Furthermore, macrophages are one of two major cellular reservoirs for latent HIV-1 infection and contribute

to early-stage virus transmission and dissemination throughout the host (reviewed in [37]). To this end, we observed significant see more secretion of 4 potent chemokines responsible for granulocyte recruitment, MIP1-a, MIP1-b [38], MCP-1 and RANTES [39] (Table 2) indicating that macrophage exposure to M. genitalium in reproductive tissues likely would result in significant inflammation consistent with enhanced HIV-1 replication. Our findings suggest that both infected genital ECs and recruited immune cells are responsible for secretion of IL-6 and other cytokines that may contribute to HIV-1 pathogenesis but continued research is necessary to dissect the cellular dynamics of HIV-1 Selleckchem GSK2245840 and M. genitalium co-infections. In our studies, the macrophage-stimulatory capacity of M. genitalium was not dependent upon bacterial viability. This outcome likely is due to the highly sensitive nature of macrophages. However, both heat denaturation and proteinase-K digestion significantly reduced the cytokine response (Figure 5) suggesting

that a large proportion of M. genitalium’s inflammatory capacity is indeed mediated by protein components. In addition, other findings from our group showed that M. genitalium and the antigenic CHIR98014 MG309-encoded protein activate TLR2/6 to induce pro-inflammatory PI-1840 cytokine secretion from human MDM and reproductive tract ECs [22]. Collectively, these results indicated that macrophages are highly sensitive to M. genitalium exposure and highlight the putative pressure to evade the cellular immune responses. Establishment of primary infection and persistence by M. genitalium in host tissues

is not well understood. Our findings suggest that a subset of M. genitalium organisms rapidly invade host ECs thereby exploiting an intracellular survival niche to evade the potent and effective cellular host immune responses. Studies that address directly whether reproductive ECs provide protection from macrophage phagocytosis are currently underway and will be essential to understand this mechanism of immune evasion. Importantly, M. genitalium infection resulted in acute-phase inflammatory cytokine responses from vaginal and cervical ECs. Therefore, it is possible that persistent infection of female reproductive tract tissues may indeed result in inflammatory outcomes that could affect reproductive health but continued research is necessary to fully elucidate the mechanisms of M. genitalium-induced urogenital disease in women. Conclusion Human vaginal, ecto- and endocervical ECs were susceptible to M. genitalium G37 and M2300 infection resulting in rapid intracellular localization of a subset of organisms and significant secretion of pro-inflammatory cytokines.

FEMS Microbiol Lett 2000, 187:127–132.CrossRefPubMed 43. Blaisdell JO, Hatahet Z, Wallace SS: A novel role for Escherichia coli endonuclease VIII in prevention of spontaneous G–>T transversions. J Bacteriol 1999, 181:6396–6402.PubMed PF-6463922 cell line 44. Seib KL, Tseng HJ, McEwan AG, Apicella MA, Jennings MP: Defenses against oxidative stress in Neisseria gonorrhoeae and Neisseria meningitidis : distinctive systems for different lifestyles. J Infect Dis 2004, 190:136–147.CrossRefPubMed

45. Frasch CE, Gotschlich EC: An outer membrane protein of Neisseria meningitidis group B responsible for serotype specifiCity. J Exp Med 1974, 140:87–104.CrossRefPubMed Authors’ contributions KLT carried out the molecular genetic see more studies and analysis of purified protein, performed sequence alignments

and drafted the manuscript. OHA constructed pUD, designed the phase variation studies and performed the GeSTer analysis. KA contributed to pUD construction and performed the phase variation studies. HH purified recombinant proteins. SAF participated in the bioinformatic analyses. TD supervised the molecular studies and analysis of purified protein, and assisted in manuscript writing. TT conceived the study, participated in its design and coordination and drafted the manuscript. All AZD8931 Authors read and approved the final manuscript.”
“Background The phylum Verrucomicrobia forms a distinct phylogenetically divergent phylum within the domain Bacteria, characterized by members widely distributed in soil and aquatic habitats. Cells of some species such as Verrucomicrobium

spinosum and Cepharanthine Prosthecobacter dejongeii possess cellular extensions termed prosthecae and cells of other strains occur in an ultramicrobacteria size range [1, 2]. Verrucomicrobia are significant for our understanding of both bacterial evolution and microbial ecology. At present, six monophyletic subdivisions (subphyla, classes) are recognized within the phylum Verrucomicrobia on the basis of 16S rRNA gene library studies [3, 4]. There are more than 500 different verrucomicrobia 16S rRNA gene sequences in publicly-accessible databases, but only a handful of these represent cultivated strains. The verrucomicrobia pose interesting evolutionary questions – members of at least one genus, Prosthecobacter, possess genes for a homolog of eukaryotic tubulin, unknown in other prokaryotes, along with the bacterial tubulin-like protein FtsZ. Verrucomicrobium spinosum possesses a FtsZ divergent from those in other phyla of the domain Bacteria [5–8]. In addition, some members of the verrucomicrobia have been recently found to oxidize methane and use methane as a sole source of carbon and energy, making them the only known aerobic methanotrophs outside the proteobacteria, and the only extreme acidophilic methanotrophs known [9–11]. They are thus significant for our understanding of the evolution of methanotrophy and C1 transfer biochemistry.