Journal: Infection and Immunity

Article Title: Aspartate aminotransferase is required for Salmonella expansion in the inflamed gut via TCA anaplerosis

doi: 10.1128/iai.00161-26

Figure Lengend Snippet: S . Tm does not require AspC for systemic survival following intraperitoneal injection. CBA/J mice were infected with a competitive 1:1 ratio of WT and aspC -deficient S . Tm IR715 (Δ aspC ), via intraperitoneal injection at a dose of 10 4 CFU. Mice were allowed to carry the pathogen for predetermined time points prior to humane euthanasia and sample collection. ( A ) Infection schematic. ( B ) Weight-loss percentage relative to inoculation weight in mice sacrificed 3, 4, and 5 days post-infection. ( C ) Competitive index of inoculum at each time point based on the proportion of S . Tm in liver and spleen homogenates, as well as intraperitoneal lavage fluid. ( D ) S . Tm burden of each genotype in the liver. ( E ) S . Tm burden of each genotype in CFU/g in spleen. ( F ) S . Tm burden of each genotype in the intraperitoneal fluid following lavage. N = 6 per time point. Geometric mean with geometric SD. ns, not significant; ***, P < 0.001 using multiple t -test.

Article Snippet: Seven-week-old CBA/J mice were purchased from Jackson Labs Inc., infected with 10 4 CFU of each strain, and carried for 96 h post-infection before sacrifice.

Techniques: Injection, Infection

Journal: Infection and Immunity

Article Title: Aspartate aminotransferase is required for Salmonella expansion in the inflamed gut via TCA anaplerosis

doi: 10.1128/iai.00161-26

Figure Lengend Snippet: Deletion of aspC results in a significant expansion defect only in the cecum and colon during a murine model of gastroenteritis. To interrogate the necessity of AspC via the canonical fecal-oral route of infection, we gavaged CBA/J mice with a 1:1 competitive ratio of our WT S . Tm and isogenic Δ aspC mutant. ( A ) Schematic for competitive in vivo infection. ( B ) Competition index of inoculum over time in feces. ( C and D ) Competition index of inoculum 10 d.p.i. from systemic and gut lumen samples of infected mice. To corroborate our observations, we repeated our infection with either of our strains in isolation. ( E ) Schematic for single infection. ( F ) S . Tm burden in feces over time in mice infected with either WT S . Tm or Δ aspC mutant. N = 6 per condition. Geometric mean and geometric SD. *, P < 0.05; **, P < 0.01 using Mann-Whitney ( B ), paired-end ( E ), or unpaired t -test ( F ).

Article Snippet: Seven-week-old CBA/J mice were purchased from Jackson Labs Inc., infected with 10 4 CFU of each strain, and carried for 96 h post-infection before sacrifice.

Techniques: Infection, Mutagenesis, In Vivo, Isolation, MANN-WHITNEY

Journal: Infection and Immunity

Article Title: Aspartate aminotransferase is required for Salmonella expansion in the inflamed gut via TCA anaplerosis

doi: 10.1128/iai.00161-26

Figure Lengend Snippet: Genetic inactivation of T3SSs results in a colonization defect of Δ aspC but does not alter the overall expansion defect. We constructed isogenic S . Tm Δ aspC mutants in an avirulent background (Δ invA Δ spiB ) and repeated the competitive infection experiment in CBA/J mice, comparing the avirulent strains to the S . Tm WT background. ( A ) Infection schematic of competitive infection. ( B ) Competitive index of inoculum in feces over the course of the infection. Day 3 samples were not collected. ( C and D ) Competitive index of inoculum ( C ) and CFU counts ( D ) of S . Tm strains in cecal content at 10 d.p.i. ( E and F ) Competitive index of inoculum ( E ) and CFU counts ( F ) of S . Tm strains in colon content at 10 d.p.i. N = 6. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 using unpaired ( B ) or paired t -test ( E, F ).

Article Snippet: Seven-week-old CBA/J mice were purchased from Jackson Labs Inc., infected with 10 4 CFU of each strain, and carried for 96 h post-infection before sacrifice.

Techniques: Construct, Infection

Journal: bioRxiv

Article Title: Toxoplasma gondii associates with human Benign Prostatic Hyperplasia and induces prostatic hyperplasia and accompanying urinary dysfunction in mice

doi: 10.64898/2026.04.23.720409

Figure Lengend Snippet: Systemic infection with Toxoplasma infects and inflames the mouse prostate but has mouse strain-distinct effects on hyperplasia. It has previously been shown that systemic Toxoplasma infects and induces inflammation in rodent prostates and induces nodular hyperplasia in the CBA/j strain of mice. The applicability of CBA/j mice to prostate modeling was unclear. To confirm this finding, we assessed infectability, inflammation, and formation of microglandular hyperplasia and nodule formation across mouse strains. A, a rosette of Toxoplasma surrounded by severe lymphocytic and monocytic inflammation in following systemic infection in CBA/j mice. B, Systemic Toxoplasma infection induces inflammation in mice in several strains (B57, CBA/J, and CD-1) as determined by H&E and crude inflammation scoring. However, only CBA/j mice exhibit a significant formation of glandular nodules [C,D] with microglandular hyperplasia among the strains. C, a region of Toxoplasma- associated microglandular hyperplasia and putative forming nodules; D, calculations of percent of mice in each strain and group that exhibit microglandular hyperplasia and/or forming nodules among mouse strains infected with Toxoplasma versus control. n=10, comparisons made, infected versus control in 2×2 table with Chi-square analysis with Yates correction.

Article Snippet: Male and female CBA/j, C57Bk6/j, (Jackson Laboratories) or CD-1 (Charles River) mice were housed in the Laboratory Animal Resource Center (LARC) at Indiana University School of Medicine under the National Institutes of Health Guide for the Care and Use of Laboratory Animals, after all protocols were approved by the Indiana University School of Medicine Animal Care and Use Committee (IACUC).

Techniques: Infection, Control

Journal: bioRxiv

Article Title: Toxoplasma gondii associates with human Benign Prostatic Hyperplasia and induces prostatic hyperplasia and accompanying urinary dysfunction in mice

doi: 10.64898/2026.04.23.720409

Figure Lengend Snippet: Toxoplasma infected mouse and uninfected control mouse number of spots counted at 28 d.p.i and 60 d.p.i in several different size categories collected. A, C57 mouse void pattern analysis including all spot sizes counted in the initial VoidWhizzard software analysis used B, C57 void pattern analysis including only the small size bin (0.1-0.25 cm) category representing spotting or irregular behavior and the larger bin size (4.0 cm) representing normal void behavior. C, CBA/J mouse void pattern analysis including the same spot size categories as B, and D, CD-1 mouse void pattern analysis including the same spot size categories as B. The left column indicates 28 d.p.i while the right indicates 60 d.p.i.

Article Snippet: Male and female CBA/j, C57Bk6/j, (Jackson Laboratories) or CD-1 (Charles River) mice were housed in the Laboratory Animal Resource Center (LARC) at Indiana University School of Medicine under the National Institutes of Health Guide for the Care and Use of Laboratory Animals, after all protocols were approved by the Indiana University School of Medicine Animal Care and Use Committee (IACUC).

Techniques: Infection, Control, Software