Tumour necrosis factor‐alpha and leukotriene B<sub>4</sub> mediate the neutrophil migration in immune inflammation

Canetti, Cláudio; Silva, João; Ferreira, Sérgio Henrique; Cunha, Fernando de Queiróz

doi:10.1038/sj.bjp.0704403

Cited by 82 publications

(130 citation statements)

References 37 publications

(37 reference statements)

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“…The release of TNF-a in this model is dependent on antigen presentation and MIP-1a production. TNF-a, in turn, promoted neutrophil recruitment through an LTB 4 -dependent mechanism [47]. In the present study we describe, for the first time, the finding that SGE inhibits neutrophil recruitment in a Th1-type immune response.…”

Section: Discussionsupporting

confidence: 55%

“…Effects of SGE on leukocyte migration induced by OVA in immunized mice As previously shown [47], compared with naive or CFAinjected animals, i.p. administration of OVA (10 lg/ cavity) in immunized mice induced significant neutrophil migration at 4 h after challenge (Fig.…”

Section: Resultsmentioning

confidence: 56%

“…Since OVA-induced neutrophil migration in immunized mice depends on TNF-a released by CD4 + T lymphocytes, which acts through an LTB 4 -dependent mechanism [47], we next analyzed the effect of SGE on TNF-a and LTB 4 production in OVA-immunized mice. The release of IL-1b, which is also a neutrophil chemotactic mediator, was also investigated.…”

Section: Productionmentioning

confidence: 99%

“…Meanwhile, the release of anti-inflammatory mediators, including IL-10, IL-4 and lipoxin down-modulates the neutrophil recruitment [45,46]. Recently, our group demonstrated that neutrophil migration during an immune peritonitis in mice induced by ovalbumin (OVA) requires CD4 + T cell-derived TNF-a, which promotes neutrophil recruitment through an LTB 4 -dependent mechanism [47]. Furthermore, the release of TNF-a by CD4 + T cells is dependent on MIP-1a release [48].…”

Section: Introductionmentioning

confidence: 99%

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Effect of salivary gland extract ofLeishmania vector,Lutzomyia longipalpis, on leukocyte migration in OVA-induced immune peritonitis

Monteiro¹,

Nogueira²,

Souza³

et al. 2005

Eur. J. Immunol.

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Salivary gland extracts (SGE) from Lutzomyia longipalpis potentate L. major infection by inducing a Th2 immune response. However, the effect of SGE on the effector phase of immune response is not known. Herein, we demonstrate that SGE inhibited neutrophil migration in ovalbumin (OVA)-induced peritonitis in immunized mice. SGE pretreatment of mice inhibited OVA-induced CD4 + and CD8 + T lymphocyte migration. The OVA-induced production of TNF-a, IL-1b and leukotriene B4 (LTB 4 ), neutrophil chemotactic mediators in this model, were inhibited by SGE. On the other hand, SGE enhanced production of IL-10 and IL-4. In naive mice, SGE also blocked LTB 4 -induced neutrophil migration, but not that induced fMLP. Moreover, co-incubation of LTB 4 (but not fMLP, TNF-a and MIP-1a) with SGE inhibited the ability of LTB 4 to induce neutrophil migration in vivo and in vitro. Altogether, the results suggest that SGE has anti-inflammatory properties that are associated with inhibition of TNF-a and LTB 4 production and/or with the neutrophil chemotactic activity of LTB 4 . The effectiveness of SGE in inhibiting neutrophil migration and inflammatory mediators release in a Th1 immune inflammatory response model reinforces the need for isolation of the compounds responsible for these activities, which could be used as prototypes for the development new anti-inflammatory drugs. IntroductionParticipation of vector saliva in disease transmission has long been recognized. Saliva inoculated during blood feeding modulates the immune response allowing the infection to become established [1][2][3]. On the other hand, anti-vector saliva immunity may protect the host against some vector-borne diseases [4][5][6][7]. In leishmaniasis, there is evidence that the saliva of the vectors Lutzomyia and Phlebotomus contains substances with immunosuppressor, vasodilatator, anti-platelet and anticlotting activities [8][9][10][11][12][13]. In addition to increasing the hemorrhagic pool where sand flies feed [8,14], salivary components also induce host immunosuppression, which is fundamental for the establishment of Leishmania infection [10,[15][16][17][18][19] production and antigen presentation by infected macrophages [20][21][22]. Furthermore, they inhibit Th1 induction, enhancing the Th2-type response with an increase of IL-4 and IL-10 in the infection [23][24][25]. A predominance of the Th1 response has been reported in several inflammatory diseases, including rheumatoid arthritis, Crohn's disease, glomerulonephritis, and immune vasculitis [26][27][28][29]. The participation of neutrophils in the pathogenesis of tissue lesions in these diseases has long been recognized [30][31][32][33]. These cells are important sources of substances that promote tissue damage, such as reactive oxygen and nitrogen species, lysosomal enzymes and metalloproteases [34,35]. Indeed, the efficacy of the so-called disease modifying anti-inflammatory drugs in several inflammatory diseases, such as rheumatoid arthritis is usually associated with their ability to decrease neutro...

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Section: Discussionsupporting

confidence: 55%

Section: Resultsmentioning

confidence: 56%

Section: Productionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effect of salivary gland extract ofLeishmania vector,Lutzomyia longipalpis, on leukocyte migration in OVA-induced immune peritonitis

Monteiro¹,

Nogueira²,

Souza³

et al. 2005

Eur. J. Immunol.

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“…LTB 4 is an arachidonic acid metabolite synthesized via the 5-lipoxygenase pathway [10]. LTB 4 is a potent PMN chemoattractant and stimulates PMN to release elastase and generate superoxide radicals [5,36,47]. The role of LTB 4 in promoting self-perpetuating inflammatory injury at various mucosal surfaces is well established [17,19,41].…”

Section: In Pmnmentioning

confidence: 99%

Tilmicosin-induced bovine neutrophil apoptosis is cell-specific and downregulates spontaneous LTB4 synthesis without increasing Fas expression

et al. 2004

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-The pathology of bacterial pneumonia, such as seen in the bovine lung infected with Mannheimia haemolytica, is due to pathogen virulence factors and to inflammation initiated by the host. Tilmicosin is a macrolide effective in treating bacterial pneumonia and recent findings suggest that this antibiotic may provide anti-inflammatory benefits by inducing polymorphonuclear neutrophilic leukocyte (PMN) apoptosis. Using an in vitro bovine system, we examined the cellspecificity of tilmicosin, characterized the changes in spontaneous leukotriene B 4 (LTB 4 ) synthesis by PMN exposed to the macrolide, and assessed its effects on PMN Fas expression. Previous findings demonstrated that tilmicosin is able to induce PMN apoptosis. These results were confirmed in this study by the Annexin-V staining of externalized phosphatidylserine and the analysis with flow cytometry. The cell-specificity of tilmicosin was assessed by quantification of apoptosis in bovine PMN, mononuclear leukocytes, monocyte-derived macrophages, endothelial cells, epithelial cells, and fibroblasts cultured with the macrolide. The effect of tilmicosin on spontaneous LTB 4 production by PMN was evaluated via an enzyme-linked immunosorbent assay. Finally, the mechanisms of tilmicosin-induced PMN apoptosis were examined by assessing the effects of tilmicosin on surface Fas expression on PMN. Tilmicosin-induced apoptosis was found to be at least partially cell-specific, as PMN were the only cell type tested to die via apoptosis in response to incubation with tilmicosin. PMN incubated with tilmicosin under conditions that induce apoptosis spontaneously produced less LTB 4 , but did not exhibit altered Fas expression. In conclusion, tilmicosin-induced apoptosis is specific to PMN, inhibits spontaneous LTB 4 production, and occurs through a pathway independent of Fas upregulation. macrolide / neutrophil / apoptosis / pasteurellosis / inflammation

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Neutrophil recruitment in immunized mice depends on MIP‐2 inducing the sequential release of MIP‐1α, TNF‐α and LTB₄

et al. 2006

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Neutrophils are thought to play an important role in the tissue damage observed in various autoimmune diseases. Chemokines, cytokines and leukotrienes have recognized roles in the orchestration of neutrophil migration. We have recently shown that antigeninduced neutrophil migration into the peritoneum of immunized mice is mediated by macrophage-inflammatory protein (MIP)-1a which interacts with CCR1 and induces the sequential release of TNF-a and leukotriene B 4 (LTB 4 ). The present study investigates the role of MIP-2 and CXCR2 in the cascade of events leading to mediator generation and neutrophil influx. Antigen challenge of immunized mice induced the expression of CXCR2 and the production of KC and MIP-2 proteins. Antigen-induced neutrophil migration was inhibited by a CXCR2 receptor antagonist (repertaxin) or an anti-MIP-2 antibody, but not by an anti-KC antibody. Administration of MIP-2 promoted a dose-dependent neutrophil migration in naive mice which was inhibited by repertaxin, anti-TNF-a, anti-MIP-1a antibodies or by MK886 (leukotriene synthesis inhibitor). MIP-2 administration induced the release of MIP-1a, TNF-a and LTB 4 , and the release of the latter two was inhibited by anti-MIP-1a antibody treatment. Our studies highlight the intricate balance between mediator production and action during an immune-mediated inflammatory response and suggest a mediator cascade leading to neutrophil influx following antigen challenge of immunized mice: MIP-2 ? MIP-1a ? TNF-a ? LTB 4 .

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Tumour necrosis factor‐alpha and leukotriene B₄ mediate the neutrophil migration in immune inflammation

Cited by 82 publications

References 37 publications

Effect of salivary gland extract ofLeishmania vector,Lutzomyia longipalpis, on leukocyte migration in OVA-induced immune peritonitis

Effect of salivary gland extract ofLeishmania vector,Lutzomyia longipalpis, on leukocyte migration in OVA-induced immune peritonitis

Tilmicosin-induced bovine neutrophil apoptosis is cell-specific and downregulates spontaneous LTB4 synthesis without increasing Fas expression

Neutrophil recruitment in immunized mice depends on MIP‐2 inducing the sequential release of MIP‐1α, TNF‐α and LTB₄

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Tumour necrosis factor‐alpha and leukotriene B4 mediate the neutrophil migration in immune inflammation

Cited by 82 publications

References 37 publications

Effect of salivary gland extract ofLeishmania vector,Lutzomyia longipalpis, on leukocyte migration in OVA-induced immune peritonitis

Effect of salivary gland extract ofLeishmania vector,Lutzomyia longipalpis, on leukocyte migration in OVA-induced immune peritonitis

Tilmicosin-induced bovine neutrophil apoptosis is cell-specific and downregulates spontaneous LTB4 synthesis without increasing Fas expression

Neutrophil recruitment in immunized mice depends on MIP‐2 inducing the sequential release of MIP‐1α, TNF‐α and LTB4

Contact Info

Product

Resources

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Tumour necrosis factor‐alpha and leukotriene B₄ mediate the neutrophil migration in immune inflammation

Neutrophil recruitment in immunized mice depends on MIP‐2 inducing the sequential release of MIP‐1α, TNF‐α and LTB₄