Chemokines synergize in the recruitment of circulating neutrophils into inflamed tissue

Struyf, Sofie; Gouwy, Mieke; Dillen, Chris; Opdenakker, Ghislain; Damme, Jozef Van

doi:10.1002/eji.200425753

Cited by 86 publications

(78 citation statements)

References 32 publications

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“…This process leads to the rapid adhesion of neutrophils to the vascular endothelium and the rapid decrease in levels of circulating neutrophils. This decrease in circulating leukocytes is normally due to leukocyte rolling movement along the vessel wall and the subsequent solid adhesion to the endothelial cells and migration into tissues (28). Thus, we investigated the effect of VAMP8 in the recruitment and activation of acute inflammatory leukocytes in vivo in C5a-induced systemic and localized inflammatory models, and showed that, following C5a i.v.…”

Section: Discussionmentioning

confidence: 99%

VAMP8 Is Essential in Anaphylatoxin-Induced Degranulation, TNF-α Secretion, Peritonitis, and Systemic Inflammation

Pushparaj

Tay

Wang

et al. 2009

The Journal of Immunology

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VAMP8, a member of the soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor (SNARE) family of fusion proteins, initially characterized in endosomal and endosomal-lysosomal fusion, may also function in regulated exocytosis. VAMP8 physiological function in inflammation has not been elucidated. In this paper, we show that deficiency of VAMP8 protects mice from anaphylatoxin (C5a)-induced neutropenia, peritonitis, and systemic inflammation. We show that, in vivo, VAMP8 deletion inhibits neutropenia and phagocyte recruitment. We also show that in macrophages, VAMP8 localizes on secretory granules and degranulation is inhibited in VAMP8-deficient macrophages. Moreover, VAMP8−/− mice show reduced systemic inflammation with inhibition of serum TNF-α levels, whereas IL-1β, IL-6, and MIP1α release are not affected. In wild-type macrophages, TNF-α colocalizes with VAMP8-positive vesicles, and in VAMP8-deficient macrophages, the TNF-α release is inhibited. Furthermore, VAMP8 regulates the release of TNF-α and β-hexosaminidase triggered by fMLP, and VAMP8−/− mice are protected from fMLP-induced peritonitis. These data demonstrate that the VAMP8 vesicle-associated-SNARE is required for the proper trafficking of secretory lysosomal granules for exocytosis in macrophages and for the release of the potent proinflammatory cytokine, TNF-α.

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Section: Discussionmentioning

confidence: 99%

VAMP8 Is Essential in Anaphylatoxin-Induced Degranulation, TNF-α Secretion, Peritonitis, and Systemic Inflammation

Pushparaj

Tay

Wang

et al. 2009

The Journal of Immunology

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“…Previous reports have suggested that SDF-1 may participate in the recruitment of neutrophils in arthritis (41)(42)(43)(44) and peritonitis (45). Interestingly, SDF-1 expression has also been implicated in the trafficking of myeloid progenitors during injury and inflammation to the liver (58,59) and the peritoneum (60), suggesting that the same chemokine interactions that maintain neutrophils and their precursors within the marrow (29, 38 -40) may be effective in recruiting these cells to extramedullary sites.…”

Section: Discussionmentioning

confidence: 98%

“…How the CXCR4/ SDF-1 axis might participate in the development of inflammation is poorly understood, but several reports support a role for this pathway in the tissue migration of leukocytes, including neutrophils, in animal models of arthritis (41)(42)(43)(44) and peritonitis (45). A role for SDF-1 in lung inflammation has been suggested by animal models of asthma in which a CXCR4 blockade attenuates both the lymphocyte and eosinophil responses and reduces airway hyperreactivity (46,47).…”

Section: A Cute Lung Injury (Ali)mentioning

confidence: 99%

Pulmonary Stromal-Derived Factor-1 Expression and Effect on Neutrophil Recruitment during Acute Lung Injury

Petty

Sueblinvong

Lenox

et al. 2007

The Journal of Immunology

117

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The severe and protracted inflammation that characterizes acute lung injury (ALI) is driven by the ongoing recruitment of neutrophils to the lung. Although much of the cytokine signaling responsible for the initial phase of ALI has been elaborated, relatively little is known about the mechanisms governing the recruitment of neutrophils from the bone marrow to the lung in the later period of this disease. Given its previously described chemoattractant effects on marrow neutrophils, we investigated whether stromal-derived factor-1 (SDF-1) (CXCL12) might participate in this later phase of recruitment. Using immunohistochemistry to examine both banked human lung specimens from patients with ALI and lungs from mice with LPS-induced pneumonitis, we found that pulmonary SDF-1 expression increases during ALI. We further determined that both lung SDF-1 protein expression and mRNA expression rise in a delayed but sustained pattern in this mouse model and that the major source of the increase in expression appears to be the lung epithelium. Lastly, we found that expression of the SDF-1 receptor CXCR4 rises in a similar temporal pattern on neutrophils in both the blood and airspace of LPS-injured mice and that Ab-mediated SDF-1 blockade significantly attenuates late but not early pulmonary neutrophilia in this model. These results implicate SDF-1 in neutrophil recruitment to the lung in the later period of acute lung injury and suggest a novel role for this cytokine in coordinating the transition from the inflammatory response to the initiation of tissue repair.

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“…35,36 Thus, whether blocking C5a affects the recruitment of neutrophil/macrophages into inflamed colons, thereby dampens inflammatory responses was addressed. Because complement activation represents an early event during TNBS colitis as described above, colon tissues from anti-C5a-treated and control mice were isolated at 4 h, 24 h, and 4 days after colitis induction and neutrophil/macrophage infiltrates were examined.…”

Section: Blockade Of C5a Activity Restrains Infiltration Of Polymorphmentioning

confidence: 99%

Blockade of complement activation product C5a activity using specific antibody attenuates intestinal damage in trinitrobenzene sulfonic acid induced model of colitis

Chen¹,

Yang

Gao

et al. 2011

Laboratory Investigation

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Complement represents a chief component of innate immunity in host defense. However, excessive complement activation has been involved in the pathogenesis of inflammatory diseases. In this study, we investigated the contribution of complement to intestinal pathology of patients and rodents with inflammatory bowel disease. The expression of complement effectors (C3a and C3) was increased remarkably in inflamed colons of IBD patients compared with those of normal counterparts. In accordance with this, the sustained activation of complement in serum and colon (including elevated C3a and C5a levels, enhanced hemolytic activity, downregulated expression of C5a receptors) was observed, following the establishment of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis, which peaked at 24 h. Mice pretreated with neutralizing anti-C5a antibodies (À2, 0, and 2 days after TNBS instillation) had significantly reduced weight loss and improved macroscopic/microscopic scores, comparable to the efficacy of prednisolone treatment. Strikingly, treatment with anti-C5a at 24 h after TNBS instillation showed remarkable therapeutic effects, whereas prednisolone did not. The efficacy of anti-C5a administration was associated with decreased release of proinflammatory chemokines and cytokines, inhibition of infiltration of neutrophils into colons, and enhanced Th2 response. These findings suggest a disease-promoting role of complement, particular C5a, in the pathology of TNBS-induced colitis in mice, indicating possible therapeutic potentials for C5a-specific antibody in IBD. The inflammatory bowel diseases (IBDs) encompassing Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory disorders of gastrointestinal tract, characterized by dysfunction of mucosal T cells, abnormal cytokine production, cellular inflammation, and ultimately damage to the intestinal lining. 1 Although the etiology of IBD remains unknown, there is circumstantial evidence to link IBD to the mucosal immune system's failure to attenuate immunity to endogenous antigen. 1 In recent years, several animal IBD models have been developed. 2,3 Although the relationship of many of these models to human disease is imperfect, the hapten-induced model of colonic inflammation in which 2,4,6-trinitrobenzene sulfonic acid (TNBS) is delivered intrarectally to BALB/c mice displays human CD-like features, notably predominantly IL-12-driving Th1 activity of the mucosal CD4 þ T-cell population and transmural mononuclear inflammation. 3 More recently, a pathogenic role of IL-23, the cytokine sharing p40 subunits with IL-12, has been evidenced in the development of CD. 4 Deficiency of IL-23-specific subunits (p19) leads to failure of colitis induction in a T-cell transfer model. This effect is attributed to suppression of IL-17 production and Th17 differentiation in the colons. 5 The factors that initiate intestinal pathology of CD and elicit Th1/Th17 immune reaction, however, are still

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Chemokines synergize in the recruitment of circulating neutrophils into inflamed tissue

Cited by 86 publications

References 32 publications

VAMP8 Is Essential in Anaphylatoxin-Induced Degranulation, TNF-α Secretion, Peritonitis, and Systemic Inflammation

VAMP8 Is Essential in Anaphylatoxin-Induced Degranulation, TNF-α Secretion, Peritonitis, and Systemic Inflammation

Pulmonary Stromal-Derived Factor-1 Expression and Effect on Neutrophil Recruitment during Acute Lung Injury

Blockade of complement activation product C5a activity using specific antibody attenuates intestinal damage in trinitrobenzene sulfonic acid induced model of colitis

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