@article{winston_rivera_cai_thanissery_montgomery_patterson_theriot_2020, title={Ursodeoxycholic Acid (UDCA) Mitigates the Host Inflammatory Response during Clostridioides difficile Infection by Altering Gut Bile Acids}, volume={88}, ISSN={["1098-5522"]}, DOI={10.1128/IAI.00045-20}, abstractNote={Clostridioides difficile infection (CDI) is associated with increasing morbidity and mortality posing an urgent threat to public health. Recurrence of CDI after successful treatment with antibiotics is high, thus necessitating discovery of novel therapeutics against this enteric pathogen. Administration of the secondary bile acid ursodeoxycholic acid (UDCA; ursodiol) inhibits the life cycles of various strains of C. difficilein vitro, suggesting that the FDA-approved formulation of UDCA, known as ursodiol, may be able to restore colonization resistance against C. difficilein vivo However, the mechanism(s) by which ursodiol is able to restore colonization resistance against C. difficile remains unknown. Here, we confirmed that ursodiol inhibits C. difficile R20291 spore germination and outgrowth, growth, and toxin activity in a dose-dependent manner in vitro In a murine model of CDI, exogenous administration of ursodiol resulted in significant alterations in the bile acid metabolome with little to no changes in gut microbial community structure. Ursodiol pretreatment resulted in attenuation of CDI pathogenesis early in the course of disease, which coincided with alterations in the cecal and colonic inflammatory transcriptome, bile acid-activated receptors nuclear farnesoid X receptor (FXR) and transmembrane G-protein-coupled membrane receptor 5 (TGR5), which are able to modulate the innate immune response through signaling pathways such as NF-κB. Although ursodiol pretreatment did not result in a consistent decrease in the C. difficile life cycle in vivo, it was able to attenuate an overly robust inflammatory response that is detrimental to the host during CDI. Ursodiol remains a viable nonantibiotic treatment and/or prevention strategy against CDI. Likewise, modulation of the host innate immune response via bile acid-activated receptors FXR and TGR5 represents a new potential treatment strategy for patients with CDI.}, number={6}, journal={INFECTION AND IMMUNITY}, author={Winston, Jenessa A. and Rivera, Alissa J. and Cai, Jingwei and Thanissery, Rajani and Montgomery, Stephanie A. and Patterson, Andrew D. and Theriot, Casey M.}, year={2020}, month={May} }
 @article{manning_birkenheuer_briley_montgomery_harris_vanone_gookin_2016, title={Intermittent At-Home Suctioning of Esophageal Content for Prevention of Recurrent Aspiration Pneumonia in 4 Dogs with Megaesophagus}, volume={30}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.14527}, abstractNote={Background Megaesophagus carries a poor to guarded prognosis due to death from aspiration pneumonia. Options for medical management of regurgitation are limited to strategic oral or gastrostomy tube feeding. Objectives To describe the use and efficacy of intermittent esophageal suctioning to prevent regurgitation and associated episodes of aspiration pneumonia in dogs with megaesophagus. Animals Four dogs with acquired idiopathic megaesophagus and recurrent aspiration pneumonia. Methods Retrospective review of medical records of dogs with megaesophagus in which intermittent suctioning of esophageal content was employed for management of recurrent aspiration pneumonia. Results Intermittent suctioning of the esophagus was initiated in 4 dogs after failure of strict gastrostomy tube feeding failed to prevent regurgitation and repeated episodes of aspiration pneumonia. Suctioning was accomplished by esophagostomy tube in 3 dogs and per os in 1 dog. After initiation of esophageal suctioning, dogs survived for a median of 13.5 additional months (range, 10–30 months) during which time 2 dogs had no additional episodes of aspiration pneumonia and 2 dogs had infrequent episodes of pneumonia, but aspiration was suspected to be a contributing factor in their death. Complications included clogging of the esophagostomy tube, esophagostomy site infections, and esophagitis. Conclusions and Clinical Importance Use of intermittent esophageal suctioning in dogs with megaesophagus that continue to regurgitate despite gastrostomy tube feedings can reduce or abolish clinical episodes of aspiration pneumonia.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Manning, K. and Birkenheuer, A. J. and Briley, J. and Montgomery, S. A. and Harris, J. and Vanone, S. L. and Gookin, J. L.}, year={2016}, pages={1715–1719} }
 @article{meichner_montgomery_borst_murphy_grindem_2016, title={Pathology in Practice}, volume={249}, ISSN={["1943-569X"]}, DOI={10.2460/javma.249.9.1023}, abstractNote={
In collaboration with the American College of Veterinary Pathologists}, number={9}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Meichner, Kristina and Montgomery, Stephanie A. and Borst, Luke B. and Murphy, K. Marcia and Grindem, Carol B.}, year={2016}, month={Nov}, pages={1023–1026} }
 @misc{donohoe_holley_collins_montgomery_whitmore_hillhouse_curry_renner_greenwalt_ryan_et al._2014, title={A gnotobiotic mouse model demonstrates that dietary fiber protects against colorectal tumorigenesis in a microbiota- and butyrate-dependent manner}, volume={4}, number={12}, journal={Cancer Discovery}, author={Donohoe, D. R. and Holley, D. and Collins, L. B. and Montgomery, S. A. and Whitmore, A. C. and Hillhouse, A. and Curry, K. P. and Renner, S. W. and Greenwalt, A. and Ryan, E. P. and et al.}, year={2014}, pages={1387–1397} }
 @article{stevens_montgomery_phillips_wester_jennings_2014, title={Pathology in Practice}, volume={245}, ISSN={["1943-569X"]}, DOI={10.2460/javma.245.1.57}, abstractNote={An 11-year-old 13.5-kg (29.7-lb) castrated male Beagle was evaluated at the General Practice at the North Carolina State University College of Veterinary Medicine because of a 1-month history of excessive panting. Clinical and Gross FindingsOn initial evaluation, the dog was panting.Abdominal palpation elicited signs of pain and revealed an approximately 8 X 4-cm mass within the left, caudoventral aspect of the abdomen.Abnormalities revealed by a CBC and serum biochemical analysis were minimal and considered unremarkable.Three-view abdominal radiography revealed many soft tissue nodules within the abdominal fat.}, number={1}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Stevens, Brenda J. and Montgomery, Stephanie A. and Phillips, Kathryn L. and Wester, Maggie W. and Jennings, Samuel H.}, year={2014}, month={Jul}, pages={57–59} }
 @article{ashbrook_burrack_silva_montgomery_heise_morrison_dermody_2014, title={Residue 82 of the Chikungunya virus E2 attachment protein modulates viral dissemination and arthritis in mice}, volume={89}, number={21}, journal={Journal of Virology}, author={Ashbrook, A. W. and Burrack, K. S. and Silva, L. A. and Montgomery, S. A. and Heise, M. T. and Morrison, T. E. and Dermody, T. S.}, year={2014}, pages={12180–12192} }
 @article{hawman_stoermer_montgomery_pal_oko_diamond_morrison_2013, title={Chronic joint disease caused by persistent Chikungunya virus infection is controlled by the adaptive immune response}, volume={87}, number={24}, journal={Journal of Virology}, author={Hawman, D. W. and Stoermer, K. A. and Montgomery, S. A. and Pal, P. and Oko, L. and Diamond, M. S. and Morrison, T. E.}, year={2013}, pages={13878–13888} }
 @article{stoermer_burrack_oko_montgomery_borst_gill_morrison_2012, title={Genetic Ablation of Arginase 1 in Macrophages and Neutrophils Enhances Clearance of an Arthritogenic Alphavirus}, volume={189}, ISSN={["0022-1767"]}, DOI={10.4049/jimmunol.1201240}, abstractNote={Abstract Chikungunya virus (CHIKV) and Ross River virus (RRV) cause a debilitating, and often chronic, musculoskeletal inflammatory disease in humans. Macrophages constitute the major inflammatory infiltrates in musculoskeletal tissues during these infections. However, the precise macrophage effector functions that affect the pathogenesis of arthritogenic alphaviruses have not been defined. We hypothesized that the severe damage to musculoskeletal tissues observed in RRV- or CHIKV-infected mice would promote a wound-healing response characterized by M2-like macrophages. Indeed, we found that RRV- and CHIKV-induced musculoskeletal inflammatory lesions, and macrophages present in these lesions, have a unique gene-expression pattern characterized by high expression of arginase 1 and Ym1/Chi3l3 in the absence of FIZZ1/Relmα that is consistent with an M2-like activation phenotype. Strikingly, mice specifically deleted for arginase 1 in neutrophils and macrophages had dramatically reduced viral loads and improved pathology in musculoskeletal tissues at late times post-RRV infection. These findings indicate that arthritogenic alphavirus infection drives a unique myeloid cell activation program in inflamed musculoskeletal tissues that inhibits virus clearance and impedes disease resolution in an arginase 1-dependent manner.}, number={8}, journal={JOURNAL OF IMMUNOLOGY}, author={Stoermer, Kristina A. and Burrack, Adam and Oko, Lauren and Montgomery, Stephanie A. and Borst, Luke B. and Gill, Ronald G. and Morrison, Thomas E.}, year={2012}, month={Oct}, pages={4047–4059} }
 @article{morrison_oko_montgomery_whitmore_lotstein_gunn_elmore_heise_2011, title={A mouse model of chikungunya virus-induced musculoskeletal inflammatory disease evidence of arthritis, tenosynovitis, myositis, and persistence}, volume={178}, number={1}, journal={American Journal of Pathology}, author={Morrison, T. E. and Oko, L. and Montgomery, S. A. and Whitmore, A. C. and Lotstein, A. R. and Gunn, B. M. and Elmore, S. A. and Heise, M. T.}, year={2011}, pages={32–40} }