The anti mac-1 monoclonal antibody inhibits neutrophil sequestration in lung and liver in a septic murine model

Morisaki, T.; Goya, Tadanobu; Toh, Hiroto; Nishihara, Kazuyoshi; Torisu, Motomichi

doi:10.1016/s0090-1229(05)80008-x

Cited by 42 publications

(26 citation statements)

References 16 publications

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“…In vitro studies showed that either anti-CD11a or anti-CD11b mAbs reduced PMN adhesion to endothelial cells by ‫ف‬ 50%, whereas these mAbs in combination or mAbs directed against the common ␤ subunit (CD18) fully prevented the PMN adhesion response (5,32). Infusion of anti-CD18 mAbs also inhibited lung PMN sequestration in animal models (5,16). However, the specific function of ␤ 2 integrin family members is unclear since mice made genetically deficient in CD11b did not show reduced PMN emigration across the endothelial barrier (11,19).…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown protective effects of both anti-CD11/ CD18 and anti-ICAM-1 mAbs in models of acute lung injury (including that induced by septicemia) (5,16,17). Protection in these models has been universally attributed to inhibition of PMN sequestration in the lungs (5,16,17).…”

Section: Introductionmentioning

confidence: 99%

“…Protection in these models has been universally attributed to inhibition of PMN sequestration in the lungs (5,16,17). However, the results using mAbs have not always agreed with experiments in mice made genetically deficient in adhesion molecules (5,(18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

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In vivo expression of neutrophil inhibitory factor via gene transfer prevents lipopolysaccharide-induced lung neutrophil infiltration and injury by a beta2 integrin-dependent mechanism.

Zhou

Bergenfeldt

et al. 1998

J. Clin. Invest.

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Abstract. Expression of a control protein, chloramphenicol acetyltransferase (CAT), by the same strategy, had no effect on these responses. In vitro studies showed that NIF prevented mouse PMN adhesion consistent with the inhibition of lung uptake after LPS challenge in NIF transgene-expressing mice. We conclude that pulmonary vascular expression of NIF, a specific ␤ 2 integrinbinding protein, is a potentially useful gene transfer strategy in modulating the infiltration of PMN across the alveolarcapillary epithelial barrier and in preventing lung vascular endothelial injury. (

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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In vivo expression of neutrophil inhibitory factor via gene transfer prevents lipopolysaccharide-induced lung neutrophil infiltration and injury by a beta2 integrin-dependent mechanism.

Zhou

Bergenfeldt

et al. 1998

J. Clin. Invest.

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“…A consistent PMN response in human and animal models of endotoxemia is loss of L-selectin and the expression of CD11b/CD18 integrin (Mac-1) [11,[28][29][30][31]. These early changes in PMN adhesive protein expression are associated temporally with vascular sequestration, and antibody studies provide evidence both for and against the involvement of CD18 integrins in pulmonary and hepatic leukostasis [32][33][34]. Extensive work performed in rabbits suggests that prolonged pulmonary PMN localization during inflammation is dependent on CD18, whereas the early sequestration (1-4 min) may be due to CD18-independent changes in cytosolic calcium, cytoskeletal derangement, and increased PMN stiffness [35,36].…”

Section: Vascular Sequestration and Adhesionmentioning

confidence: 99%

Neutrophil migration during endotoxemia

Wagner

Roth

1999

Journal of Leukocyte Biology

176

125

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Endotoxemia is marked by a global activation of inflammatory responses, which can lead to shock, multiple organ failure, and the suppression of immune and wound healing processes. Neutrophils (PMNs) play a central role in some of these responses by accumulating in tissues and releasing reactive oxygen species and proteases that injure host structures. This review focuses on altered PMN migratory responses that occur during endotoxemia and their consequences in the development of pulmonary infection. The inflammatory mediators that might be responsible for these altered responses are discussed. The oxidant potential of PMNs is increased after exposure to endotoxin both in vitro and during clinical and experimental endotoxemia. However, other functions such as chemotaxis and phagocytosis are often depressed in these same cells. Endotoxin exposure renders PMNs hyperadhesive to endothelium. The sum of these effects produces activated inflammatory cells that are incapable of leaving the vasculature. As such, the endotoxic PMN is more likely to promote tissue injury from within microvascular beds than to clear pathogens from extravascular sites. Moreover, the functional characteristics of endotoxic PMNs are similar to those observed during trauma, burn injury, sepsis, surgery, and other inflammatory conditions. Accordingly, several clinical conditions might have a common effector in the activated, yet migratorially dysfunctional, PMN. Direct effects of endotoxin on PMNs as well as effects of endogenous mediators released during endotoxemia are discussed. Understanding PMN behavior during endotoxemia may provide basic and critical insights that can be applied to a number of inflammatory scenarios. J. Leukoc. Biol. 66: 10-24; 1999.

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“…In contrast, a rapid accumulation of inflammatory cells, consisting mostly of neutrophils, occurred in lungs and livers after i.p. injection of lipopolysaccharide (LPS), as previously reported by Morisaki et al [18]. LPS is a potent activator of macrophages and induces the production of neutrophil chemotactic factors, such as IL-8, in a non-specific manner [19][20][21].…”

Section: Discussionmentioning

confidence: 99%

CD4+ T cell-mediated fatal hyperinflammatory reactions in mice infected with Penicillium marneffei

Kudeken

Kawakami

Saitô

1997

Clinical and Experimental Immunology

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SUMMARYIn the present study, we demonstrate that all mice survived when a low dose of Penicillium marneffei was instilled intratracheally, while severe infection induced by instillation of 1 × 10 8 and 1 × 10 7 colony-forming units (CFU) killed all and 50% of mice, respectively, within 14 days, although the number of live microorganisms in the lungs of these animals was found to decrease with time. The cellular inflammatory responses in the lungs were much more striking in mice with severe infection than in animals infected with a low dose of microorganisms. The number of leucocytes, macrophages, neutrophils and lymphocytes in the lungs increased progressively during infection, and were more than 50 times higher on day 11 than in the control count. CD4 þ T cells were the predominant cells in the lungs, and played an important role in hyperinflammatory host reactions, because neutralizing anti-CD4 MoAb increased the survival rate in infected mice despite the presence of a high number of live microorganisms in the lungs. Our results indicate that severe infection with P. marneffei induces fatal hyperinflammatory host reactions, mediated to a large extent by CD4 þ T cells, although the infection is well controlled. However, the contribution of endogenous tumour necrosis factor-alpha (TNF-a) remains unsubstantiated, since administration of neutralizing anti-TNF-a MoAb in the present study failed to prolong survival in infected mice.

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The anti mac-1 monoclonal antibody inhibits neutrophil sequestration in lung and liver in a septic murine model

Cited by 42 publications

References 16 publications

In vivo expression of neutrophil inhibitory factor via gene transfer prevents lipopolysaccharide-induced lung neutrophil infiltration and injury by a beta2 integrin-dependent mechanism.

In vivo expression of neutrophil inhibitory factor via gene transfer prevents lipopolysaccharide-induced lung neutrophil infiltration and injury by a beta2 integrin-dependent mechanism.

Neutrophil migration during endotoxemia

CD4+ T cell-mediated fatal hyperinflammatory reactions in mice infected with Penicillium marneffei

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