24 research outputs found
From Troubled Childhood to Rhodes Scholar. Caylin Moore. Honors Fall Convocation 2021
No full textBy taking advantage of the limited educational opportunities in his community, Caylin Moore excelled through high school and college. As a student-athlete at Texas Christian University, he became founder and president of S.P.A.R.K., a community outreach organization encouraging youth to pursue education as a means of community uplift. He went on to become a US-UK Fulbright Summer Institute fellow at the University of Bristol and a Public Policy and International Affairs Junior Summer Institute fellow at Princeton University. After graduating from TCU, the Rhodes scholarship allowed him to study public policy and earn a master’s degree in Latin American studies at the University of Oxford. Moore received critical acclaim for his debut book, “A Dream Too Big: The Story of an Improbable Journey from Compton to Oxford” (Thomas Nelson, June 2019). The book, which details his against-all-odds journey from the poverty of a gang-ridden Los Angeles community to becoming a Rhodes scholar, has been featured by ABC’s “Good Morning America,” the Hallmark Channel and other many other media outlets. Moore’s book also was named a Good Morning America Anchor’s Favorite Books of 2019 and was an Amazon bestseller in sociology of urban areas. It has drawn widespread praise from notable figures. New York Times bestselling author Ron Hall called his book “an inspiring tale that should be mandatory reading for every student, parent, and anyone else interested in the success of those who will shape and define our future.” Emmy Award-winning anchor and pro football Hall of Famer Michael Strahan said, “What an inspiring story. How he was able to use his wits and his smarts to stay out of trouble and to excel in life … I thought that this book needed to be put out there in the forefront because you can never have a dream too big to accomplish.” Pursuing a Ph.D. in sociology at Stanford University, Moore focuses his research on issues of gang violence, poverty and how they are affected by policies that have been implemented to harm African American and Latino communities.https://egrove.olemiss.edu/hoco_convo/1003/thumbnail.jp
Celebrated Author Caylin Moore Set for Honors Convocation Keynote
No full textRhodes scholar and inspirational speaker to discuss \u27A Dream Too Big\u2
Retelling Tales: Patience Agbabi\u27s Queering of Chaucer\u27s The Man of Law\u27s Tale
No full textGeoffrey Chaucer’s The Canterbury Tales is recognized as a formative text within the canon of English literature. Because of his widely known status, Chaucer and his writings have become the central focus of many medievalists; this does not simply mean the increased presence of critical writings, but also creative works that are inspired by The Canterbury Tales. Patience Agbabi’s Telling Tales is a contemporary poetic retelling of The Canterbury Tales in which she explores the origins of ideas such as diaspora, colonization, racialized thinking, social hierarchy, and binary thinking, only to question these ideas in her own writing. Author Seth Lerer argues, “Constructing literary systems entails positing not just a present of performance but a past of cultural identity. It necessitates the self-conscious invention of a history to literature and, in turn, a definition of the poet’s self-appointed role in mediating that history to a present reading, commissioning, or judging community” (Lerer 4). Although Lerer is discussing the ratification of Chaucer into the modern canon of English literature, he is creating a clear line of historical foundations for the practice of rewriting. Agbabi is continuing Chaucer’s practice of drawing on his own surroundings to create a tale of the present. Patience Agbabi rewrites “The Man of Law’s Tale” into a queer and transnational tale by extracting points of origin from the Middle Ages and rewriting them from a contemporary point of view
Hijacking host cell highways: manipulation of the host actin cytoskeleton by obligate intracellular bacterial pathogens
No full textIntracellular bacterial pathogens replicate within eukaryotic cells and display unique adaptations that support key infection events including invasion, replication, immune evasion, and dissemination. From invasion to dissemination, all stages of the intracellular bacterial life cycle share the same three-dimensional cytosolic space containing the host cytoskeleton. For successful infection and replication, many pathogens hijack the cytoskeleton using effector proteins introduced into the host cytosol by specialized secretion systems. A subset of effectors contains eukaryotic-like motifs that mimic host proteins to exploit signaling and modify specific cytoskeletal components such as actin and microtubules. Cytoskeletal rearrangement promotes numerous events that are beneficial to the pathogen, including internalization of bacteria, subversion of cell intrinsic immunity, structural support for bacteria-containing vacuoles, altered vesicular trafficking, actin-dependent bacterial movement, and pathogen dissemination. This review highlights a diverse group of obligate intracellular bacterial pathogens that manipulate the host cytoskeleton to thrive within eukaryotic cells and discusses underlying molecular mechanisms that promote these dynamic host-pathogen interactions
Dining in: intracellular bacterial pathogen interplay with autophagy
No full textIntracellular bacterial pathogens have evolved many ways to manipulate host cells for successful infection. Many of these pathogens use specialized secretion systems to inject bacterial proteins into the host cytosol that manipulate cellular processes to favor infection. Autophagy is a eukaryotic cellular remodeling process with a critical role in many diseases, including bacterial clearance. A growing field of research highlights mechanisms used by intracellular bacteria to manipulate autophagy as a pro-survival strategy. This review focuses on a select group of bacterial pathogens with diverse intracellular lifestyles that exploit autophagy-derived nutrients and membrane for survival. This group of pathogens uses secretion systems and specific effectors to subvert distinct components of autophagy. By understanding how intracellular pathogens manipulate autophagy, we gain insight not only into bacterial pathogenesis but also host cell signaling and autophagolysosome maturation
Evaluation of IL-1 blockade as a host-directed therapy for tuberculosis in mice and macaques [preprint]
No full textFull author list omitted for brevity. For the full list of authors, see article.In 2017, there were over 550,000 estimated new cases of multi-drug/rifampicin resistant tuberculosis (MDR/RR-TB), emphasizing a need for new treatment strategies. Linezolid (LZD) is a potent antibiotic for antibiotic-resistant Gram-positive infections and is an effective treatment for TB. However, extended LZD use can lead to LZD-associated host toxicities, most commonly bone marrow suppression. LZD toxicities may be mediated by IL-1, a pathway important for early immunity during M. tuberculosis infection that later contributes to pathology. We hypothesized LZD efficacy could be enhanced by modulation of IL-1 pathway to reduce BM toxicity and TB associated-inflammation. We used two animal models of TB to test our hypothesis, mice and cynomolgus macaques. Antagonizing IL-1 in chronically-infected mice reduced lung neutrophil numbers and partially restored the erythroid progenitor populations that are depleted by LZD. In macaques, we found no conclusive evidence of BM suppression associated with LZD, indicating our treatment time may have been short enough to avoid the toxicities observed in humans. Though treatment was only 1 month, the majority of granulomas were sterilized with reduced inflammation (assessed by PET/CT) in animals treated with both LZD and IL-1 receptor antagonist (IL-1Rn). However, overall lung inflammation was significantly reduced in macaques treated with both IL-1Rn and LZD, compared to LZD alone. Importantly, IL-1Rn administration did not noticeably impair the host response against Mtb or LZD efficacy in either animal model. Together, our data support that inhibition of IL-1 in combination with LZD has potential to be an effective HDT for TB
Evaluation of IL-1 Blockade as an Adjunct to Linezolid Therapy for Tuberculosis in Mice and Macaques
No full textIn 2017 over 550,000 estimated new cases of multi-drug/rifampicin resistant tuberculosis (MDR/RR-TB) occurred, emphasizing a need for new treatment strategies. Linezolid (LZD) is a potent antibiotic for drug-resistant Gram-positive infections and is an effective treatment for TB. However, extended LZD use can lead to LZD-associated host toxicities, most commonly bone marrow suppression. LZD toxicities may be mediated by IL-1, an inflammatory pathway important for early immunity during M. tuberculosis infection. However, IL-1 can contribute to pathology and disease severity late in TB progression. Since IL-1 may contribute to LZD toxicity and does influence TB pathology, we targeted this pathway with a potential host-directed therapy (HDT). We hypothesized LZD efficacy could be enhanced by modulation of IL-1 pathway to reduce bone marrow toxicity and TB associated-inflammation. We used two animal models of TB to test our hypothesis, a TB-susceptible mouse model and clinically relevant cynomolgus macaques. Antagonizing IL-1 in mice with established infection reduced lung neutrophil numbers and partially restored the erythroid progenitor populations that are depleted by LZD. In macaques, we found no conclusive evidence of bone marrow suppression associated with LZD, indicating our treatment time may have been short enough to avoid the toxicities observed in humans. Though treatment was only 4 weeks (the FDA approved regimen at the time of study), we observed sterilization of the majority of granulomas regardless of co-administration of the FDA-approved IL-1 receptor antagonist (IL-1Rn), also known as Anakinra. However, total lung inflammation was significantly reduced in macaques treated with IL-1Rn and LZD compared to LZD alone. Importantly, IL-1Rn administration did not impair the host response against Mtb or LZD efficacy in either animal model. Together, our data support that inhibition of IL-1 in combination with LZD has potential to be an effective HDT for TB and the need for further research in this area
Coxiella burnetii Subverts p62/Sequestosome 1 and Activates Nrf2 Signaling in Human Macrophages
No full textABSTRACT
Coxiella burnetii
is the causative agent of human Q fever, a debilitating flu-like illness that can progress to chronic disease presenting as endocarditis. Following inhalation,
C. burnetii
is phagocytosed by alveolar macrophages and generates a lysosome-like replication compartment termed the parasitophorous vacuole (PV). A type IV secretion system (T4SS) is required for PV generation and is one of the pathogen's few known virulence factors. We previously showed that
C. burnetii
actively recruits autophagosomes to the PV using the T4SS but does not alter macroautophagy. In the current study, we confirmed that the cargo receptor p62/sequestosome 1 (SQSTM-1) localizes near the PV in primary human alveolar macrophages infected with virulent
C. burnetii
. p62 and LC3 typically interact to select cargo for autophagy-mediated degradation, resulting in p62 degradation and LC3 recycling. However, in
C. burnetii
-infected macrophages, p62 was not degraded when cells were starved, suggesting that the pathogen stabilizes the protein. In addition, phosphorylated p62 levels increased, indicative of activation, during infection. Small interfering RNA experiments indicated that p62 is not absolutely required for intracellular growth, suggesting that the protein serves a signaling role during infection. Indeed, the Nrf2-Keap1 cytoprotective pathway was activated during infection, as evidenced by sustained maintenance of Nrf2 levels and translocation of the protein to the nucleus in
C. burnetii
-infected cells. Collectively, our studies identify a new p62-regulated host signaling pathway exploited by
C. burnetii
during intramacrophage growth.
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Vasodilator-Stimulated Phosphoprotein Activity Is Required for Coxiella burnetii Growth in Human Macrophages
No full text
