Gene Expression and Production of Tumor Necrosis Factor Alpha, Interleukin-1beta  (IL-1beta ), IL-8, Macrophage Inflammatory Protein 1alpha  (MIP-1alpha ), MIP-1beta , and Gamma Interferon-Inducible Protein 10 by Human Neutrophils Stimulated with Group B Meningococcal Outer Membrane Vesicles

doi:10.1128/IAI.68.12.6917-6923.2000

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Infection and Immunity, December 2000, p. 6917-6923, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Gene Expression and Production of Tumor Necrosis Factor Alpha, Interleukin-1 $beta$ (IL-1 $beta$ ), IL-8, Macrophage Inflammatory Protein 1 $alpha$ (MIP-1 $alpha$ ), MIP-1 $beta$ , and Gamma Interferon-Inducible Protein 10 by Human Neutrophils Stimulated with Group B Meningococcal Outer Membrane Vesicles

José A. Lapinet,¹^,² Patrizia Scapini,¹ Federica Calzetti,¹ Oliver Pérez,² and Marco A. Cassatella¹^,^*

Department of Pathology, Section of General Pathology, University of Verona, 37134 Verona, Italy,¹ and Finlay Institute, 11600, Havana, Cuba²

Received 26 July 2000/Accepted 8 September 2000

Accumulation of polymorphonuclear neutrophils (PMN) into the subarachnoidal space is one of the hallmarks of Neisseria meningitidisinfection. In this study, we evaluated the ability of outer membranevesicles (OMV) from N. meningitidis B to stimulate cytokine productionby neutrophils. We found that PMN stimulated in vitro by OMV produceproinflammatory cytokines and chemokines including tumor necrosisfactor alpha (TNF- $alpha$ ), interleukin-1 $beta$ (IL-1 $beta$ ), IL-8, macrophageinflammatory protein 1 $alpha$ (MIP-1 $alpha$ ), and MIP-1 $beta$ . A considerable inductionof gamma interferon (IFN- $gamma$ )-inducible protein 10 (IP-10) mRNAtranscripts, as well as extracellular IP-10 release, was alsoobserved when neutrophils were stimulated by OMV in combinationwith IFN- $gamma$ . Furthermore, PMN stimulated by OMV in the presenceof IFN- $gamma$ demonstrated an enhanced capacity to release TNF- $alpha$ , IL-1 $beta$ ,IL-8, and MIP-1 $beta$ compared to stimulation with OMV alone. In linewith its downregulatory effects on neutrophil-derived proinflammatorycytokines, IL-10 potently inhibited TNF- $alpha$ , IL-1 $beta$ , IL-8, and MIP-1 $beta$ production triggered by OMV. Finally, a neutralizing anti-TNF- $alpha$ monoclonal antibody (MAb) did not influence the release of IL-8and MIP-1 $beta$ induced by OMV, therefore excluding a role for endogenousTNF- $alpha$ in mediating the induction of chemokine release by OMV.In contrast, the ability of lipopolysaccharide from N. meningitidisB to induce the production of IL-8 and MIP-1 $beta$ was significantlyinhibited by anti-TNF- $alpha$ MAb. Our results establish that, in responseto OMV, neutrophils produce a proinflammatory profile of cytokinesand chemokines which may not only play a role in the pathogenesisof meningitis but may also contribute to the development of protectiveimmunity to serogroup Bmeningococci.

^* Corresponding author. Mailing address: Department of Pathology, Section of General Pathology, Strada Le Grazie 4, I-37134Verona, Italy. Phone: 39-045-8027130. Fax: 39-045-8027127. E-mail:MCNCSS{at}borgoroma.univr.it.

Infection and Immunity, December 2000, p. 6917-6923, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

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Gene Expression and Production of Tumor Necrosis Factor Alpha, Interleukin-1 (IL-1), IL-8, Macrophage Inflammatory Protein 1 (MIP-1), MIP-1, and Gamma Interferon-Inducible Protein 10 by Human Neutrophils Stimulated with Group B Meningococcal Outer Membrane Vesicles