interleukin-8 and Cross-Infection

Despite improvements in the management of community-acquired pneumonia (CAP), morbidity and mortality are still high, especially in patients with more severe disease. Early and appropriate antibiotics remain the cornerstone in the treatment of CAP. However, two aspects seem to contribute to a worse outcome: an uncontrolled inflammatory reaction and an inadequate immune response. Adjuvant treatments, such as corticosteroids and intravenous immunoglobulins, have been proposed to counterbalance these effects. The use of corticosteroids in patients with severe CAP and a strong inflammatory reaction can reduce the time to clinical stability, the risk of treatment failure, and the risk of progression to acute respiratory distress syndrome. The administration of intravenous immunoglobulins seems to reinforce the immune response to the infection in particular in patients with inadequate levels of antibodies and when an enriched IgM preparation has been used; however, more studies are needed to determinate their impact on outcome and to define the population that will receive more benefit.

Topics: Adrenal Cortex Hormones; Cross Infection; Hospital Mortality; Humans; Immunity, Innate; Immunoglobulins; Interleukin-10; Interleukin-6; Interleukin-8; Pneumonia; Review Literature as Topic; Systemic Inflammatory Response Syndrome

Effective host defense against bacterial infection is dependent on the activation and recruitment of phagocytic cells. The initiation, maintenance, and resolution of this inflammatory response in the setting of bacterial pneumonia is dependent on the expression of cytokines. As the complexities of the host-pathogen interaction are further dissected and unraveled, immunologic manipulation of cytokine expression will likely become an important adjuvant therapy in the treatment of serious lung infections.

Topics: Animals; Biological Therapy; Cross Infection; Cytokines; Granulocyte Colony-Stimulating Factor; Humans; Interleukin-10; Interleukin-12; Interleukin-8; Pneumonia, Bacterial; Tumor Necrosis Factor-alpha

The staphylococcal bi-component leukotoxins constitute a family included in the super-family of the beta-sheet-structured pore-forming toxins. They may be produced by Staphylococcus aureus and by Staphylococcus intermedius and their target cells vary according to the molecules. The mode of action proceeds by the sequential binding of the class S proteins, then by that of the class F proteins at the surface of the membranes. Then, the activation of cellular calcium-channels precedes the pore formation which seems to be sensitive to several monovalent cations. The cell response is inflammatory and includes the neosynthesis as well as the secretion of leukotriene B4, interleukin -8, histamine. The injection of leukotoxins to rabbits generates cell chemotaxis , vasodilatation, and tissue necrosis. The association of the production of leukotoxins with clinical syndromes concerns several aspects of the pathology of S. aureus, and confers to these leukotoxins an important role of virulence factors.

Topics: Animals; Bacterial Proteins; Bacterial Toxins; Calcium Channels; Cations, Divalent; Cattle; Cell Membrane Permeability; Chemotaxis, Leukocyte; Cross Infection; Erythrocytes; Exotoxins; Female; Hemolysin Proteins; Histamine Release; Humans; Interleukin-8; Ion Transport; Leukocidins; Leukotriene B4; Male; Mastitis, Bovine; Models, Biological; Necrosis; Neutrophils; Rabbits; Staphylococcal Infections; Staphylococcus aureus; T-Lymphocytes; Vasodilation; Virulence; Vitreous Body

The inflammatory response plays a critical role in postoperative nosocomial infections, which are the most common postoperative complications causing adverse events and poor postoperative outcomes. This study aimed to explore the ability of early inflammation-related factor levels to predict the occurrence of nosocomial infections after abdominal surgery.. The study included 146 patients with open abdominal surgery (a nosocomial infection group (NI group, n=42) and a no-nosocomial infection group (NNI group, n=104)). After 1:1 matching, the patients were divided into a matching nosocomial infection group (M-NI group, n=25) and a matching no-nosocomial infection group (M-NNI group, n=25). Serum levels of interleukin (IL)-6, IL-8, IL-10, IL-12, IL-18, macrophage migration inhibitory factor (MIF), and monocyte chemotactic protein (MCP-1) were tested at three time points (pre-operation, 0-hour post-operation (POD1) and 24-hour post-operation (POD2)). The area under the receiver operating characteristic curve (AUC-ROC) was used to test the predictive abilities.. There were significant differences in the levels of IL-6, IL-12, and IL-18 between the M-NI and M-NNI groups (p < 0.05), but not in the levels of other inflammatory factors. MIF, IL-8, and MCP-1 levels were higher in the M-NI group than in the M-NNI group at POD2 (p < 0.05). In the ROC analysis, the AUC for prediction of nosocomial infection using a combination of IL-6 and IL-18 at POD1 was 0.9616, while the AUCs for IL-6 alone and IL-12 alone were 0.8584 and 0.8256, respectively.. The combination of the levels of inflammatory factors, IL-6 and IL-18, at the 0-hour postoperative time point, significantly improved the predictive ability to the development of postoperative infection during perioperative period. Our study suggests the importance of monitoring postoperative inflammatory markers.

Topics: Abdomen; Biomarkers; Cross Infection; Humans; Interleukin-10; Interleukin-12; Interleukin-18; Interleukin-6; Interleukin-8; Macrophage Migration-Inhibitory Factors; Monocyte Chemoattractant Proteins; Postoperative Complications

We investigated the expression levels of virulence factors (ompA, omp33-36 and carO) in five clinical isolates and in a standard ATCC 19606 strain of Acinetobacter baumannii to determine their effect on the virulence characteristics of the isolates.. The mRNA levels of omps and proinflammatory cytokines were analyzed by quantitative real-time PCR. For adherence assay, after human lung epithelial cells (A549) were co-cultured with A. baumannii at 37 °C for 2 h, the cell-adherent bacteria was counted. Pearson correlation analysis was used to compare the omps mRNA levels, the proinflammatory cytokines and the number of adherent bacteria.. The mRNA levels of ompA in the clinical isolates were higher and similar compared with those in ATCC 19606, whereas the mRNA levels of omp33-36 in the clinical isolates were lower and similar compared with those in ATCC 19606. The mRNA levels of carO in the clinical isolates were significantly higher than those in ATCC 19606. The number of cell-adherent clinical isolates was higher than that of cell-adherent ATCC 19606. Furthermore, the number of cell-adherent clinical isolates was positively and significantly correlated with ompA mRNA level. The mRNA levels of TNF-α, IL-6 and IL-8 in A549 cells co-cultured with the clinical isolates were lower than those in A549 cells co-cultured with ATCC 19606. Moreover, the mRNA levels of TNF-α, IL-6 and IL-8 were negatively and significantly correlated with those of carO in the isolates.. These results provide insights into the renewed virulence characteristics of A. baumannii clinical isolates that depend on cell adherence capacity and the expression level of omp mRNAs.

Topics: A549 Cells; Acinetobacter baumannii; Bacterial Adhesion; Bacterial Outer Membrane Proteins; Coculture Techniques; Cross Infection; Humans; Interleukin-6; Interleukin-8; Porins; RNA, Messenger; Tumor Necrosis Factor-alpha; Virulence Factors

Mortality of sepsis is still high. Crucial for therapeutic response are the early start of treatment as well as the choice of antibiotics or antibiotic combinations. β-lactam antibiotics with bactericidal mode of action are often recommended in guidelines. But this antibiotic class can trigger the immune system to a maximum by releasing cell wall components or exotoxins. This may lead to a worsening of the patient's clinical situation. In contrast, antibiotics with bacteriostatic action often inhibit bacterial protein synthesis with decrease of production of virulence factors and minimize release of cell wall components. The purpose of this review is to summarise the significance of some bacteriostatic antibiotics and to discuss whether a combination of bactericidal and bacteriostatic agents may improve the course of the illness.

Topics: Animals; Anti-Bacterial Agents; Bacteria; Bacterial Infections; beta-Lactams; Cell Wall; Critical Care; Cross Infection; Drug Therapy, Combination; Exotoxins; Guideline Adherence; Humans; Immunization; Interleukin-8; Sepsis; Staphylococcal Infections; Staphylococcus aureus; Virulence Factors

Based on the implication of soluble triggering receptor expressed on myeloid cells (sTREM-1) in the septic cascade, it was investigated whether it participates or not in posttraumatic systemic inflammatory response syndrome (SIRS).. Blood was sampled on days 1, 4, 7, and 15 from 69 patients with SIRS after multiple injuries and upon presentation of a septic complication. Concentrations of sTREM-1, tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-6, IL-8, and interferon-gamma were determined by an enzyme immunoassay. Samples drawn on day 1 from 10 trauma patients without SIRS served as controls.. In 26 patients with SIRS without septic complication, sTREM-1, TNFalpha, and IL-8 remained stable over follow-up; IL-6 decreased and interferon-gamma increased on days 4 and 7 compared with day 1. TNFalpha was the only variable being higher upon advent of septic shock compared with patients without SIRS and upon presentation of SIRS, sepsis, and severe sepsis (p of comparisons with all subgroups <0.0001). Mortality of patients with sTREM-1 greater than 180 pg/mL was 5.3% compared with 28.0% of those with sTREM-1 lower than 180 pg/mL (p 0.035). sTREM-1 higher than 40 pg/mL had sensitivity 56.5% and specificity 91.7% for the differential diagnosis between SIRS and sepsis after multiple injuries.. This is the first study providing evidence about the participation of sTREM-1 in posttraumatic SIRS. Its levels are increased and remain constant over time in patients who did not develop any complications whereas it seems to behave as an anti-inflammatory mediator.

Topics: Adult; Aged; Bacteremia; Cross Infection; Diagnosis, Differential; Enzyme-Linked Immunosorbent Assay; Female; Gram-Negative Bacterial Infections; Humans; Injury Severity Score; Interferon-gamma; Interleukin-6; Interleukin-8; Male; Membrane Glycoproteins; Middle Aged; Multiple Organ Failure; Multiple Trauma; Pneumonia, Bacterial; Predictive Value of Tests; Prognosis; Prospective Studies; Pyelonephritis; Receptors, Immunologic; Shock, Septic; Systemic Inflammatory Response Syndrome; Time Factors; Triggering Receptor Expressed on Myeloid Cells-1; Tumor Necrosis Factor-alpha

An important and persistent laboratory finding has been that males and females respond differently after traumatic injury and hemorrhagic shock. We have previously presented clinical data showing that male gender is independently associated with a 40% higher rate of multiple organ failure (MOF) and a 25% higher rate of nosocomial infection (NI) after injury; however, the mechanism responsible for this dimorphic response after injury has not been adequately characterized clinically.. Data were obtained from a multicenter prospective cohort study evaluating clinical outcomes in severely injured adults with blunt hemorrhagic shock. Proteomic analysis of serum inflammatory cytokines, on days 0, 1, and 4 postinjury, was performed on 46 males and 34 females. Repeated measures ANOVA were used to compare serial IL-1beta, TNF-alpha, IL-6, IL-8, and IL-10 serum levels across gender, while controlling for important confounders. Logistic regression modeling was then used to analyze the independent risk of MOF and NI associated with gender.. IL-6 serum levels were statistically higher in males relative to females (p = 0.008). This higher level of IL-6 expression in males remained statistically significant over time even after controlling for differences in age, initial base deficit, ISS, and 12-hour blood transfusion requirements (p = 0.025). No differences in IL-1beta serum levels (p = 0.543), TNF-alpha, (p = 0.200) IL-8 (p = 0.107), and IL-10 (p = 0.157) were found. Males had a higher crude incidence of MOF and an 11-fold higher independent risk of MOF.. Persistently elevated IL-6 levels in males are associated with a higher rate of MOF. It is not known if this excessive IL-6 expression in males is causal or only a marker for poor outcome. Further studies are required to elucidate if this early, persistent IL-6 expression is responsible for the gender-based differential outcomes after injury.

Topics: Adult; Analysis of Variance; APACHE; Cross Infection; Humans; Injury Severity Score; Interleukin-1; Interleukin-10; Interleukin-6; Interleukin-8; Length of Stay; Male; Multiple Organ Failure; Prospective Studies; Risk Factors; Sex Factors; Shock, Hemorrhagic; Tumor Necrosis Factor-alpha; Wounds, Nonpenetrating

Inflammation due to perinatal infection (PI) and perinatal asphyxia (PA) may cause damage to various tissues and very often to the immature brain of the fetus and the newborn. Previously, we have shown that the neonatal immune system has the ability to produce increased chemokine protein levels in the serum during the inflammatory response caused by PI and PA.. The aim of our present study was to investigate mRNA levels of the proinflammatory chemokines interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) in peripheral blood leukocytes from infected and asphyxiated neonates.. Forty-two premature neonates were studied; 11 with PI, 16 with PA and 15 without PA and PI, were used as controls. IL-8 and MCP-1 mRNA levels were investigated in whole blood and in phytohemagglutinin-activated lymphocytes using semi-quantitative polymerase chain reaction and real-time polymerase chain reaction, respectively.. IL-8 mRNA levels were significantly increased in whole blood both during PA and PI, while MCP-1 mRNA levels were not. In vitro activated lymphocytes expressed significantly increased IL-8 mRNA levels during PI, whereas no increase was observed during PA. MCP-1 mRNA levels were significantly increased in activated lymphocytes during PA, while no increase was observed during PI.. Our data show that chemokine mRNA levels expressed by activated lymphocytes during inflammation caused by PIs are different to those expressed during PAs. These findings might have important implications during the administration of specific chemokine antagonists in order to prevent or reduce tissue damage caused by inflammation.

Topics: Asphyxia Neonatorum; Chemokine CCL2; Cross Infection; Gene Expression; Humans; Infant, Newborn; Interleukin-8; Leukocytes, Mononuclear; Lymphocyte Activation; Mitogens; Phytohemagglutinins; RNA, Messenger

To determine the pathogens causing pneumonia in community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP) and to investigate serum levels of interleukin-6 (IL-6), interleukin-8 (IL-8) and CRP in pneumonia caused by different aetiological agents.. Eighty-seven children (mostly < 5 years of age) were recruited in a prospective study, 55 of them with CAP without prior antibiotic treatment and 32 with HAP. Thirty healthy outpatient children served as controls.. The causative micro-organisms were determined by serological and microbiological methods in 40 cases with CAP (72.7%) and 30 with HAP (93.7%). In CAP, M. pneumoniae was the most common causative agent (43.6%), followed by S. pneumoniae (20%) and C. pneumoniae (18.1%). Bacteria alone were the sole causative agents in only 21.8% of cases with HAP. Pseudomonas aeruginosa (34.3%) and K. pneumoniae (32.5%) were the most frequently isolated. Although IL-6 and IL-8 levels were raised, there was no statistical difference between the CAP and HAP groups, or between bacterial and mycoplasma infections; neither was there a difference in CRP levels between these two groups.. The causes of pneumonia differ between CAP and HAP. Levels of IL-6, IL-8 and CRP are raised in pneumonia but are unhelpful in differentiating the various aetiologies.

Topics: Analysis of Variance; Biomarkers; C-Reactive Protein; Child, Preschool; Community-Acquired Infections; Cross Infection; Diagnosis, Differential; Female; Humans; Infant; Interleukin-6; Interleukin-8; Male; Pneumonia, Bacterial; Prospective Studies; Statistics, Nonparametric

The inflammatory response induced by perinatal infections and asphyxia is considered to participate in neonatal brain damage. Inflammatory responses are characterized by the expression of chemokines. Although chemokine levels have been investigated in healthy newborns, their role during neonatal pathological conditions has not been studied. The aim of our study was to examine chemokine serum levels in asphyxiated and infected neonates.. Peripheral blood samples were obtained from perinatally asphyxiated and infected neonates during the first days of life and from neonates who developed nosocomial infections. Serum levels of interleukin-8 (IL-8), interferon-gamma-inducible protein-10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1alpha (MIP-1alpha), and regulated upon activation, normal T cells expressed and secreted (RANTES) were determined.. In perinatally asphyxiated neonates, IL-8 levels were significantly elevated on the 1st day of life. In perinatally infected neonates, IL-8 and IP-10 levels were significantly increased on the 1st day of life, while RANTES levels were significantly lower and remained so until the 4th day. In nosocomially infected neonates, IL-8, IP-10 and MIP-1alpha levels were significantly increased on diagnosis of infection.. The neonatal immune system is able to produce chemokines for the induction of an inflammatory response during perinatal asphyxia and perinatal or nosocomial infections. Blockade of inflammatory chemokines could possibly contribute to the prevention of brain damage.

Topics: Asphyxia Neonatorum; Chemokine CCL2; Chemokine CCL3; Chemokine CCL4; Chemokine CCL5; Chemokine CXCL10; Chemokines; Cross Infection; Humans; Infant, Newborn; Infections; Interleukin-8; Macrophage Inflammatory Proteins

Chronic lung disease (CLD) of the newborn is associated with pulmonary inflammation. However, the origin of this inflammation is not known. We evaluated the impact of airway infection on bronchoalveolar inflammation in mechanically ventilated preterm infant at risk for CLD (n = 68). Mean and maximum concentrations of the inflammatory mediators (IM) interleukin-1 and interleukin-8 were assayed in the tracheobronchial aspirate fluid (TAF) of neonates with perinatal airway infection (Ureaplasma urealyticum, or bacteria), postnatal nosocomial airway infection, or respiratory disease without airway infection from days 1-10 of postnatal age. Patients with CLD (n = 23;) exhibited increased levels of IM in TAF compared to neonates without CLD. Within the three subgroups, concentrations of IM were increased in CLD patients with perinatal infection and in CLD patients with respiratory disease without airway infection, but not in CLD patients with nosocomial airway infection. Although airway colonization with Gram-negative bacteria was more frequently found in CLD patients within the first month of life, there were no differences between levels of IM in patients colonized with Gram-negative bacteria or coagulase-negative staphyloccoci. We conclude that perinatal infections with Ureaplasma urealyticum or bacteria and respiratory disease without infection, but not nosocomial airway infection, contribute to the bronchopulmonary inflammatory response in neonates with CLD.

Topics: Cross Infection; Female; Humans; Immunoglobulin A, Secretory; Infant, Newborn; Infant, Premature; Infant, Very Low Birth Weight; Inflammation Mediators; Interleukin-1; Interleukin-8; Lung Diseases; Male; Perinatal Care; Pneumonia; Prospective Studies; Respiration, Artificial; Respiratory Tract Infections; Trachea; Ureaplasma Infections

Nosocomial pneumonia (NP) in injured patients is a significant clinical problem. We hypothesize that the pathogenesis of NP in injured patients involves an imbalanced cytokine response within the alveolar airspace that may inhibit effector cell function.. Proinflammatory (IL-8) and anti-inflammatory (IL-10) levels were measured in bronchoalveolar lavage (BAL) fluid from multitrauma patients on admission, 24, 48, and 72 hours post-injury and following lipopolysaccharide (LPS) induction of alveolar cells. Patients were compared based on IL-8 levels and the development of NP.. A high level of IL-8 on admission was associated with the development of NP. In addition, levels of IL-8 were significantly greater in NP-positive patients at all time points. The IL-10 levels decreased from admission values in NP-negative patients but increased in NP-positive patients. Furthermore, a high level of IL-10 ( > 120 pg/mL) at 72 hours post-injury was associated with the development of NP. Alveolar cells from NP-positive patients produced significantly more IL-10 in response to LPS than cells from NP-negative patients.. The pathogenesis of NP in injured patients involves an early and severe IL-8 process within the lung followed by an exaggerated IL-10 response that may inhibit effector cell function.

Topics: Adult; Aged; Cross Infection; Female; Humans; Interleukin-10; Interleukin-8; Lipopolysaccharides; Male; Middle Aged; Pneumonia, Bacterial

To examine whether the determination of interleukin 8 (IL-8) and C-reactive protein (CRP) in neonates with suspected nosocomial bacterial infection (NBI) is feasible and cost-effective in reducing antibiotic therapy.. Between April 1996 and May 1997, IL-8 was measured 260 times along with blood cultures, CRP, and immature-to-total-neutrophil (IT) ratio for suspected NBI in term and preterm neonates. All infants were retrospectively analyzed for NBI. Sensitivity, specificity, positive and negative predictive values, and 95% confidence intervals were calculated for IL-8, CRP, and IT ratio. Receiver-operating characteristic curves were analyzed to determine optimal thresholds. Between June 1997 and June 1998, IL-8 was measured 215 times in newborn infants with suspected NBI and the decision to start antibiotic therapy was based on increased IL-8 and/or CRP values. A cost-effectiveness analysis was performed and sensitivity, specificity, and receiver-operating characteristic curves were reevaluated.. At the first suspicion of NBI, the combination of IL-8 >/= 53 pg/mL and/or CRP >10 mg/L detected culture-proven NBI with 96% sensitivity. The combined culture-proven and clinical NBI were detected with 93% sensitivity and 80% specificity. The use of IL-8 reduced unnecessary antibiotic therapy for suspected NBI by 73% and was cost-effective when compared with initiating antibiotic therapy based on clinical signs alone or based on clinical signs and an increased IT ratio and/or CRP.. The combination of IL-8 and/or CRP is a reliable and early test for the diagnosis of NBI in newborn infants. Using the combination of IL-8 and/or CRP to restrict antibiotic therapy to truly infected infants reduces unnecessary antibiotic therapy and is cost-effective.

Topics: Anti-Bacterial Agents; Bacterial Infections; Biomarkers; C-Reactive Protein; Cost-Benefit Analysis; Cross Infection; Drug Utilization; Humans; Infant, Newborn; Interleukin-8; Predictive Value of Tests; Retrospective Studies; Sensitivity and Specificity

Systemic inflammatory response syndrome (SIRS) and infections are frequently associated with the development and progression of acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS). We investigated, at onset and during the progression of ARDS, the relationships among (1) clinical variables and biological markers of SIRS, (2) infections defined by strict criteria, and (3) patient outcome. Biological markers of SIRS included serial measurements of inflammatory cytokines (IC)-tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL) 1 beta, 2, 4, 6, and 8-in plasma and BAL fluid.. We prospectively studied two groups of ARDS patients: 34 patients treated conventionally (group 1) and nine patients who received glucocorticoid rescue treatment for unresolving ARDS (group 2). Individual SIRS criteria and SIRS composite score were recorded daily for all patients. Plasma IC levels were measured by enzyme-linked immunosorbent assay on days 1, 2, 3, 5, 7, 10, and 12 of ARDS and every third day thereafter while patients received mechanical ventilation. Unless contraindicated, bilateral BAL was performed on day 1, weekly, and when ventilator-associated pneumonia was suspected. Patients were closely monitored for the development of nosocomial infections (NIs).. ICU mortality was similar among patients with and without sepsis on admission (54% vs 40%; p < 0.45). Among patients with sepsis-induced ARDS, mortality was higher in those who subsequently developed NIs (71% vs 18%; p < 0.05). At the onset of ARDS, plasma TNF-alpha, IL-1 beta, IL-6, and IL-8 levels were significantly higher (p < 0.0001) in nonsurvivors (NS) and in those with sepsis (p < 0.0001). The NS group, contrary to survivors (S), had persistently elevated plasma IC levels over time. In 17 patients, 36 definitive NIs (17 in group 1 and 19 in group 2) were diagnosed by strict criteria. No definitive or presumed NIs caused an increase in plasma IC levels above patients' preinfection baseline. Daily SIRS components and SIRS composite scores were similar among S and NS and among patients with and without sepsis-induced ARDS, were unaffected by the development of NI, and did not correlate with plasma IC levels.. Sepsis as a precipitating cause of ARDS was associated with higher plasma IC levels. However, NIs were not associated with an increase in SIRS composite scores, individual SIRS criteria, or plasma IC levels above patients' preinfection baseline. SIRS composite scores over time were similar in S and NS. SIRS criteria, including fever, were found to be nonspecific for NI. Irrespective of etiology of ARDS, plasma IC levels, but not clinical criteria, correlated with patient outcome. These findings suggest that final outcome in patients with ARDS is related to the magnitude and duration of the host inflammatory response and is independent of the precipitating cause of ARDS or the development of intercurrent NIs.

Topics: Adult; Bacterial Infections; Biomarkers; Bronchoalveolar Lavage Fluid; Cause of Death; Critical Care; Cross Infection; Disease Progression; Enzyme-Linked Immunosorbent Assay; Female; Follow-Up Studies; Glucocorticoids; Humans; Interleukin-1; Interleukin-2; Interleukin-4; Interleukin-6; Interleukin-8; Male; Multiple Organ Failure; Outcome Assessment, Health Care; Pneumonia; Prospective Studies; Respiration, Artificial; Respiratory Distress Syndrome; Survival Rate; Systemic Inflammatory Response Syndrome; Tumor Necrosis Factor-alpha

One hundred five (70%) of 151 patients hospitalized in the intensive care unit and undergoing mechanical ventilation had bronchial secretions that tested positive for interleukin-8 within 36 hours of admission. Arterial blood, mixed venous blood, and urine collected simultaneously all tested negative, except for 11 patients admitted with intra-abdominal septic foci. The presence of interleukin-8 in the pulmonary air space early in the course of hospitalization was significantly associated with patients with multiple injuries, the need for greater ventilatory support, the occurrence of pulmonary dysfunction, and a 66% incidence of nosocomial bacterial pneumonia. We conclude that the early local production of interleukin-8 in the lungs is an early marker of pulmonary injury and may be involved in the pathogenesis of nosocomial bacterial pneumonia.

Topics: Adult; Blotting, Northern; Bronchi; Cross Infection; Female; Humans; Intensive Care Units; Interleukin-8; Male; Middle Aged; Multiple Trauma; Pneumonia, Pneumococcal; Prospective Studies