Effect of pulmonary blood flow on the exchange between the circulating and marginating pool of polymorphonuclear leukocytes in dog lungs.

Martin, B. A.; Wright, Joanne L.; Thommasen, Harvey V.; Hogg, James C.

doi:10.1172/jci110567

Cited by 89 publications

(39 citation statements)

References 16 publications

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“…The geometrical complexity of the capillary bed, as well as the considerably smaller size of capillaries (as small as 2 m wide) are responsible for neutrophil (6 -8 m) concentration in the capillary bed (13)(14)(15)(16)(17)(18). Neutrophil transit time and velocity are thus already reduced in the capillary bed, rendering the rolling process mediated by selectins unnecessary, as confirmed by various studies (10, 19 -21).…”

mentioning

confidence: 76%

“…3). Due to the complexity of the capillary network and the small size of capillaries, a large number of neutrophils are normally sequestered in the capillary bed of lungs, even in the absence of inflammation (15,17,18,52). Indeed, the 13 units of MPO detected in the lungs of infected WT and galectin-3 deficient mice represents around 1 ϫ 10 7 neutrophils (53-55).…”

Section: Myeloperoxidase (Mpo) Levels In the Lungs Of Galectin-3 Nullmentioning

confidence: 99%

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Role of Galectin-3 in Leukocyte Recruitment in a Murine Model of Lung Infection by Streptococcus pneumoniae

Nieminen

St-Pierre

Bhaumik

et al. 2008

The Journal of Immunology

105

119

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Pneumonia can be caused by a variety of pathogens, among which Streptococcus pneumoniae causes one of the most common forms of community-acquired pneumonia. Depending on the invading pathogen, the elements of the immune response triggered will vary. For most pathogens, such as Escherichia coli, neutrophil recruitment involves a well-described family of adhesion molecules, β2-integrins. In the case of streptococcal pneumonia, however, neutrophil recruitment occurs mainly through a β2-integrin-independent pathway. Despite decades of research on this issue, the adhesion molecules involved in neutrophil recruitment during lung infection by S. pneumoniae have not been identified. We have previously shown that galectin-3, a soluble mammalian lectin, can be found in lungs infected by S. pneumoniae, but not by E. coli, and can mediate the adhesion of neutrophils on the endothelial cell layer, implying its role in the recruitment of neutrophils to lungs infected with S. pneumoniae. In this study, using galectin-3 null mice, we report further evidence of the involvement of this soluble lectin in the recruitment of neutrophils to S. pneumonia-infected lungs. Indeed, in the absence of galectin-3, lower numbers of leukocytes, mainly neutrophils, were recruited to the infected lungs during infection by S. pneumoniae. In the case of β2-integrin-dependent recruitment induced by lung infection with E. coli, the number of recruited neutrophils was not reduced. Thus, taken together, our data suggest that galectin-3 plays a role as a soluble adhesion molecule in the recruitment of neutrophils to lungs infected by S. pneumoniae, which induces β2-integrin-independent migration.

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mentioning

confidence: 76%

Section: Myeloperoxidase (Mpo) Levels In the Lungs Of Galectin-3 Nullmentioning

confidence: 99%

Role of Galectin-3 in Leukocyte Recruitment in a Murine Model of Lung Infection by Streptococcus pneumoniae

Nieminen

St-Pierre

Bhaumik

et al. 2008

The Journal of Immunology

105

119

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“…Using cone-plate viscometry, we report that LFA-1, Mac-1, and ICAM-3 contribute approximately equally to neutrophil aggregate formation at shear rates on the order of 100 s Ϫ1 . Such purely ␤ 2 integrin-dependent adhesion may be physiologically important at low shears that predominate in the pulmonary microcirculation and other organs, in particular under conditions of acute inflammation (35)(36)(37). Furthermore, these adhesion molecules may contribute to vascular occlusion via the formation of adhesive interactions between leukocytes and platelets (38).…”

Section: Discussionmentioning

confidence: 99%

Shear and Time-Dependent Changes in Mac-1, LFA-1, and ICAM-3 Binding Regulate Neutrophil Homotypic Adhesion

Neelamegham

Taylor

Shankaran

et al. 2000

The Journal of Immunology

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We examined the relative contributions of LFA-1, Mac-1, and ICAM-3 to homotypic neutrophil adhesion over the time course of formyl peptide stimulation at shear rates ranging from 100 to 800 s−1. Isolated human neutrophils were sheared in a cone-plate viscometer and the kinetics of aggregate formation was measured by flow cytometry. The efficiency of cell adhesion was computed by fitting the aggregate formation rates with a model based on two-body collision theory. Neutrophil homotypic adhesion kinetics varied with shear rate and was most efficient at 800 s−1, where ∼40% of the collisions resulted in adhesion. A panel of blocking Abs to LFA-1, Mac-1, and ICAM-3 was added to assess the relative contributions of these molecules. We report that 1) LFA-1 binds ICAM-3 as its primary ligand supporting homotypic adhesion, although the possibility of other ligands was also detected. 2) Mac-1 binding to an unidentified ligand supports homotypic adhesion with an efficiency comparable to LFA-1 at low shear rates of ∼100 s−1. Above 300 s−1, however, Mac-1 and not LFA-1 were the predominant molecules supporting cell adhesion. This is in contrast to neutrophil adhesion to ICAM-1-transfected cells, where LFA-1 binds with a higher avidity than Mac-1 to ICAM-1. 3) Following stimulation, the capacity of LFA-1 to support aggregate formation decreases with time at a rate ∼3-fold faster than that of Mac-1. The results suggest that the relative contributions of β2 integrins and ICAM-3 to neutrophil adhesion is regulated by the magnitude of fluid shear and time of stimulus over a range of blood flow conditions typical of the venular microcirculation.

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“…This technique often results in inaccurate assessments especially in the presence of low CO and tricuspid regurgitation. 35 In our study, therefore, we excluded significant tricuspid regurgitation, and the mean CO determined by catheter was 4.5 L/min.…”

Section: Study Limitationmentioning

confidence: 99%

Isolation of Oligotrophic Denitrifiers Carrying Previously Uncharacterized Functional Gene Sequences

Ishii

Ashida

Otsuka

et al. 2011

Appl Environ Microbiol

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Background-The shape of right ventricular outflow tract (RVOT) has been assumed to be circular. The aim of this study was to assess RVOT morphology using 3-dimensional transesophageal echocardiography (3D TEE). Methods and Results-This prospective study included 114 patients who underwent 3D TEE. Two-dimensional (2D) TEE measured maximum and minimum RVOT diameters (RVOTD max and min) during a cardiac cycle. 3D TEE determined RVOT area (RVOTA) max and min, RVOT fractional area change, and RVOT shape index (RVOTSI; vertical/horizontal RVOTD). Cardiac output (CO) was calculated using 2D TEE, 3D TEE, and a Swan-Ganz catheter in 23 patients. All patients were classified into group 1 (RVOTSI ≤1) or group 2 (RVOTSI >1) based on the RVOT shapes.

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Effect of pulmonary blood flow on the exchange between the circulating and marginating pool of polymorphonuclear leukocytes in dog lungs.

Cited by 89 publications

References 16 publications

Role of Galectin-3 in Leukocyte Recruitment in a Murine Model of Lung Infection by Streptococcus pneumoniae

Role of Galectin-3 in Leukocyte Recruitment in a Murine Model of Lung Infection by Streptococcus pneumoniae

Shear and Time-Dependent Changes in Mac-1, LFA-1, and ICAM-3 Binding Regulate Neutrophil Homotypic Adhesion

Isolation of Oligotrophic Denitrifiers Carrying Previously Uncharacterized Functional Gene Sequences

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