Immunogenic properties of the Rv2190c protein.

<p>N-terminal truncated Rv2190c was purified and analyzed for immunogenic properties by Dot-Blot ELISA against various sera. <b>A.</b> Immunogenic response in the human serum of an individual with latent TB (PPD-Pos.) (left panel) as opposed to a negligible response in a PPD negative human serum (right panel). <b>B.</b> Immunogenic response in serum from an <i>M. bovis</i> infected rabbit (left panel) and weak responses from sera raised against WhiB6 protein (middle panel) or pre-bleeds (right panel). i) 2ng of Rv2190c and ii) 2ng of BSA.</p

The <i>M. tuberculosis Rv2190c</i> causes decreased lung histopathology in the mouse.

<p>Formalin-fixed lung sections from mice infected with WT, <i>Rv2190c</i> mutant and complement strains were stained with hematoxylin and eosin and visualized using light microscopy. Scale bar = 0.1 mm.</p

The <i>M. tuberculosis Rv2190c</i> mutant is attenuated <i>in vivo</i>.

<p><b>A. </b><i>M. tuberculosis</i> aerosol implantation in the lungs of BALB/c mice for the <i>Rv2190c</i> mutant, complement and WT (CDC1551) strains for the time-to-death experiment, determined day 1 post-infection. <b>B.</b> Survival curves for the time-to-death experiment. <b>C–D.</b> Lung (C) and spleen (D) CFU counts for BALB/c mice infected via aerosol with ∼3.4 log₁₀CFUs of WT, <i>Rv2190c</i> mutant and complement <i>M. tuberculosis</i> strains. <b>E.</b> Gross pathology of infected mouse lungs at 112 days post-infection.</p

<i>Rv2190c</i> expression peaks at log phase and is involved in the response to cell wall disruption.

<p><b>A.</b> Fold change of <i>Rv2190c</i> expression (relative to level at the start of the growth curve) over increasing cell density in 7H9 broth in wild-type <i>M. tuberculosis</i> CDC1551, normalized to <i>sigA</i> expression. pc: post-clumping. <b>B.</b> Fold-change of <i>Rv2190c</i> expression after exposure to oxidative (cumene), disulfide (diamide) and detergent (SDS) stress conditions, relative to expression levels prior to addition of stressors and normalized to <i>sigA</i>. <b>C.</b> Survival of WT, the <i>Rv2190c</i> mutant and complement <i>M. tuberculosis</i> strains following 24 hours of lysozyme exposure. <b>D.</b> PDIMs for <i>M. tuberculosis</i> WT and Rv2190c mutant strains analyzed by thin layer chromatography using hexane∶diethyl ether∶acetic acid solvent. <b>E.</b> PDIMs analyzed using petroleum ether∶diethyl ether solvent.</p

Comparative lung histopathology in guinea pigs infected with <i>M. tuberculosis</i> H37Rv with different histories of in vitro and in vivo passaging.

<p>* Not passaged in mice.</p><p>** Passaged in mice.</p

Comparison of inflammatory granulomatous pathology in the lungs of guinea pigs three weeks after aerosol infection with one of two H37Rv strains (unpassaged TAMU, top, and mouse-passaged JHU, bottom).

<p>Comparison of inflammatory granulomatous pathology in the lungs of guinea pigs three weeks after aerosol infection with one of two H37Rv strains (unpassaged TAMU, top, and mouse-passaged JHU, bottom).</p

A. Multiplication of mouse-passaged and -unpassaged <i>M. tuberculosis</i> clinical isolate in BALB/c mice.

<p>A. Growth in lungs of the isolate following intravenous infection. B. Growth in lungs following aerosol infection of mouse-passaged clinical isolate in comparison with regularly mouse-passaged H37Rv strain (JHU) in BALB/c mice. Errors are SD.</p

Comparison of bacterial multiplication in the lungs of C57BL/6 mice by passaged and unpassaged <i>dosR</i> deletion mutants and their parental <i>M. tuberculosis</i> H37Rv strain following aerosol infection.

<p>Errors are SD.</p

Mouse passaged JHU <i>M. tuberculosis</i> H37Rv strain compared to in vitro propagated TAMU H37Rv strain in guinea pigs after aerosol infection.

<p>Errors are SEM.</p