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Infection and Immunity, February 2004, p. 1204-1209, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.1204-1209.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Haemophilus influenzae Porin Induces Toll-Like Receptor 2-Mediated Cytokine Production in Human Monocytes and Mouse Macrophages

Marilena Galdiero,1 Massimiliano Galdiero,1* Emiliana Finamore,2 Fabio Rossano,1 Maria Gambuzza,3 Maria Rosaria Catania,1 Giuseppe Teti,3 Angelina Midiri,3 and Giuseppe Mancuso3

Dipartimento di Medicina Sperimentale, Sezione di Microbiologia e Microbiologia Clinica,1 Dipartimento di Patologia Generale, Facoltà di Medicina e Chirurgia, Seconda Università degli Studi di Napoli, 80138 Naples,2 Dipartimento di Patologia e Microbiologia Sperimentale, Università degli Studi di Messina, 98125 Messina, Italy3

Received 2 July 2003/ Returned for modification 5 August 2003/ Accepted 28 October 2003

The production of proinflammatory cytokines is likely to play a major pathophysiological role in meningitis and other infections caused by Haemophilus influenzae type b (Hib). Previous studies have shown that Hib porin contributes to signaling of the inflammatory cascade. We examined here the role of Toll-like receptors (TLRs) and the TLR-associated adaptor protein MyD88 in Hib porin-induced production of tumor necrosis factor alpha (TNF-{alpha}) and interleukin-6 (IL-6). Hib porin-induced TNF-{alpha} and IL-6 production was virtually eliminated in macrophages from TLR2- or MyD88-deficient mice. In contrast, macrophages from lipopolysaccharide (LPS)-hyporesponsive C3H/HeJ mice, which are defective in TLR4 function, responded normally to Hib porin. Moreover anti-TLR2 antibodies but not anti-TLR4 antibodies significantly reduced Hib porin-stimulated TNF-{alpha} and IL-6 release from the human monocytic cell line THP-1. These data indicate that the TLR2/MyD88 pathway plays an essential role in Hib porin-mediated cytokine production. These findings may be useful in the development of alternative therapies aimed at reducing excessive inflammatory responses during Hib infections.

* Corresponding author. Mailing address: Dipartimento di Medicina Sperimentale, Sezione di Microbiologia e Microbiologia Clinica, Facoltà di Medicina e Chirurgia, Seconda Università di Napoli, Via De Crecchio 7, 80138 Naples, Italy. Phone: 39 081 5667646. Fax: 39 081 5667578. E-mail: massimiliano.galdiero{at}unina2.it.

Editor: F. C. Fang

Infection and Immunity, February 2004, p. 1204-1209, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.1204-1209.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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