Haemophilus influenzae Porin Induces Toll-Like Receptor 2-Mediated Cytokine Production in Human Monocytes and Mouse Macrophages
Authors: Emiliana Finamore
Fabio Rossano
Marilena Galdiero
Giuseppe Teti
Maria Rosaria Catania
Giuseppe Mancuso
Massimiliano Galdiero
Angelina Midiri
Maria Gambuzza
Journal: Infection and Immunity (2004)
Discipline: IMMUNOLOGY
Keywords: proinflammatory cytokines; Haemophilus influenzae type b; Hib porin; Toll-like receptors; TLR-associated adaptor protein MyD88
Affiliations: Dipartimento di Medicina Sperimentale, Sezione di Microbiologia e Microbiologia Clinica, Seconda Università degli Studi di Napoli, 80138 Naples, Italy., Dipartimento di Medicina Sperimentale, Sezione di Microbiologia e Microbiologia Clinica, Dipartimento di Patologia Generale, Facoltà di Medicina e Chirurgia, Seconda Università degli Studi di Napoli, 80138 Naples, Dipartimento di Patologia e Microbiologia Sperimentale, Università degli Studi di Messina, 98125 Messina, Italy

Abstract:  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. 

Retracted: No

PubPeer comments:
 Adding some more papers to the ones found by Dr. Bik and me. Dr. Bik:  This paper is part of a set of at least 14 papers with shared authors (always including one with the last name Galdiero), spanning 1995-2008, that all appear to show the same gels. The porin gels appear to all represent the same sample (Salmonella typhimurium porins), but the LPS gels represent Salmonella, Pasteurella multocida, or Pasteurella haemolytica). Sometimes fewer or more lanes are visible, and in each paper the data are represented as novel. Here is a compilation of most of these gels, as made by Edentulina Martensi, for which I thank this PubPeer user. Here are the papers: - Mariateresa Vitiello et al., Immunology and Cell Biology (1995), DOI: 10.1038 icb.1995.70 - https: pubpeer.com publications 17EC2E40E190E2FCC6F181A2293361 - M. Galdiero et al., Immunology (1995), PMID: 8567029 - https: pubpeer.com publications DECE082D02578F84676293D3A3D307 - L. Sommese et al., J Med Microbiology (1996), DOI: 10.1099 00222615-45-1-40 - https: pubpeer.com publications 7DF0A919C0BB60C8DD14EA1AA8DF34 - M Galdiero et al., Immunology (1998), DOI: 10.1046 j.1365-2567.1998.00492.x - https: pubpeer.com publications BE8182500B61343C93C4D083288F5A - Giuseppe Iovane et al., Veterinary Immunology and Immunopathology (1998), DOI: 10.1016 S0165-2427(98)00183-4 https: pubpeer.com publications 6B20332BB1333F6A9128F81ADE8047 - M. Galdiero et al., Clin Exp Immunol (1999), DOI: 10.1046 j.1365-2249.1999.00904.x - https: pubpeer.com publications 7489649618C468805E4E8A2DA683BB - Antonella Marcatili et al., Research in Microbiology (2000), DOI: 10.1016 S0923-2508(00)00142-X - https: pubpeer.com publications AE562BC01FEC2640B955C330A0B013 - M. Galdiero et al., Microbiology (2001), DOI: 10.1099 00221287-147-10-2697 - https: pubpeer.com publications 511A96912036B49FECC6CEB6F1CBF2 - Massimiliano Galdiero et al., Infection and Immunity (2002), DOI: 10.1128 iai.70.2.558-568.2002 - https: pubpeer.com publications A8765584CC85E943BCA5CB79901DAC - M. Galdiero et al., Journal of Infection (2003), DOI: 10.1053 jinf.2002.1068 - https: pubpeer.com publications FED37BABEA925C28B2CF7BF86CE5B8 - M. Galdiero et al., Clin Microbiol Infect (2003), DOI: 10.1046 j.1469-0691.2003.00728.x - https: pubpeer.com publications FC98EF7F5F87C7AE81F88F12D9C8F4 - M. Vitiello et al., Cytokine (2004), DOI: 10.1016 j.cyto.2004.03.010 - https: pubpeer.com publications 47A3D51AB3A1C226D75197C36D5753 - M. Galdiero et al., Med Microbiol Immunol (2005), DOI: 10.1007 s00430-003-0209-7 - https: pubpeer.com publications 850E4A39A93C3F04AC922264AFC923 - M. Vitiello et al., Cytokine (2008), DOI: 10.1016 j.cyto.2007.11.021 - https: pubpeer.com publications 1EB6BE6DC91E81C414E128642A2FA9 ![file] ![file] ![file]  Here my edit: - M. Galdiero et al., Immunobiology (2000) DOI: 10.1016 S0171-2985(00)80030-3 https: pubpeer.com publications DBF917296422998A5EC5E6A50170A9 - G. Iovane et al., FEMS Immunology and Medical Microbiology (1998) DOI: 10.1111 j.1574-695x.1998.tb01108.x https: pubpeer.com publications 6A9702D24AB5F8283FCB210414880C - Marilena Galdiero et al., INFECTION AND IMMUNITY (2004), DOI: 10.1128 IAI.72.2.1204u20131209.2004 https: pubpeer.com publications 81F27E6CD12B2FCE200A53F1EDE8A9 In particular, in the lattest, of the rows in Figure 1 has a lot of similarities in common with another one in another paper , but there is one big difference (green arrow). Here compared: ![file] ,