Important role of CD18 in TNF- α -induced leukocyte adhesion in muscle and skin venules in vivo

Zhang, X W; Schramm, René; Liu, Qing; Ekberg, Henrik; Jeppsson, Bengt; Thorlacius, Henrik

doi:10.1007/s000110050627

Cited by 12 publications

(10 citation statements)

References 30 publications

(21 reference statements)

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“…Mori et al (35) reported that, in skin wounds, the TNF-␣ receptor p55 induces the expression of leukocyte adhesion molecules (E-selectin, ICAM-1, and vascular cellular adhesion molecule-1) and the release of chemokines [macrophage inflammatory protein-2 (MIP-2) and MCP-1] for neutrophils and monocytes. Furthermore, local injection of TNF-␣ into skeletal muscle induces rolling (23,46), adhesion (45,46), and extravasation (47) of leukocytes (predominately neutrophils) in cremaster muscle arterioles and venules. Zhang et al (47) reported that the extravasation of neutrophils from cremaster venules after local injection of TNF-␣ was dependent on two mouse neutrophil chemoattractants, cytokine-induced neutrophil chemoattractant (KC) and MIP-2.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α promotes the accumulation of neutrophils and macrophages in skeletal muscle

Peterson¹,

Feeback²,

Baas³

et al. 2006

Journal of Applied Physiology

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α promotes the accumulation of neutrophils and macrophages in skeletal muscle

Peterson¹,

Feeback²,

Baas³

et al. 2006

Journal of Applied Physiology

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“…Cell surface antigen immunostaining was performed as previously described (55). Leukocytes from peripheral blood of both wild-type and iNOS Ϫ/Ϫ mice subjected to CLP and from wild-type mice subjected to L-CLP and treated with AG (30 mg kg Ϫ1 , 30 min before surgery) were blocked with 10% normal goat serum for 20 min at 4°C and then stained with monoclonal antibody for 30 min at 4°C (anti-CD62L and anti-CD18).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Leukocyte Rolling by Nitric Oxide during Sepsis Leads to Reduced Migration of Active Microbicidal Neutrophils

et al. 2002

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We developed two models of sepsis with different degrees of severity, sublethal and lethal sepsis, induced by cecal ligation and puncture. Lethal sepsis induced by cecal ligation and puncture (L-CLP) resulted in failure of neutrophil migration to the infection site and high mortality. Treatment of septic animals with aminoguanidine (AG), a nitric oxide (NO) synthase inhibitor, precluded the failure of neutrophil migration and protected the animals from death. However, cytokine-induced NO synthase (iNOS)-deficient (iNOS ؊/؊ ) mice subjected to L-CLP did not present neutrophil migration failure, but 100% lethality occurred. iNOS ؊/؊ mice subjected to sublethal sepsis induced by cecal ligation and puncture (SL-CLP) also suffered high mortality despite the occurrence of neutrophil migration. This apparent paradox could be explained by the lack of microbicidal activity in neutrophils of iNOS ؊/؊ mice present at the infection site due to their inability to produce NO. Notably, SL-and L-CLP iNOS ؊/؊ mice showed high bacterial numbers in exudates. The inhibition of neutrophil migration by NO is due to inhibition of a neutrophil/endothelium adhesion mechanism, since a reduction in leukocyte rolling, adhesion, and emigration was observed in L-CLP wild-type mice. These responses were prevented by AG treatment and were not observed in the iNOS ؊/؊ L-CLP group. There was no significant change in L-selectin expression in neutrophils from L-CLP mice. Thus, it seems that the decrease in leukocyte rolling is due to a defect in the expression of adhesion molecules on endothelial surfaces mediated by iNOS-derived NO. In conclusion, the results indicate that despite the importance of NO in neutrophil microbicidal activity, its generation in severe sepsis reduces neutrophil migration by inhibiting leukocyte rolling and their firm adhesion to the endothelium, in effect impairing the migration of leukocytes and consequently their fundamental role in host cell defense mechanisms.

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“…The absence of neutrophil accumulation in CD18−/− mice after lengthening contractions is consistent with the established role of CD18 in the diapedesis of neutrophils into a variety of injured and/or inflamed tissues including skeletal muscle. Specifically, previous investigators have reported that neutrophil accumulation in skeletal muscle after treatment with TNF-α or during the reperfusion of ischaemic muscle is dependent on CD18 (Palazzo et al 1998;Zhang et al 2000). Frenette et al (2003) has recently reported P-and E-selectins, which cause rolling Post-lengthening contractions A, percentage of myofibres expressing eMHC.…”

Section: Post-lengthening Contractionsmentioning

confidence: 99%

Neutrophils contribute to muscle injury and impair its resolution after lengthening contractions in mice

Pizza

Peterson

Baas

et al. 2005

The Journal of Physiology

200

199

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We tested the hypotheses that: (1) neutrophil accumulation after contraction-induced muscle injury is dependent on the β 2 integrin CD18, (2) neutrophils contribute to muscle injury and oxidative damage after contraction-induced muscle injury, and (3) neutrophils aid the resolution of contraction-induced muscle injury. These hypotheses were tested by exposing extensor digitorum longus (EDL) muscles of mice deficient in CD18 (CD18 −/− ; Itgb2 tm1Bay) and of wild type mice (C57BL/6) to in situ lengthening contractions and by quantifying markers of muscle inflammation, injury, oxidative damage and regeneration/repair. Neutrophil concentrations were significantly elevated in wild type mice at 6 h and 3 days post-lengthening contractions; however, neutrophils remained at control levels at these time points in CD18−/− mice. These data indicate that CD18 is required for neutrophil accumulation after contraction-induced muscle injury. Histological and functional (isometric force deficit) signs of muscle injury and total carbonyl content, a marker of oxidative damage, were significantly higher in wild type relative to CD18−/− mice 3 days after lengthening contractions. These data show that neutrophils exacerbate contraction-induced muscle injury. After statistically controlling for differences in the force deficit at 3 days, wild type mice also demonstrated a higher force deficit at 7 days, a lower percentage of myofibres expressing embryonic myosin heavy chain at 3 and 7 days, and a smaller cross sectional area of central nucleated myofibres at 14 days relative to CD18−/− mice. These observations suggest that neutrophils impair the restoration of muscle structure and function after injury. In conclusion, neutrophil accumulation after contraction-induced muscle injury is dependent on CD18. Furthermore, neutrophils appear to contribute to muscle injury and impair some of the events associated with the resolution of contraction-induced muscle injury.

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Important role of CD18 in TNF- α -induced leukocyte adhesion in muscle and skin venules in vivo

Cited by 12 publications

References 30 publications

Tumor necrosis factor-α promotes the accumulation of neutrophils and macrophages in skeletal muscle

Tumor necrosis factor-α promotes the accumulation of neutrophils and macrophages in skeletal muscle

Inhibition of Leukocyte Rolling by Nitric Oxide during Sepsis Leads to Reduced Migration of Active Microbicidal Neutrophils

Neutrophils contribute to muscle injury and impair its resolution after lengthening contractions in mice

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