title: Neisseria gonorrhoeae enhances infection of dendritic cells by HIV type 1.
abstract: Clinical studies indicate that Neisseria gonorrhoeae (gonococci (GC)) has the capacity to enhance HIV type 1 (HIV-1) infection. We studied whether GC enhances HIV infection of activated dendritic cells (DCs). The results show that GC can dramatically enhance HIV replication in human DCs during coinfection. The GC component responsible for HIV infection enhancement may be peptidoglycan, which activates TLR2. TLR2 involvement is suggested by bacterial lipoprotein, a TLR2-specific inducer, which stimulates a strong enhancement of HIV infection by human DCs. Moreover, participation of TLR2 is further implicated because GC is unable to stimulate expression of HIV in DCs of TLR2-deficient HIV-1-transgenic mice. These results provide one potential mechanism through which GC infection increases HIV replication in patients infected with both GC and HIV.
authors.affiliation: Department of Microbiology and Immunology, Division of Infectious Diseases, Walther Oncology Center, Walther Oncology Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
authors.forename: Jizhong
authors.initials: J
authors.lastname: Zhang
authors.forename: Geling
authors.initials: G
authors.lastname: Li
authors.forename: Andre
authors.initials: A
authors.lastname: Bafica
authors.forename: Milica
authors.initials: M
authors.lastname: Pantelic
authors.forename: Pei
authors.initials: P
authors.lastname: Zhang
authors.forename: Hal
authors.initials: H
authors.lastname: Broxmeyer
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Lee
authors.initials: L
authors.lastname: Wetzler
authors.forename: Johnny J
authors.initials: JJ
authors.lastname: He
authors.forename: Tie
authors.initials: T
authors.lastname: Chen
mesh_terms: D000818:Animals; D015703:Antigens, CD; D015704:CD4 Antigens / Q000096:biosynthesis; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism / Q000382:microbiology* / Q000821:virology*; D005260:Female; D015658:HIV Infections / Q000276:immunology / Q000382:microbiology / Q000821:virology; D015497:HIV-1 / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity; D006367:HeLa Cells; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis; D006801:Humans; D007136:Immunoglobulins / Q000096:biosynthesis; D037181:Lectins, C-Type / Q000096:biosynthesis; D008074:Lipoproteins / Q000502:physiology; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009000:Monocytes / Q000276:immunology / Q000382:microbiology / Q000821:virology; D009344:Neisseria gonorrhoeae / Q000276:immunology*; D010457:Peptidoglycan / Q000494:pharmacology; D019713:Receptors, CCR5 / Q000096:biosynthesis; D019718:Receptors, CXCR4 / Q000096:biosynthesis; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors; D015854:Up-Regulation / Q000276:immunology; D000097802:CD83 Antigen; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin
chemical_list: D015703:Antigens, CD; D015704:CD4 Antigens; D015815:Cell Adhesion Molecules; D015395:Histocompatibility Antigens Class I; D007136:Immunoglobulins; D037181:Lectins, C-Type; D008074:Lipoproteins; D008562:Membrane Glycoproteins; D010457:Peptidoglycan; D019713:Receptors, CCR5; D019718:Receptors, CXCR4; D011956:Receptors, Cell Surface; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors; D000097802:CD83 Antigen; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin; C495342:TLR2 protein, human