Video recording in the delivery room: current status, implications and implementation.

Many factors determine the performance and success of delivery room management of newborn babies. Improving the quality of care in this challenging surrounding has an important impact on patient safety and on perinatal morbidity and mortality. Video recording (VR) offers the advantage to record and store work as done rather than work as recalled. It provides information about adherence to algorithms and guidelines, and technical, cognitive and behavioural skills. VR is feasible for education and training, improves team performance and results of research led to changes of international guidelines. However, studies thus far have not provided data regarding whether delivery room video recording affects long-term team performance or clinical outcomes. Privacy is a concern because data can be stored and individuals can be identified. We describe the current state of clinical practice in high- and low-resource settings, discuss ethical and medical-legal issues and give recommendations for implementation with the aim of improving the quality of care and outcome of vulnerable babies. IMPACT: VR improves performance by health caregivers providing neonatal resuscitation, teaching and research related to delivery room management, both in high as well low resource settings. VR enables information about adherence to guidelines, technical, behavioural and communication skills within the resuscitation team. VR has ethical and medical-legal implications for healthcare, especially recommendations for implementation of VR in routine clinical care in the delivery room. VR will increase the awareness that short- and long-term outcomes of babies depend on the quality of care in the delivery room.

Implementation and effectiveness of a video-based debriefing programme for neonatal resuscitation.

BACKGROUND: Approximately 5%-10% of newly born babies need intervention to assist transition from intra- to extrauterine life. All providers in the delivery ward are trained in neonatal resuscitation, but without clinical experience or exposure, training competency is transient with a decline in skills within a few months. The aim of this study was to evaluate whether neonatal resuscitations skills and team performance would improve after implementation of video-assisted, performance-focused debriefings. METHODS: We installed motion-activated video cameras in every resuscitation bay capturing consecutive compromised neonates. The videos were used in debriefings led by two experienced facilitators, focusing on guideline adherence and non-technical skills. A modification of Neonatal Resuscitation Performance Evaluation (NRPE) was used to score team performance and procedural skills during a 7 month study period (2.5, 2.5 and 2 months pre-, peri- and post-implementation) (median score with 95% confidence interval). RESULTS: We compared 74 resuscitation events pre-implementation to 45 events post-implementation. NRPE-score improved from 77% (75, 81) to 89% (86, 93), P < 0.001. Specifically, the sub-categories "group function/communication", "preparation and initial steps", and "positive pressure ventilation" improved (P < 0.005). Adequate positive pressure ventilation improved from 43% to 64% (P = 0.03), and pauses during initial ventilation decreased from 20% to 0% (P = 0.02). Proportion of infants with heart rate > 100 bpm at 2 min improved from 71% pre- vs. 82% (P = 0.22) post-implementation. CONCLUSION: Implementation of video-assisted, performance-focused debriefings improved adherence to best practice guidelines for neonatal resuscitation skill and team performance.

"Mothers get really exhausted!" The lived experience of pregnancy in extreme heat: Qualitative findings from Kilifi, Kenya.

Heat exposure in pregnancy is associated with a range of adverse health and wellbeing outcomes, yet research on the lived experience of pregnancy in high temperatures is lacking. We conducted qualitative research in 2021 in two communities in rural Kilifi County, Kenya, a tropical savannah area currently experiencing severe drought. Pregnant and postpartum women, their male spouses and mothers-in-law, community health volunteers, and local health and environment stakeholders were interviewed or participated in focus group discussions. Pregnant women described symptoms that are classically regarded as heat exhaustion, including dizziness, fatigue, dehydration, insomnia, and irritability. They interpreted heat-related tachycardia as signalling hypertension and reported observing more miscarriages and preterm births in the heat. Pregnancy is conceptualised locally as a 'normal' state of being, and women continue to perform physically demanding household chores in the heat, even when pregnant. Women reported little support from family members to reduce their workload at this time, reflecting their relative lack of autonomy within the household, but also potentially the 'normalisation' of heat in these communities. Climate change risk reduction strategies for pregnant women in low-resource settings need to be cognisant of local household gender dynamics that constrain women's capacity to avoid heat exposures.

National guidelines for treatment of jaundice in the newborn.

UNLABELLED: Jaundice is the most common reason for instituting treatment in otherwise healthy as well as sick newborn infants. Herein, we describe the process employed in Norway to forge agreement on a set of treatment guidelines that are now used across the country. The Norwegian Pediatric Association was a key resource in this process, which involved contacts with all paediatric departments in Norway. We have also performed an international survey regarding the use of such national guidelines, showing that the majority of those queried confirm having national guidelines. The evidence base for any neonatal jaundice guideline is weak; therefore, it is not surprising that the various guidelines differ both in format and in specifics. In the Norwegian guidelines, treatment indications are based on bilirubin concentrations and related to birth weight. Postnatal age is also factored in because jaundice develops gradually during the first 3-4 days before it levels off. CONCLUSION: Following the introduction of these guidelines, fewer babies in Norway receive phototherapy, and no cases of chronic kernicterus have been reported during this period.

Recent-onset childhood arthritis--association with Streptococcus pyogenes in a population-based study.

OBJECTIVES: To assess the frequency of Streptococcus pyogenes in children with early arthritis, compare the characteristics in patients with post-streptococcal ReA (PSReA) with those in patients with other types of arthritis, and describe the occurrence of carditis in PSRA. PATIENTS: In a population-based Norwegian study, the physicians were asked to refer all children with suspected arthritis. The arthritis patients were followed up at 6 weeks, 6 months and 18 months. The presence of S. pyogenes was based on throat smear or antibodies. Echocardiography was performed in the patients with ARF or PSRA. RESULTS: Thirty-two (18%) of the 173 children with arthritis tested positive for S. pyogenes. The percentage of positive tests rose steadily with age and peaked at ages 8-11 (35%). Six weeks after admission arthritis was present in 33% of the PSRA patients, which was less frequent than in the juvenile idiopathic arthritis (JIA) patients (P < 0.001), but more frequent than in the transient arthritis patients (P = 0.012). Hip arthritis was more frequent and knee/ankle arthritis, ANA and HLA-B27 were less frequent in PSRA than in JIA (P < 0.001, P = 0.009 and P = 0.029, respectively). The PSRA patients were older than those with transient arthritis (P = 0.007). One child with ARF had carditis. CONCLUSIONS: Streptococcus pyogenes was present in 18% of children with arthritis. The patient characteristics, clinical presentation and early disease course in PSRA was different from that of JIA and transient arthritis.

Immunohistochemical localization of coagulation, fibrinolytic and antifibrinolytic markers in adenocarcinoma of the lung.

Extravascular coagulation and fibrinolysis are intimately involved in and modulate cancer cell growth, invasion and metastasis. Samples from resection specimens of patients with primary lung cancer (adenocarcinomas) were tested with monoclonal (MAb) and polyclonal (PAb) antibodies against various factors of the coagulation or fibrinolysis systems, or against antigens of inflammatory or proliferating cells. MAb Ki-67 specific to nuclear antigens of proliferating cells showed a distinct but variable staining of cell nuclei throughout the tumor tissue. Nests of tumor tissue stained with cytokeratin-specific antibodies (PKK1), whereas other parts were negative. Fibrin(ogen) and fibronectin were found throughout the tumor tissue stroma and in the alveolar lining, and the most densely stained areas were at the transition zone between normal and tumor tissue. Fibrinolytic system components like tissue plasminogen activators (t-PA), and urokinase (u-PA), and their inhibitors PAI-1 and PAI-2 were all studied. All specimens were negative for t-PA (except endothelial linings), whereas urokinase-specific antibodies stained loosely packed tumor cells and macrophages within the tumor stromal tissue and alveolar septa. Both PAI-1 and PAI-2 were most prominently expressed within interstitial and alveolar macrophages. A weaker staining of tumor tissue cells was demonstrated. Inflammatory cells like macrophages and T lymphocytes were located in aggregates or diffusely spread within tumor stromal tissue. The inflammatory reaction was most intense at the border between normal lung and tumor tissue.

Characterization of cytoadhesion molecules on human monocytes and tissue macrophages.

The presence of proteins antigenically related to the GPIIb/IIIa complex expressed on platelets have been investigated on tissue macrophages recovered by bronchoalveolar lavage (lung alveolar macrophages, LAM) or peritoneal lavage (peritoneal macrophages, PM) as well as on monocytes. Polyclonal antibodies (pab) directed against human platelet GPIIb/IIIa and the vitronectin receptor (VnR), and mouse monoclonal antibodies (mab) against human GPIIb, GPIIIa or the GPIIb/IIIa-complex were used. Triton X-100 extracts of bronchoalveolar cells (BAC) (containing 94% LAM) and the ultrasedimentable fraction of cell-free bronchoalveolar lavage (US) reacted with the polyclonal antibodies against the GPIIb/IIIa-complex and the VnR, but only with one (P4) of the mabs. Cell microscopy after immunogold labelling and alkaline phosphatase immunostaining, as well as immunofluorescence using the P4 mab and the polyclonal anti-GPIIb/IIIa clearly demonstrated positive membrane staining of LAM, PM and monocytes. Both BAC and US extracts gave rise to immunoprecipitates in crossed and rocket immunoelectrophoresis using anti-GPIIb/IIIa and anti-VnR. Our data indicate that monocytes and their monocyte-derived tissue counterparts constitutively express GPIIb/IIIa-like antigen(s) on their membrane. The presence of such antigen(s) on tissue macrophages makes it unlikely that platelet contamination is responsible for these findings.

Dissociation of the aggregating effect and the inhibitory effect upon cyclic adenosine monophosphate accumulation by adrenaline and adenosine diphosphate in human platelets.

Recent evidence indicates that adrenaline and adenosine diphosphate each have separate stimulus-response pathways for induction of aggregation and inhibition of cAMP accumulation. We have used a natural model to test the validity of this evidence, i.e. patients from two kindreds with an inherited bleeding disorder due to absent aggregation to adrenaline and no secondary wave response to large concentrations of adenosine diphosphate. Our studies showed that the inhibitory effect of adrenaline and adenosine diphosphate on PGE1-induced increase of cAMP in the patients was not different from that of the controls both for adrenaline and adenosine diphosphate. These results therefore support the present evidence that both adrenaline and adenosine diphosphate apply separate pathways in these two platelet functions.

Local activation of the coagulation and fibrinolysis systems in lung disease.

Extravascular coagulation and fibrinolysis is an integral part of inflammatory reactions. Disordered expression of procoagulant and profibrinolytic factors by mononuclear phagocytes of the lung (i.e. lung alveolar macrophages (LAM) and interstitial macrophages) may have important bearings on inflammatory lung tissue destruction and repair. Based on this hypothesis we have measured the presence of trigger molecules and activation products of the coagulation and fibrinolytic system in cell-free bronchoalveolar lavage fluid and in bronchoalveolar cells. Patient groups with chronic obstructive disease (COLD) (n = 76), idiopathic pulmonary fibrosis (IPF) (n = 29), sarcoidosis (n = 22), lung cancer (n = 36), pneumonia (n = 39), acquired immunodeficiency syndrome (AIDS) (n = 17) and a control group (n = 60) were studied by bronchoalveolar lavage (BAL). In all patient groups tissue thromboplastin (TPL) and fibrinopeptide A (FPA) were significantly increased compared to controls. Plasminogen activator (PA) activity was significantly lower in patients than in normals, and usually associated with high levels of antifibrinolytic activity. The level of PA inhibitor (PAI-2) was not significantly higher in any patient group compared to controls. The sensitivity of the method for fibrin degradation products (FDP) analysis was not high enough to detect FDP in BAL fluid of control individuals, whereas such products could be demonstrated in 25-53% of patients in various categories. We conclude that disordered expression of procoagulant and plasminogen activator activities in bronchoalveolar lavage fluid may reflect a milieu that favours accumulation of fibrin in inflammatory lung tissue and form the basis for the development of pulmonary fibrosis.

Polymorphism of a platelet polypeptide.

Polymorphism of a platelet protein is described. The gene products are represented by two peptides of MW around 30 kD. The allele frequency was estimated to 0.85 and 0.15, the common variant being of slightly higher MW and about 2 charge units more acidic than the other. The peptides were neither released nor phosphorylated, and subcelluar fractionation indicated localization to the cytosol. Attempts to raise antibodies failed, and further characterization could not be done, but the peptides seem to differ from all reasonably well characterized platelet proteins so far.

Heterogeneity of procoagulant activity and cytokine release in subpopulations of alveolar macrophages and monocytes.

We have studied the expression of tissue factor (TF) and fibrinopeptide A (FPA) generation as well as the release capacity of TNF-alpha, IL-1beta, and IL-6 in density-defined subpopulations of alveolar macrophages (AM) and monocytes (Mo). TF was equally expressed on all AM subpopulations and Mo, while the FPA-forming capacity was at the same level in low density AM as in Mo and was significantly (P < 0.05) higher in low density AM than in high density AM. The lipopolysaccharide (LPS)-induced release of TNF-alpha was higher (P < 0.05) in high density AM than in low density AM and in Mo. IL-1beta release was undetectable in unstimulated AM and in LPS-stimulated low density AM, while the LPS-induced IL-1beta release in high density AM was low compared to the levels demonstrated in Mo. LPS-stimulated IL-6 release was not distinctively different in the AM subpopulations and Mo. The presented study showed that FPA generation and LPS-stimulated TNF-alpha release were dependent on the density (i.e., maturity) of AM. This implies that a skewed distribution of AM subpopulations induced by disease processes may profoundly influence the inflammatory reactions, including extravascular activation of coagulation.

CD14 expression and binding of lipopolysaccharide to alveolar macrophages and monocytes.

We have studied the expression of the lipopolysaccharide (LPS) receptor CD14 on monocytes (Mo) and alveolar macrophages (AM), including density- and size-defined subpopulations. Bronchoalveolar lavage (BAL) was performed on eleven healthy non-smokers and blood sampled from 5 of them, and the levels of cell CD14 expression was investigated using flow cytometry. The influence of LPS stimulation on the CD14 expression of AM was studied at various intervals during prolonged incubation. Further, the relationship between CD14 expression and LPS binding to Mo and subpopulations of AM was studied by measuring fluorescein isothiocyanate (FITC)-LPS binding (flow cytometry) and binding of radioiodinated LPS (125I-LPS). The CD14 expression was 13-fold higher (P < 0.02) on Mo than on unfractionated and high density AM. The CD14 level on the latter was higher than on low density AM, and also higher (P < 0.05) on small AM compared to large (flow cytometrically defined) AM. LPS stimulation had a downregulating effect on AM CD14 level, but after several hours of continuing decreased expression, an increased (P < 0.05) CD14 expression was demonstrated, indicating de novo synthesis. The binding of LPS to subpopulations of AM and isolated Mo was not significantly different, but the binding of FITC-LPS to Mo in whole blood was higher than to AM (P < 0.02). The presented results indicate that AM of different size and maturity have different and variable (activation dependent) CD14 levels. The LPS binding capacity was, however, not proportional to the CD14 expression, indicating that LPS binding mechanisms unrelated to CD14 levels were also operable.

Maternal allergy influences the proliferation of neonatal T cells expressing CCR4, CXCR5 or CD103.

BACKGROUND: Elevated proliferative response to allergen in cord blood mononuclear cells (CBMCs) is related to subsequent allergy development of the neonate and has been suggested as a screening marker for high allergy risk. OBJECTIVE: To characterize the proliferating cells in CBMCs from a neonatal group influenced by maternal allergy compared with a control group without known allergic heredity. METHODS: CBMCs were stimulated with bovine beta-lactoglobulin (beta-LG) and proliferation was analysed by radioactive thymidine incorporation and expressed both as the traditional stimulation index (SI) and SI corrected by eliminating non-specific proliferation. After beta-LG combined with endotoxin stimulation, cellular expression of IL-4 and IFN-gamma mRNA was determined by quantitative RT-PCR and adhesion as well as chemokine receptors were analysed by three-colour flow cytometry in proliferating T cells (CD3+ Ki-67+). RESULTS: The percentage of CCR4+ cells correlated weakly with concurrent IL-4 expression (r(S)=0.5, P<0.05), while CXCR3 correlated strongly with IFN-gamma expression (r(S)=0.83, P<0.001). In the allergy risk group, the percentage of proliferating T cells expressing CCR4 or integrin alphaE (CD103) was significantly reduced compared with the control group, while CXCR5 and the corrected SI were relatively increased (CCR4: P=0.01; integrin alphaE: P=0.03; CXCR5: P=0.04; SI: P=0.04). CONCLUSION: Our results implied delayed maturation of immune functions involved in cellular migration, cell-cell interaction and immunoregulatory functions in neonates with hereditary allergy risk. The alterations observed in this subject group suggested that the corrected SI as well as proliferation of CCR4+, CXCR5+ or CD103+ T cells in allergen-stimulated CBMCs might serve as early screening markers for allergy risk.

Impaired interleukin (IL)-4-associated generation of CCR4-expressing T cells in neonates with hereditary allergy risk.

Reduced microbial exposure in early life may contribute to the increase of atopic diseases in 'westernized' societies but the underlying mechanisms remain elusive. The objective of this study was to examine how exposure to bacterial lipopolysaccharide (LPS) during early antigen encounter might influence the maturation of neonatal lymphoid cells, and to define possible differences in this respect between neonates with high risk of allergy due to a family history (FH(+)) and controls with no apparent hereditary risk (FH(-)). Cord blood mononuclear cells from the FH(+) or FH(-) group were stimulated with pure LPS or beta-lactoglobulin (beta-LG) in the presence of LPS. T cell expression of chemokine receptors CCR4 and CXCR3 was determined by flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR). Cellular expression of interleukin (IL)-4 was analysed by quantitative RT-PCR, whereas interferon (IFN)-gamma was analysed by both quantitative RT-PCR and immunoassay. Stimulation with LPS, or beta-LG together with LPS, induced up-regulation of CCR4 (P < 0.05) and CXCR3 (P < 0.05). For CCR4, such up-regulation was related to the level of IL-4 produced by the same T cells (r(S) = 0.49, P = 0.03), while CXCR3 expression was negatively correlated with the IL-4 levels (r(S) = -0.56, P = 0.02). Compared with the FH(-) group, the FH(+) group showed a significantly lower capacity for generation of CCR4(+) T cells (mean percentage of total T cells: FH(+), 2.42%versus FH(-), 5.74%; P < 0.01), whereas induction of CXCR3 and IFN-gamma did not differ significantly between the two groups. When the immune system in early life encounters antigen together with LPS, the T cell potential for compartmentalized interaction with other immune cells might be increased by elevated CCR4- and CXCR3-expression levels. In neonates at hereditary allergy risk, this putative homeostatic mechanism could theoretically be jeopardized due to decreased up-regulation of CCR4. Conversely, Th1 responses to antigen in the presence of LPS did not appear to be reduced compared with controls.

[Pathogenetic mechanisms in acute respiratory failure in adults]. / Patogenetiske mekanismer ved akutt lungesviktsyndrom hos voksne.

A large variety of mediators and mediator systems are involved in the pathogenesis of acute respiratory failure in adults, and the complexity of the syndrome should be considered in both prophylaxis and therapy. The locally accentuated and organ-related activation of several mediator systems over a long period of time is likely to be responsible for the irreversible damage to cells and tissue. Surfactant dysfunction or degradation, regardless of the cause, contributes to the pathophysiology of severe respiratory failure, and might be a common denominator in the pathogenesis of the syndrome. Cytokines from macrophages are important, since these mediators have the potential to convert a primarily functional and reversible systemic reaction into irreversible damage to specific organs.

[Integrins, structure and function]. / Integriner, struktur og funksjon.

Integrins are molecules of central importance in physiological and pathological processes. Integrins are an important factor in intercellular adhesion processes and cell migration leading to normal architecture of tissue, in inflammatory and tumour cell migration and in reparatory processes of damaged tissue. The integrin designation is derived from the role of these substances in integrating processes within and outside the cell. Therefore these membrane proteins play a role in cell growth, differentiation and gene expression. The role played by integrins in cell signal transduction and inflammation is discussed in this article. During the past few years we have seen an explosion of research in this field, which may lead to therapeutic benefits in a few years time.

Allergen-stimulated expression of CD154 (CD40 ligand) on CD3+ lymphocytes in atopic, but not in nonatopic individuals. Modulation by bacterial lipopolysaccharide.

The intention of this study was to mimic a naturally occurring stimulation by allergens and bacterial infection in order to determine whether specific allergen-induced, inflammatory responses may be changed or modified by bacterial products. Blood leukocytes from six atopic and six nonatopic individuals were examined for their surface expression of CD154, CD11a, and HLA-DR molecules and for secretion of IgE, eosinophil cationic protein (ECP), and the cytokines interleukin (IL)-4 and IL-5. Signals through CD154 are required for activation and proliferation of effector cells associated with the allergic, inflammatory response. HLA-DR and CD11a/CD18-mediated interactions are also involved in T- and B-cell functions. Birch-pollen (BP) allergens induced CD154 expression on CD3-positive lymphocytes only in atopic individuals. In nonatopics, the expression of CD154 could be induced only after exposure to BP and subsequent lipopolysaccharide (LPS) stimulation. Levels of CD154 expression were always higher in atopics than nonatopics. CD11a and HLA-DR expressions were upregulated, irrespective of atopic state, after BP and/or LPS stimulation. The increased secretion of IL-5 and total IgE in BP-supplemented cell cultures indicated that an allergic response had occurred. In conclusion, the results of this report do not support the hypothesis of a changed inflammatory response stimulated by the combined action of bacteria and allergens, as compared to allergen provocation alone.

Antigenic specificity of human alveolar macrophages and blood monocytes studied by an immunofluorescence technique.

Lung alveolar macrophages (AM) and blood monocytes (BM) are part of the mononuclear phagocyte system (MPS) and have been shown to be composed of several functionally and biochemically distinct subsets. AM and BM were each fractionated into four subfractions by centrifugation over Percoll, 95 per cent of the monocytes having a higher buoyant density than the high-density AM fraction. Antigen distribution within the cell subfractions was studied by an immunofluorescence technique using a panel of ten monoclonal antibodies (MoAbs) reacting with separate antigenic determinants previously found on mononuclear phagocytes. Several antigens were present on both types of cells (Ki-M1, Ki-M6, Leu-M3, Leu-M5, 1D5, Dako-Ma, and HLA-DR), while other antigens were expressed exclusively on BM (MAS 072 and MAS 081) or on AM (Ki-M8). Ki-M1, Leu-M3, Leu-M5, and HLA-DR were expressed to a greater degree on the surface of AM (95-96 per cent of cells) than on BM (56-68 per cent), while an inverse relationship was noted for 1D5 antigen (present on 41 per cent of BM and 11 per cent of AM). Ki-M6 and Dako-Ma MoAbs recognized an intracellularly restricted antigen present in both AM and BM. Ki-M1, Ki-M8, MAS 072, MAS 081, Leu-M3, Leu-M5, 1D5, and HLA-DR were expressed both in the cytoplasm and at the cell surface. Some antigens (1D5, Leu-M3, MAS 072, MAS 081, and Dako-Ma) showed an uneven distribution among subsets of both AM and BM.(ABSTRACT TRUNCATED AT 250 WORDS)

Procoagulant activities in human alveolar macrophages.

The coexistence of fibrin and tissue macrophages is a common finding in the histopathology of chronic lung inflammatory diseases. Human lung alveolar macrophages (LAM) obtained by lavage of healthy donors can initiate the coagulation sequence by expressing procoagulant factors. The procoagulants of LAM were in this study identified to be either thromboplastin (tissue factor) or a direct factor X activator, probably a thromboplastin/factor VII complex. LAM did not show inducible thromboplastin synthesis as did monocytes when stimulated in vitro. LAM were separated into four subpopulations by density gradient centrifugation. The specific thromboplastin activity of subpopulation cells varied inversely with their density. Low-density subpopulations of LAM released microvesicles from their surface which could be recovered in the culture medium, and which expressed procoagulant activities with the same characteristics as the LAM procoagulants. These findings suggest that alveolar macrophages and the membrane vesicles shed from their surface contribute to local fibrin deposition in the lungs by expressing procoagulant factors.

Expression of leukocyte integrins and tissue factor in mononuclear phagocytes.

Coagulation is intimately involved in the pathology of inflammation. The leukocyte beta2-integrins have several functions, including serving as receptors for coagulation factor X and fibrinogen. Tissue factor (TF) is a receptor for factor VII and a very potent trigger of coagulation. The intention of this study was to examine a possible coexpression of beta2-integrins (CD11b/CD18 and CD11c/CD18) and the procoagulant TF in alveolar macrophages (AM) and blood monocytes, i.e. cells of the same differentiation lineage. The expression of beta2-integrins in human AM isolated by bronchoalveolar lavage and in blood monocytes was analysed by flow cytometry, whereas TF activity was analysed in a one-stage clotting assay. In monocytes, TF activity, CD11b and CD11c expression were highly inducible by lipopolysaccharide (LPS), with a 13-, 19- and four-fold increase, respectively. In AM, TF and beta2-integrins were all constitutively expressed, but the expression could not be further enhanced by LPS stimulation. CD11b and CD11c expression varied inversely with the cell size of AM, in contrast to TF activity which is known to be proportional to AM cell size. In vitro expression of beta2-integrins and tissue factor in lipopolysaccharide-stimulated blood monocytes seems to be intimately coregulated, whereas the expression of these receptors in alveolar macrophages seems to be unresponsive to lipopolysaccharide. These results indicate that blood monocytes and alveolar macrophages have different roles and use different mechanisms in cell-induced fibrin formation.