Combinatorial requirements for adhesion molecules in mediating neutrophil emigration during bacterial peritonitis in mice

Mizgerd, Joseph P.; Quinlan, William M.; LeBlanc, Brian W.; Kutkoski, Gregory J.; Bullard, Daniel C.; Beaudet, Arthur L.; Doerschuk, Claire M.

doi:10.1002/jlb.64.3.291

Cited by 31 publications

(26 citation statements)

References 30 publications

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“…It has been reported that neutrophil emigration into the inflamed peritoneal cavity of galectin-3 null mice is reduced at late stages of inflammation, at which point inflammatory macrophages, which could release galectin-3, begin to be recruited (49,76). Interestingly, several reports suggest that during late stages of peritonitis or during pathogen-induced peritonitis, neutrophil recruitment into the inflamed peritoneal cavity is ␤ 2 -integrin-independent (11,77,78). In addition, it is suggested that the induction of the ␤ 2 -integrin-independent emigration of neutrophils mostly depends on the presence of macrophages (79).…”

Section: Discussionmentioning

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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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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Section: Discussionmentioning

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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“…Increased adhesion of leukocytes to endothelial cells through LFA-1/ICAM-1 binding is needed for the activation of immune function and responsible for the progression of inflammation (17,36,37). Selective inhibition of LFA-1 function, and consequently, of immune function and inflammation, can be achieved using a mAb against LFA-1, or a synthetic small molecule derived from compounds mimicking ICAM-1 (18, 38 -40).…”

Section: Discussionmentioning

confidence: 99%

Spermine, a Natural Polyamine, Suppresses LFA-1 Expression on Human Lymphocyte

Soda¹,

Kano²,

Nakamura³

et al. 2005

The Journal of Immunology

113

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Natural polyamines, spermine, spermidine, and putrescine, play a pivotal role in the regulation of gene expression; therefore, the age-dependent decreases and the disease-dependent increases in polyamine synthesis suggest a possible contribution of polyamines to the age-related and disease-associated changes in cellular function. In this study, we examined the effects of polyamines on the cellular function and the expression of adhesion molecules on human PBMCs from healthy volunteers. Flow cytometry revealed that PBMCs cultured with spermine decreased mean fluorescent intensities (MFIs) of CD11a and CD18 in the lymphocyte light-scattered region, but not in the monocyte region. This suppression was observed in a dose- and time-dependent manner and found nonspecifically on all cell subsets we tested (CD3+, CD4+, CD8+, CD19+, CD45RA+, CD45RO+, CD4+CD45RA+, CD4+CD45RO+, CD8+CD45RA+, CD8+CD45RO+). The decreases of CD11a and CD18 MFIs were accompanied by the decrease in adherent capacity of PBMCs to HUVECs. Spermine did not hinder cell activities or cell viability. Among 42 healthy volunteers (mean, 49.5 years old; from 26 to 69), blood spermine levels inversely correlated with the CD11a MFIs of cells in the lymphocyte region (r = −0.48; p = 0.001), but not with those in the monocyte region. The effects of spermidine seemed weaker than those of spermine, and blood spermidine levels had no correlation with CD11a MFIs of the lymphocyte region. Putrescine had no effect on the expressions of membrane molecules. Polyamines, especially spermine, decrease LFA-1 (CD11a/CD18) expression on human lymphocyte and adhesion capacity of PBMCs to HUVECs.

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“…[1][2][3][4][5][6][7] Mice deficient in multiple leukocyte adhesion molecules, including CD18 integrins; E-and P-selectin; Eand P-selectin and ICAM-1; E-, P-, and L-selectin; E-, P-, and L-selectin and ICAM-1; CD18 and E-selectin; and CD18 and P-selectin show more severe neutrophilia. 3,[8][9][10][11][12][13][14] A few adhesion molecule-deficient mice, including mice lacking Mac-1, Eselectin, or both E-and L-selectin, have normal circulating neutrophil concentrations. 2,3,15 Although the existence of physiologic mechanisms controlling peripheral neutrophil counts has been proposed as early as 1991, 16 the reason for elevated neutrophil counts in adhesion molecule knockout mice is not known.…”

Section: Introductionmentioning

confidence: 99%

Increased granulopoiesis through interleukin-17 and granulocyte colony-stimulating factor in leukocyte adhesion molecule–deficient mice

Forlow

Schurr

Kolls

et al. 2001

Blood

174

164

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Many mutant mice deficient in leukocyte adhesion molecules display altered hematopoiesis and neutrophilia. This study investigated whether peripheral blood neutrophil concentrations in these mice are elevated as a result of accumulation of neutrophils in the circulation or altered hematopoiesis mediated by a disrupted regulatory feedback loop. Chimeric mice were generated by transplanting various ratios of CD18 ؉/؉ and CD18 ؊/؊ unfractionated bone marrow cells into lethally irradiated wild-type mice, resulting in approximately 0%, 10%, 50%, 90%, or 100% CD18 null neutrophils in the blood. The presence of only 10% CD18 ؉/؉ neutrophils was sufficient to prevent the severe neutrophilia seen in mice reconstituted with CD18 ؊/؊ bone marrow cells. These data show that the neutrophilia in CD18 ؊/؊ mice is not caused by enhanced neutrophil survival or the inability of neutrophils to leave the vascular compartment. In CD18 ؊/؊ , CD18 ؊/؊ E ؊/؊ , CD18 ؊/؊ P ؊/؊ , EP ؊/؊ , and EPI ؊/؊ mice, levels of granulocyte colony-stimulating factor (G-CSF) and interleukin-17 (IL-17) were elevated in proportion to the neutrophilia seen in these mice, regardless of the underlying mutation. Antibiotic treatment or the propensity to develop skin lesions did not correlate with neutrophil counts. Blocking IL-17 or G-CSF function in vivo significantly reduced neutrophil counts in severely neutrophilic mice by approximately 50% (P < .05) or 70% (P < .01), respectively. These data show that peripheral blood neutrophil numbers are regulated by a feedback loop involving G-CSF and IL-17 and that this feedback loop is disrupted when neutrophils cannot migrate into peripheral tissues. IntroductionAdhesion molecule-deficient mice have provided valuable information in elucidating leukocyte recruitment mechanisms. Many of the mice deficient in leukocyte adhesion molecules display secondary phenotypes, including altered hematopoiesis and neutrophilia, which have not been fully investigated. Mice lacking P-selectin, leukocyte function-associated antigen-1, intercellular adhesion molecule-1 (ICAM-1), core-2 glucosaminyltransferase, P-and L-selectin, P-selectin and ICAM-1, or L-selectin and ICAM-1 are mildly neutrophilic. [1][2][3][4][5][6][7] Mice deficient in multiple leukocyte adhesion molecules, including CD18 integrins; E-and P-selectin; Eand P-selectin and ICAM-1; E-, P-, and L-selectin; E-, P-, and L-selectin and ICAM-1; CD18 and E-selectin; and CD18 and P-selectin show more severe neutrophilia. 3,[8][9][10][11][12][13][14] A few adhesion molecule-deficient mice, including mice lacking Mac-1, Eselectin, or both E-and L-selectin, have normal circulating neutrophil concentrations. 2,3,15 Although the existence of physiologic mechanisms controlling peripheral neutrophil counts has been proposed as early as 1991, 16 the reason for elevated neutrophil counts in adhesion molecule knockout mice is not known. One candidate mechanism for neutrophilia is passive accumulation of circulating neutrophils because of altered neutrophil survival. Although mice l...

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Combinatorial requirements for adhesion molecules in mediating neutrophil emigration during bacterial peritonitis in mice

Cited by 31 publications

References 30 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

Spermine, a Natural Polyamine, Suppresses LFA-1 Expression on Human Lymphocyte

Increased granulopoiesis through interleukin-17 and granulocyte colony-stimulating factor in leukocyte adhesion molecule–deficient mice

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