after anesthesia or trauma (femur fracture + 40% hemorrhage). Four groups, anesthesia + vehicle (C), anesthesia + NS-398 (CN), trauma + vehicle (T), or trauma + NS-398 (TN), were studied. On Day 7 after trauma, mice were sacrificed, serum was collected, and splenic macrophages were evaluated for PGE(2), LTB(4), IL-6, TNF-alpha, and NO production. Additionally, macrophage COX-2 mRNA, IkappaB-alpha, and NF-kappaB were evaluated. In a separate study, mice (n = 10-11/group) were traumatized and given NS-398 over 7 days, and then cecal ligation and puncture (CLP) were performed. Mice were then followed for survival over 10 days (via log-rank test). NS-398 treatment of injured mice decreased PGE(2) production compared to T (3.9 +/- 0.3 vs 3.1 +/- 0.4 pg/microg protein), and significantly decreased IL-6, NO, and TNF-alpha production. NS-398 treatment also attenuated COX-2 mRNA levels and NF-kappaB activation. These cellular events correlate with a significant survival advantage in TN versus T mice after CLP. These data suggest that a specific COX-2 inhibitor not only suppresses PGE(2), but normalizes proinflammatory cytokines after trauma through changes that may partly be mediated via transcriptional events. This correlates with significantly increased survival in TN mice given a septic challenge and suggests that COX-2 inhibitors contribute to modulating the inflammatory response and improving survival after trauma.

Topics: Animals; Bacterial Infections; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dinoprostone; Female; Femoral Fractures; Interleukin-6; Isoenzymes; Leukotriene B4; Macrophages; Mice; Mice, Inbred BALB C; NF-kappa B; Nitric Oxide; Nitrobenzenes; Prostaglandin-Endoperoxide Synthases; RNA, Messenger; Spleen; Sulfonamides; Survival Analysis; Tumor Necrosis Factor-alpha; Wounds and Injuries

There are little data describing noncellular changes in bronchial inflammation during exacerbations of chronic bronchitis. The relationship between sputum colour and airway inflammation at presentation has been assessed during an exacerbation in patients with chronic bronchitis and a primary care diagnosis of chronic obstructive pulmonary disease. Sputum myeloperoxidase, neutrophil elastase, leukotriene B4 (LTB4), interleukin-8 (IL-8), sol:serum albumin ratio and serum C-reactive protein were measured in patients presenting with an exacerbation and mucoid (n = 27) or purulent sputum (n = 42). Mucoid exacerbations were associated with little bronchial or systemic inflammation at presentation, and sputum bacteriology was similar to that obtained in the stable state. Purulent exacerbations were associated with marked bronchial and systemic inflammation (p < 0.025 for all features) and positive sputum cultures (90%). Resolution was related to a significant reduction in LTB4 (p < 0.01), but no change in IL-8, suggesting that LTB4 may be more important in neutrophil recruitment in these mild, purulent exacerbations. In the stable state, IL-8 remained higher in patients who had experienced a purulent exacerbation (2p < 0.02). The presented results indicate that exacerbations of chronic bronchitis, defined by sputum colour, differ in the degree of bronchial and systemic inflammation. Purulent exacerbations are related to bacterial infection, and are associated with increased neutrophilic inflammation and increased leukotriene B4 concentrations.

Topics: Acute Disease; Adult; Aged; Aged, 80 and over; Bacterial Infections; Bronchitis; Female; Humans; Inflammation Mediators; Leukotriene B4; Male; Middle Aged; Neutrophils; Primary Health Care; Pulmonary Disease, Chronic Obstructive; Sputum

Neutrophils recruited to the airways in chronic obstructive pulmonary disease (COPD) are thought to mediate tissue destruction. Neutrophil recruitment is increased during bacterial exacerbations. The inflammatory process was studied in patients with an acute exacerbation of COPD in order to ascertain the role of leukotriene B4 (LTB4). The sputum of eight subjects with a bacterial exacerbation of COPD was analysed for neutrophil products (myeloperoxidase, elastase) and chemoattractants (interleukin-8 (IL-8) and LTB4). The contribution of LTB4 to the chemotactic activity of the sputum sol phase was determined using the LTB4 receptor antagonist LY293111. The concentrations of the serum acute phase proteins alpha1-proteinase inhibitor, alpha1-antichymotrypsin and C-reactive protein were measured. All patients received appropriate broad-spectrum antibiotic treatment for 7-14 days. Initially, the sputum myeloperoxidase activity was high, indicating neutrophil influx; this was associated with high levels of IL-8 and LTB4. All these concentrations fell with treatment (p<0.01). The chemotactic activity of the sputum was raised on presentation and fell with treatment (p<0.01). LTB4 contributed approximately 30% of the total chemotactic activity on presentation; this diminished with therapy. All acute phase proteins were raised on presentation and fell with therapy (p<0.01). These findings suggest that leukotriene B4 contributes to neutrophil influx into the airway in chronic obstructive pulmonary disease and may influence disease progression.

Topics: Acute-Phase Proteins; Aged; Bacterial Infections; Bronchitis; Case-Control Studies; Female; Humans; Leukotriene B4; Male; Middle Aged; Neutrophil Infiltration; Neutrophils; Sputum

Neutrophil elastase is capable of generating many of the features of chronic bronchial disease. In patients with COPD, airways inflammation with neutrophil recruitment and elastase release is positively correlated with colonizing bacterial load in the stable clinical state (p < 0.0005). In addition, alpha(1)-antitrypsin deficiency is associated with a greater neutrophil load, higher elastase activity, leukotriene-B(4) concentration, and serum protein leak than matched patients without deficiency (p < 0.005). These data confirm an effect of bronchial colonization on airways inflammation in COPD and indicate the role of alpha(1)-antitrypsin in its modulation.

Topics: alpha 1-Antitrypsin Deficiency; Bacteria; Bacterial Infections; Biomarkers; Bronchi; Bronchitis; Humans; Leukocyte Elastase; Leukotriene B4; Peroxidase; Sputum

Patients with homozygous (PiZ) alpha(1)-antitrypsin (AAT) deficiency have not only low baseline serum AAT levels (approximately 10 to 15% normal) but also an attenuated acute phase response. They are susceptible to the development of premature emphysema but may also be particularly susceptible to lung damage during bacterial exacerbations when there will be a significant neutrophil influx. The purposes of the present study were to assess the inflammatory nature of acute bacterial exacerbations of chronic obstructive pulmonary disease (COPD) in subjects with AAT deficiency, to compare this with COPD patients without deficiency, and to monitor the inflammatory process and its resolution following appropriate antibacterial therapy. At the start of the exacerbation, patients with AAT deficiency had lower sputum AAT (p < 0.001) and secretory leukoprotease inhibitor (SLPI; p = 0.02) with higher elastase activity (p = 0.02) compared with COPD patients without deficiency. Both groups had a comparable acute phase response as assessed by C-reactive protein (CRP) but the AAT-deficient patients had a minimal rise in serum AAT (to < 6 microM). After treatment with antibiotics, in patients with AAT deficiency, there were significant changes in many sputum proteins including a rise in SLPI levels, and a reduction in myeloperoxidase (MPO) and elastase activity (p < 0. 005 for all measures); the sputum chemoattractants interleukin-8 (IL-8) and leukotriene B(4) (LTB(4)) fell (p < 0.01), and protein leak (sputum/serum albumin ratio) became lower (p < 0.01). The changes were rapid and within 3 d of the commencement of antibiotic therapy the biochemical markers had decreased significantly, but took a variable time thereafter to return to baseline values. In conclusion, patients with AAT deficiency had evidence of increased elastase activity at the start of the exacerbation when compared with nondeficient COPD patients which probably reflects a deficient antiproteinase screen (lower sputum AAT and SLPI). The increased bronchial inflammation at presentation resolved rapidly with 14 d of antibiotic therapy.

Topics: Acute Disease; Acute-Phase Reaction; Aged; alpha 1-Antitrypsin; alpha 1-Antitrypsin Deficiency; Bacterial Infections; Bronchi; C-Reactive Protein; Female; Humans; Inflammation Mediators; Interleukin-8; Leukotriene B4; Lung Diseases, Obstructive; Male; Middle Aged; Pancreatic Elastase; Peroxidase; Phenotype; Proteinase Inhibitory Proteins, Secretory; Proteins; Respiratory Tract Infections; Secretory Leukocyte Peptidase Inhibitor; Serine Proteinase Inhibitors; Serum Albumin; Sputum

The inflammatory indicators in the tracheobronchial aspirate (TA) of 81 ventilated preterm infants with microbial colonisation of the airways and in non-colonised neonates were analysed on the first day of life. TA was assessed for chemotactic activity, neutrophil cell count, and concentrations of leukotriene B4, C5a, interleukin-1, interleukin-8, elastase-alpha 1-proteinase inhibitor, free elastase and albumin. Concentrations of mediators were related to concentrations of the secretory component of IgA. The infants' gestational age was mean (SD) 27.9 (2.0) weeks, birthweight 945 (179) g. In 12 infants (15%) microbial colonisation of the airways was present (Ureaplasma urealyticum n = 7; bacteria n = 5). Compared with non-colonised neonates (n = 69), chemotactic activity, neutrophil count, and concentrations of interleukin-1, leukotriene B4 and elastase-alpha 1-proteinase inhibitor were significantly higher in the colonised group. The difference was most pronounced for IL-1 concentrations, both with and without correction for secretory component. There was also a trend towards increased concentrations of interleukin-8 in the latter group. There were no differences for concentrations of C5a and albumin in the TA of both groups. It is concluded that airway colonisation with U urealyticum or bacteria at birth is associated with a clinically relevant bronchopulmonary inflammatory response. Increased concentrations of interleukin-1 in TA on the first day of life may be a marker of perinatal colonisation of the airways.

Topics: alpha 1-Antitrypsin; Bacterial Infections; Biomarkers; Bronchi; Female; Humans; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Interleukin-1; Interleukin-8; Leukocyte Elastase; Leukotriene B4; Male; Pancreatic Elastase; Prospective Studies; Trachea; Ureaplasma Infections; Ureaplasma urealyticum

In order to evaluate the role of polymorphonuclear leukocytes (PMNs) in acute otitis media (AOM), levels of leukotriene B4 (LTB4), a potent inflammatory product of PMNs, and interleukin-8 (IL-8), a PMN chemotactic cytokine, were measured in 271 middle ear fluid (MEF) samples from 106 children with AOM. Forty-two percent of the patients had evidence of respiratory viral infection. At the time of diagnosis, levels of both LTB4 and IL-8 were higher in the MEFs from patients with AOM associated with bacterial or bacterial and viral infection than those MEFs containing no pathogen (p < .05). Antibiotic treatment was not associated with a significant change in levels of LTB4 or IL-8 in the MEFs obtained 2 to 5 days into treatment, compared to those obtained at diagnosis. Bacteriologic failure after 2 to 5 days of treatment was associated with high LTB4 levels in the initial MEFs (p = .05). Recurrence of AOM within 1 month was associated with high IL-8 levels in the initial MEF (p = .04). Our findings suggest that LTB4 and IL-8 are produced during acute infection of the middle ear, and these PMN-related inflammatory substances may play an important role in delaying recovery or in recurrence of AOM. Effective treatment of AOM may require eradication of bacteria by antibiotics, as well as pharmacologic agents that modulate PMN functions.

Topics: Bacterial Infections; Enzyme-Linked Immunosorbent Assay; Female; Humans; Infant; Interleukin-8; Leukotriene B4; Male; Neutrophils; Otitis Media; Recurrence; Respiratory Tract Infections; Virus Diseases

To evaluate the role of bacterial peritonitis in peritoneal macrophage (PMO) Beta-2 Microglobulin (B2M) production and its relationship with PMO Interleukin-1 (IL-1) and Leukotriene B4 (LTB4) release we analyzed in 20 CAPD patients (10 with peritonitis): 1. in vivo plasma and peritoneal dialysis effluent (PDE) B2M, IL-1 and LTB4 levels; 2. in vitro B2M, IL-1 and LTB4 release by PMO. Values were compared with those seen in the plasma or with peripheral blood monocytes of 30 hemodialysis (HD) patients (10 treated with Cuprophan-CU-, 10 with Polyacrylonitrile - PAN, and 10 with Cellulose Acetate - CA). Results showed that in CAPD patients with bacterial peritonitis B2M, IL-1 and LTB4 concentrations in the PDE were significantly higher than those seen in CAPD patients without peritonitis or in the plasma of HD patients treated with PAN or CA, but were similar to those seen in HD patients treated with CU. At the same time, in vitro, PMO from CAPD patients with bacterial peritonitis produced more B2M, IL-1 and LTB4 than did PMO from CAPD patients without peritonitis or peripheral blood monocytes from HD patients treated with PAN or CA. We conclude that in CAPD patients bacterial peritonitis is able to induce PMO B2M production, probably via a cytokine-mediated process, which may be analogous to what occurs with peripheral blood monocytes of HD patients treated with CU.

Topics: Adult; Bacterial Infections; beta-Thromboglobulin; Female; Humans; Interleukin-1; Leukotriene B4; Macrophages; Male; Membranes, Artificial; Middle Aged; Peritoneal Cavity; Peritoneal Dialysis, Continuous Ambulatory; Peritonitis; Renal Dialysis

The influx of neutrophils into the lung is a prominent feature in patients with bacterial pneumonia. Since neutrophils migrate in response to chemotactic factors, chemotactic activity was evaluated in bronchoalveolar lavage (BAL) fluid obtained from 12 patients with bacterial pneumonia and ten normal control subjects. Chemotactic activity was greatly elevated in the BAL fluid of the pneumonia patients compared with control subjects (p less than 0.01). To partially characterize the chemotactic factors present in the lavage fluid of the patient group, molecular sieve chromatography was performed on the lavage fluid, and at least three peaks of chemotactic activity were identified. Since the molecular weight of the smaller peaks approximated the molecular weight of two known chemotactic factors, C5a and leukotriene B4, these factors were measured in lavage fluid by radioimmunoassay. C5a was detectable in none of the normal subjects but was detectable in four of 14 BAL samples obtained from the patients. Leukotriene B4 was detectable in all subjects and was significantly elevated in the pneumonia patients (552 +/- 95 vs 81 +/- 16 pg/ml, p less than 0.01). These findings demonstrate that elevated neutrophil chemotactic activity is present in the lungs of patients with bacterial pneumonia and suggest that C5a and leukotriene B4 may account, at least in part, for this increase.

Topics: Adolescent; Aged; Bacterial Infections; Bronchoalveolar Lavage Fluid; Bronchoscopy; Chemotaxis, Leukocyte; Chromatography, Gel; Complement C5; Complement C5a; Female; Humans; Leukocyte Count; Leukotriene B4; Male; Middle Aged; Neutrophils; Pneumonia

The effects of exogenous leukotriene B4 (LTB4) on the resistance of mouse peritoneal macrophages against Salmonella (S.) typhimurium and Pseudomonas (P.) aeruginosa infections were studied. In vitro, LTB4 added to macrophage monolayers at final concentrations of 10(-12)-10(-8) M, enhanced their phagocytosis of S. typhimurium to 2.3 times the control level and that of P. aeruginosa to 1.8 times the control level. The intracellular killing rates were also elevated by the addition of LTB4: for S. typhimurium, 83.3% (LTB4) vs 59.1% (control) and for P. aeruginosa, 46.5% (LTB4) vs 9.2% (control). In vivo, intraperitoneally injected LTB4 (5 ng) enhanced the clearance at 24 h of intraperitoneally injected S. typhimurium from the mouse peritoneal cavity (2.38 x 10(3) +/- 0.94 x 10(3) cells [LTB4] vs 5.73 x 10(5) +/- 1.90 x 10(5) [control]) and spleen (5.00 x 10(2) +/- 0.94 x 10(2) [LTB4] vs 2.47 x 10(4) +/- 0.84 x 10(4) [control]), but this effect disappeared by 48 h. In contrast, in beige mice, an experimental model of the Chédiak-Higashi syndrome that is characterized by susceptibility to bacterial infection, there was no induction of the eliminating effect by intraperitoneal injection of LTB4. Activation of macrophages by exogenous LTB4 seemed to have contributed to such an augmented resistance of macrophages to bacterial infection. This study suggested a possible use of LTB4 in bacterial infectious diseases whereby phagocytes are able to play a key role in host defense.

Topics: Animals; Ascitic Fluid; Bacterial Infections; Chediak-Higashi Syndrome; Female; Immunity, Innate; Leukotriene B4; Macrophages; Male; Mice; Mice, Inbred C57BL; Phagocytosis

In 15 patients with atopic dermatitis (AD) and without concomitant viral or bacterial infections, chemotaxis, superoxide-anion (O2-) generation, and beta-glucuronidase release of purified monocytes (MO) and neutrophils (PMN) were determined. Defined receptor-dependent stimulators (i.e., N-formyl-methionyl-leucyl-phenylalanine, C5a, and leukotriene B4, as well as native and opsonized zymosan particles) were used for phagocyte stimulation. PMN functional activities in response to the stimuli tested were found to be normal in patients with AD and without infections. MO from these patients revealed a slight enhancement of O2- production after stimulation with opsonized zymosan and a small increase of N-formyl-methionyl-leucyl-phenylalanine-induced chemotaxis. Other MO functions tested were within the normal range. However, investigations of MO and PMN functions during the course of concomitant bacterial infections of three patients with AD demonstrated striking alterations of cellular responsiveness. These changes ranged from enhanced to decreased phagocyte functions, depending on the activity of the infectious disorder. Chemotaxis of PMN and MO was depressed around the third day after onset of the infectious disease. In the beginning of infection, there was a decreased O2- generation and beta-glucuronidase release in PMNs. In MOs, both parameters were enhanced. The results of these investigations provide evidence that functional abnormalities of phagocytes observed in patients with AD are sequelae of concomitant skin infections and not signs of an intrinsic defect present in MOs and PMNs.

Topics: Adolescent; Adult; Bacterial Infections; Chemotaxis, Leukocyte; Complement C5; Complement C5a; Dermatitis, Atopic; Female; Follow-Up Studies; Glucuronidase; Humans; Immunoglobulin E; Leukotriene B4; Longitudinal Studies; Male; Middle Aged; Monocytes; N-Formylmethionine Leucyl-Phenylalanine; Neutrophils; Phagocytosis; Superoxides

This study was undertaken to examine the effects of intrauterine infection and preterm labor on the amniotic fluid concentrations of arachidonate lipoxygenase metabolites in women with premature rupture of membranes. Amniotic fluid was obtained from four groups of women with premature rupture of membranes: group 1, women without labor or infection; group 2, women with labor but without infection; group 3, women with intra-amniotic infection but without labor; and group 4, women with both infection and labor. 12-Hydroxyeicosatetraenoic acid, 15-hydroxyeicosatetraenoic acid, and leukotriene B4 were measured by radioimmunoassays. Amniotic fluid concentrations of 12-hydroxyeicosatetraenoic acid were found not to differ significantly among the four groups. Amniotic fluid concentrations of 15-hydroxyeicosatetraenoic acid in group 4 were significantly higher than in women in groups 1 and 3 (p less than 0.05). In addition, amniotic fluid concentrations in leukotriene B4 were significantly higher in group 4 than in any of the other three groups (p less than 0.05). Leukotriene B4 concentrations were higher in groups 2 and 3 than in group 1, suggesting that the presence of both labor and infection increases the concentration of this metabolite in amniotic fluid. Infection and labor had an additive effect in the elevation of amniotic fluid concentrations of leukotriene B4. These results suggest that the amniotic fluid concentrations of arachidonate lipoxygenase metabolites are affected differently by the presence of infection and labor in women with premature rupture of membranes.

Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Amniotic Fluid; Arachidonate Lipoxygenases; Bacterial Infections; Female; Fetal Membranes, Premature Rupture; Humans; Hydroxyeicosatetraenoic Acids; Leukotriene B4; Obstetric Labor, Premature; Pregnancy; Pregnancy Complications, Infectious

Topics: Bacterial Infections; Blood Bactericidal Activity; Chemotactic Factors; Exotoxins; Humans; Interleukin-8; Leukotriene B4; Neutrophils; Pseudomonas Infections; Staphylococcal Infections