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Yu X.,University of Texas at San Antonio | Korkmaz T.,University of Texas at San Antonio | Lilburn T.G.,Jamestown | Cai H.,University of Texas at San Antonio | And 3 more authors.
Proceedings - 2014 IEEE International Conference on Bioinformatics and Biomedicine, IEEE BIBM 2014 | Year: 2014

Malaria is one of the most deadly infectious diseases in the world. The malaria burden is characterized by 207 million cases and over 627,000 deaths annually. The consistent morbidity and mortality underscore an urgent need for the development of next-generation antimalarials. In this paper, we propose a network mining approach to uncover the protein-protein associations that are implicated in important cellular processes including DNA repair, genome integrity, transcriptional regulation, and pathogenesis. © 2014 IEEE. Source

Rane H.S.,University of New Mexico | Hardison S.,South Texas Center for Emerging Infectious Diseases | Hardison S.,University of Texas at San Antonio | Botelho C.,University of Minho | And 4 more authors.
Virulence | Year: 2014

We have previously demonstrated that the C. albicans pre-vacuolar protein sorting gene VPS4 is required for extracellular secretion of the secreted aspartyl proteases Sap2p and Saps4-6p. Furthermore, the vps4Δ null mutant has been shown to be markedly hypovirulent in a murine tail vein model of disseminated candidiasis. In these experiments, we sought to further define the role of the pre-vacuolar secretion pathway mediated by the pre-vacuolar sorting gene VPS4 in the pathogenesis of epithelial and mucosal infection using a broad range of virulence models. The C. albicans vps4Δ mutant demonstrates reduced tolerance of cell wall stresses compared to its isogenic, complemented control strain. In an in vitro oral epithelial model (OEM) of tissue invasion, the vps4Δ mutant caused reduced tissue damage compared to controls. Further, the vps4Δ mutant was defective in macrophage killing in vitro, and was attenuated in virulence in an in vivo Caenorhabditis elegans model representative of intestinal epithelial infection. In contrast, the vps4Δ mutant caused a similar degree of tissue damage in an in vitro uroepithelial model of Candida infection compared with controls. Furthermore, in an in vivo murine model of vaginal candidiasis there was no reduction in fungal colony burden and no differences in vaginal histopathology compared to wild-type and complemented controls. These results suggest that VPS4 contributes to several key aspects of oral epithelial but not uroepithelial infection, and in contrast to systemic infection, plays no major role in the pathogenesis of Candida vaginitis. By using a wide range of virulence models, we demonstrate that C. albicans VPS4 contributes to virulence according to the specific tissue that is infected. Thus, in order to gain a full understanding of C. albicans virulence in relation to a particular gene or pathway of interest, a selected range of infection models may need to be utilized. © 2014 Taylor & Francis Group, LLC Source

Pierce C.G.,South Texas Center for Emerging Infectious Diseases | Lopez-Ribot J.L.,South Texas Center for Emerging Infectious Diseases | Bhalla A.S.,University of Texas at San Antonio | Guo R.,University of Texas at San Antonio
Journal of Nano Research | Year: 2016

Most microorganisms grow on surfaces as biofilms rather than as individual planktonic cells, and cells within biofilms show high levels of resistance against antimicrobial drugs. Thereby biofilm formation complicates treatment and contributes to high morbidity and mortality rates associated with infections. This study explores the physical, optical, and nano-structural properties of silver and copper nanoparticles dispersed in aqueous suspensions (nanoparticulate colloidal water) and examines their in vitro activity against microbial biofilms. Silver and copper nanoparticulate colloidal water of various concentrations were prepared and studied. Their surface energies, surface charge and surface plasmonic resonance properties were determined using contact angle measurement, zeta potential measurement and optical spectrometry, respectively. A model of biofilm formation on the wells of microtiter plates was used to determine the activity of the nanoparticulate suspensions against fungal and bacterial biofilms. Scanning electron microscopy (SEM) was used to observe the nanoparticle interactions with microbial cells within the biofilms. Results show that silver nanoparticle-containing liquids have higher surface energy than their copper counterparts; and that the surface energy increases as the concentration of silver nanoparticles increases. Altogether, the effectiveness of silver nanoparticle colloidal suspensions in controlling biofilm formation is observed and reported. For a given size of silver nanoparticles studied, it is found that the effective concentrations against microbial biofilms are far lower than their cytotoxic concentrations, indicating an overall safety and a good therapeutic index thus substantial application potential. © (2016) Trans Tech Publications, Switzerland. Source

Jupelli M.,South Texas Center for Emerging Infectious Diseases | Selby D.M.,Wilford Hall Medical Center | Guentzel M.N.,South Texas Center for Emerging Infectious Diseases | Chambers J.P.,South Texas Center for Emerging Infectious Diseases | And 4 more authors.
Journal of Interferon and Cytokine Research | Year: 2010

Neonatal Chlamydia trachomatis pneumonia has been associated with respiratory sequelae in later life. We recently established a mouse model of neonatal pulmonary Chlamydia muridaum infection and found an important contribution of IFN-γ to protective immunity. In this study, we further characterized the role of Th1-type cytokines; IL-12, IFN-γ, and IFN-γ signaling using mice genetically deficient in IL-12, IFN-γ, or IFN-γ receptor 1. All 3 knockout (KO) mice challenged intranasally with C. muridarum 1 day after birth exhibited 100% mortality by day 17 post-challenge whereas wild-type (WT) animals survived the monitoring period of 1 month. The KO mice exhibited greater lung bacterial burdens and enhanced dissemination to the liver, compared to WT animals. The inflammatory cellular infiltration in C. muridarum-challenged KO animals was significantly reduced in the lungs, but markedly enhanced in the livers of the KO mice compared to similarly challenged WT mice. It was also found that a deficiency in IL-12 or IFN-γ resulted in correspondingly reduced IFN-γ or IL-12 production, respectively, suggesting an intricate interdependence in the induction of these cytokines. Collectively, these results suggest that the IL-12/ IFN-γ axis induces pulmonary cellular infiltration, induces bacterial clearance from the lung, reduces dissemination to other organs, and promotes the survival of the host during neonatal pulmonary chlamydial infection. © Copyright 2010, Mary Ann Liebert, Inc. Source

Murthy A.K.,South Texas Center for Emerging Infectious Diseases | Chaganty B.K.R.,South Texas Center for Emerging Infectious Diseases | Troutman T.,South Texas Center for Emerging Infectious Diseases | Guentzel M.N.,South Texas Center for Emerging Infectious Diseases | And 6 more authors.
PLoS ONE | Year: 2011

The role of antigen-specific secretory IgA (SIgA) has been studied extensively, whereas there is a limited body of evidence regarding the contribution of non-specific SIgA to innate immune defenses against invading pathogens. In this study, we evaluated the effects of non-specific SIgA against infection with Vibrio cholerae O139 strain MO10 and biofilm formation. Seven day old infant mice deficient in IgA (IgA-/- mice) displayed significantly greater intestinal MO10 burden at 24 hr post-challenge when compared to IgA+/+ pups. Importantly, cross-fostering of IgA-/- pups with IgA+/+ nursing dams reversed the greater susceptibility to MO10 infection, suggesting a role for non-specific SIgA in protection against the infection. Since biofilm formation is associated with virulence of MO10, we further examined the role of human non-specific SIgA on this virulence phenotype of the pathogen. Human non-specific SIgA, in a dose-dependent fashion, significantly reduced the biofilm formation by MO10 without affecting the viability of the bacterium. Such an inhibitory effect was not induced by human serum IgA, IgG, or IgM, suggesting a role for the oligosaccharide-rich secretory component (SC) of SIgA. This was supported by the demonstration that SIgA treated with endoglycosidase H, to cleave the high-mannose containing terminal chitobiose residues, did not induce a reduction in biofilm formation by MO10. Furthermore, the addition of free mannose per se, across a wide dose range, induced significant reduction in MO10 biofilm formation. Collectively, these results suggest that mannose containing oligosacchardies within human non-specific secretory IgA can alter important virulence phenotypes of Vibrio cholerae such as biofilm formation, without affecting viability of the microorganism. Such effects may contribute significantly to innate immune defenses against invading pathogens in vivo in the gastrointestinal tract. © 2011 Murthy et al. Source

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