Search

Your search keyword '"Caceres, Silvia M."' showing total 28 results
Start Over Author "Caceres, Silvia M."
28 results on '"Caceres, Silvia M."'

1. Prospective evaluation of nontuberculous mycobacteria disease in cystic fibrosis: The design of the PREDICT study

Author

Martiniano, Stacey L., Caceres, Silvia M., Poch, Katie, Rysavy, Noel M., Lovell, Valerie K., Armantrout, Emily, Jones, Marion, Anthony, Margaret, Keck, Allison, Nichols, David P., Vandalfsen, Jill M., Sagel, Scott D., Wagner, Brandie, Xie, Jing, Weaver, Katie, Heltshe, Sonya L., Daley, Charles L., Davidson, Rebecca M., and Nick, Jerry A.

Published
2024
Full Text
View/download PDF

3. Genomic Epidemiology ofMycobacterium abscessusat an Adult Cystic Fibrosis Program Reveals Low Potential for Healthcare-Associated Transmission

Author

Gross, Jane E., primary, Finklea, James D., additional, Caceres, Silvia M., additional, Poch, Katie R., additional, Hasan, Nabeeh A., additional, Jia, Fan, additional, Epperson, L. Elaine, additional, Lipner, Ettie M., additional, Vang, Charmie K., additional, Honda, Jennifer R., additional, Strand, Matthew J., additional, Nogueira de Moura, Vinicius Calado, additional, Daley, Charles L., additional, Strong, Michael, additional, and Nick, Jerry A., additional

Published
2024
Full Text
View/download PDF

6. Prospective evaluation of nontuberculous mycobacteria disease in cystic fibrosis: The design of the PREDICT study

Author

Martiniano, Stacey L., primary, Caceres, Silvia M., additional, Poch, Katie, additional, Rysavy, Noel M., additional, Lovell, Valerie K., additional, Armantrout, Emily, additional, Jones, Marion, additional, Anthony, Margaret, additional, Keck, Allison, additional, Nichols, David P., additional, Vandalfsen, Jill M., additional, Sagel, Scott D., additional, Wagner, Brandie, additional, Xie, Jing, additional, Weaver, Katie, additional, Heltshe, Sonya L., additional, Daley, Charles L., additional, Davidson, Rebecca M., additional, and Nick, Jerry A., additional

Published
2023
Full Text
View/download PDF

8. Molecular Epidemiologic Investigation of Mycobacterium intracellulare subspecies chimaera Lung Infections at an Adult Cystic Fibrosis Program

Author

Gross, Jane E., primary, Teneback, Charlotte C., additional, Sweet, Julie G., additional, Caceres, Silvia M, additional, Poch, Katie R, additional, Hasan, Nabeeh A, additional, Jia, Fan, additional, Epperson, L Elaine, additional, Lipner, Ettie M., additional, Vang, Charmie K, additional, Honda, Jennifer R., additional, Strand, Matthew J, additional, Calado Nogueira de Moura, Vinicius, additional, Daley, Charles L., additional, Strong, Michael, additional, Davidson, Rebecca M, additional, and Nick, Jerry A, additional

Published
2023
Full Text
View/download PDF

11. Blood mRNA biomarkers distinguish variable systemic and sputum inflammation at treatment initiation of inhaled antibiotics in cystic fibrosis: A prospective non-randomized trial

Author

Caceres, Silvia M., primary, Sanders, Linda A., additional, Rysavy, Noel M., additional, Poch, Katie R., additional, Jones, Caroline R., additional, Pickard, Kyle, additional, Fingerlin, Tasha E., additional, Marcus, Roland A., additional, Malcolm, Kenneth C., additional, Taylor-Cousar, Jennifer L., additional, Nichols, David P., additional, Nick, Jerry A., additional, Strand, Matthew, additional, and Saavedra, Milene T., additional

Published
2022
Full Text
View/download PDF

14. Whole Blood Gene Expression Profiling Predicts Severe Morbidity and Mortality in Cystic Fibrosis: A 5-Year Follow-Up Study

Author

Saavedra, Milene T., primary, Quon, Bradley S., additional, Faino, Anna, additional, Caceres, Silvia M., additional, Poch, Katie R., additional, Sanders, Linda A., additional, Malcolm, Kenneth C., additional, Nichols, David P., additional, Sagel, Scott D., additional, Taylor-Cousar, Jennifer L., additional, Leach, Sonia M., additional, Strand, Matthew, additional, and Nick, Jerry A., additional

Published
2018
Full Text
View/download PDF

17. Extremes of Interferon-Stimulated Gene Expression Associate with Worse Outcomes in the Acute Respiratory Distress Syndrome

Author

Nick, Jerry A., primary, Caceres, Silvia M., additional, Kret, Jennifer E., additional, Poch, Katie R., additional, Strand, Matthew, additional, Faino, Anna V., additional, Nichols, David P., additional, Saavedra, Milene T., additional, Taylor-Cousar, Jennifer L., additional, Geraci, Mark W., additional, Burnham, Ellen L., additional, Fessler, Michael B., additional, Suratt, Benjamin T., additional, Abraham, Edward, additional, Moss, Marc, additional, and Malcolm, Kenneth C., additional

Published
2016
Full Text
View/download PDF

21. Mycobacterium abscessus Induces a Limited Pattern of Neutrophil Activation That Promotes Pathogen Survival

Author

Malcolm, Kenneth C., primary, Nichols, E. Michelle, additional, Caceres, Silvia M., additional, Kret, Jennifer E., additional, Martiniano, Stacey L., additional, Sagel, Scott D., additional, Chan, Edward D., additional, Caverly, Lindsay, additional, Solomon, George M., additional, Reynolds, Paul, additional, Bratton, Donna L., additional, Taylor-Cousar, Jennifer L., additional, Nichols, David P., additional, Saavedra, Milene T., additional, and Nick, Jerry A., additional

Published
2013
Full Text
View/download PDF

22. Neutrophil Extracellular Trap (NET)-Mediated Killing of Pseudomonas aeruginosa: Evidence of Acquired Resistance within the CF Airway, Independent of CFTR

Author

Young, Robert L., primary, Malcolm, Kenneth C., additional, Kret, Jennifer E., additional, Caceres, Silvia M., additional, Poch, Katie R., additional, Nichols, David P., additional, Taylor-Cousar, Jennifer L., additional, Saavedra, Milene T., additional, Randell, Scott H., additional, Vasil, Michael L., additional, Burns, Jane L., additional, Moskowitz, Samuel M., additional, and Nick, Jerry A., additional

Published
2011
Full Text
View/download PDF

25. Mycobacterium abscessus Induces a Limited Pattern of Neutrophil Activation That Promotes Pathogen Survival.

Author

Malcolm, Kenneth C., Nichols, E. Michelle, Caceres, Silvia M., Kret, Jennifer E., Martiniano, Stacey L., Sagel, Scott D., Chan, Edward D., Caverly, Lindsay, Solomon, George M., Reynolds, Paul, Bratton, Donna L., Taylor-Cousar, Jennifer L., Nichols, David P., Saavedra, Milene T., and Nick, Jerry A.

Subjects
MYCOBACTERIUM, NEUTROPHILS, PATHOGENIC microorganisms, CYSTIC fibrosis, AIRWAY (Anatomy), MACROPHAGES, INFLAMMATION
Abstract

Mycobacterium abscessus is a rapidly growing mycobacterium increasingly detected in the neutrophil-rich environment of inflamed tissues, including the cystic fibrosis airway. Studies of the immune reaction to M. abscessus have focused primarily on macrophages and epithelial cells, but little is known regarding the neutrophil response despite the predominantly neutrophillic inflammation typical of these infections. In the current study, human neutrophils released less superoxide anion in response to M. abscessus than to Staphylococcus aureus, a pathogen that shares common sites of infection. Exposure to M. abscessus induced neutrophil-specific chemokine and proinflammatory cytokine genes. Although secretion of these protein products was confirmed, the quantity of cytokines released, and both the number and level of gene induction, was reduced compared to S. aureus. Neutrophils mediated killing of M. abscessus, but phagocytosis was reduced when compared to S. aureus, and extracellular DNA was detected in response to both bacteria, consistent with extracellular trap formation. In addition, M. abscessus did not alter cell death compared to unstimulated cells, while S. aureus enhanced necrosis and inhibited apoptosis. However, neutrophils augment M. abscessus biofilm formation. The response of neutrophils to M. abscessus suggests that the mycobacterium exploits neutrophil-rich settings to promote its survival and that the overall neutrophil response was reduced compared to S. aureus. These studies add to our understanding of M. abscessus virulence and suggest potential targets of therapy. [ABSTRACT FROM AUTHOR]

Published
2013
Full Text
View/download PDF

26. Neutrophil Extracellular Trap (NET)-Mediated Killing of Pseudomonas aeruginosa: Evidence of Acquired Resistance within the CF Airway, Independent of CFTR.

Author

Robert L. Young, Malcolm, Kenneth C., Kret, Jennifer E., Caceres, Silvia M., Poch, Katie R., Nichols, David P., Taylor-Cousar, Jennifer L., Saavedra, Milene T., Randell, Scott H., Vasil, Michael L., Burns, Jane L., Moskowitz, Samuel M., and Nick, Jerry A.

Subjects
NEUTROPHILS, PSEUDOMONAS aeruginosa, CYSTIC fibrosis transmembrane conductance regulator, NATURAL immunity, AIRWAY (Anatomy), GENOTYPE-environment interaction, MICROBIAL virulence
Abstract

The inability of neutrophils to eradicate Pseudomonas aeruginosa within the cystic fibrosis (CF) airway eventually results in chronic infection by the bacteria in nearly 80 percent of patients. Phagocytic killing of P. aeruginosa by CF neutrophils is impaired due to decreased cystic fibrosis transmembrane conductance regulator (CFTR) function and virulence factors acquired by the bacteria. Recently, neutrophil extracellular traps (NETs), extracellular structures composed of neutrophil chromatin complexed with granule contents, were identified as an alternative mechanism of pathogen killing. The hypothesis that NET-mediated killing of P. aeruginosa is impaired in the context of the CF airway was tested. P. aeruginosa induced NET formation by neutrophils from healthy donors in a bacterial density dependent fashion. When maintained in suspension through continuous rotation, P. aeruginosa became physically associated with NETs. Under these conditions, NETs were the predominant mechanism of killing, across a wide range of bacterial densities. Peripheral blood neutrophils isolated from CF patients demonstrated no impairment in NET formation or function against P. aeruginosa. However, isogenic clinical isolates of P. aeruginosa obtained from CF patients early and later in the course of infection demonstrated an acquired capacity to withstand NET-mediated killing in 8 of 9 isolates tested. This resistance correlated with development of the mucoid phenotype, but was not a direct result of the excess alginate production that is characteristic of mucoidy. Together, these results demonstrate that neutrophils can kill P. aeruginosa via NETs, and in vitro this response is most effective under non-stationary conditions with a low ratio of bacteria to neutrophils. NET-mediated killing is independent of CFTR function or bacterial opsonization. Failure of this response in the context of the CF airway may occur, in part, due to an acquired resistance against NET-mediated killing by CF strains of P. aeruginosa. [ABSTRACT FROM AUTHOR]

Published
2011
Full Text
View/download PDF

27. Enhanced In VitroFormation and Antibiotic Resistance of Nonattached Pseudomonas aeruginosaAggregates through Incorporation of Neutrophil Products

Author

Caceres, Silvia M., Malcolm, Kenneth C., Taylor-Cousar, Jennifer L., Nichols, David P., Saavedra, Milene T., Bratton, Donna L., Moskowitz, Samuel M., Burns, Jane L., and Nick, Jerry A.

Abstract

ABSTRACTPseudomonas aeruginosais a major pathogen in cystic fibrosis (CF) lung disease. Children with CF are routinely exposed to P. aeruginosafrom the natural environment, and by adulthood, 80% of patients are chronically infected. P. aeruginosain the CF airway exhibits a unique biofilm-like structure, where it grows in small clusters or aggregates of bacteria in association with abundant polymers of neutrophil-derived components F-actin and DNA, among other components. These aggregates differ substantially in size and appearance compared to surface-attached in vitrobiofilm models classically utilized for studies but are believed to share properties of surface-attached biofilms, including antibiotic resistance. However, little is known about the formation and function of surface-independent modes of biofilm growth, how they might be eradicated, and quorum sensing communication. To address these issues, we developed a novel in vitromodel of P. aeruginosaaggregates incorporating human neutrophil-derived products. Aggregates grown in vitroand those found in CF patients' sputum samples were morphologically similar; viable bacteria were distributed in small pockets throughout the aggregate. The lasAquorum sensing gene was differentially expressed in the presence of neutrophil products. Importantly, aggregates formed in the presence of neutrophils acquired resistance to tobramycin, which was lost when the aggregates were dispersed with DNase, and antagonism of tobramycin and azithromycin was observed. This novel yet simple in vitrosystem advances our ability to model infection of the CF airway and will be an important tool to study virulence and test alternative eradication strategies against P. aeruginosa.

Published
2014
Full Text
View/download PDF

28. Mycobacterium abscessusClearance by Neutrophils Is Independent of Autophagy

Author

Pohl, Kerstin, Grimm, Xue A., Caceres, Silvia M., Poch, Katie R., Rysavy, Noel, Saavedra, Milene, Nick, Jerry A., and Malcolm, Kenneth C.

Abstract

Mycobacterium abscessus, a rapidly growing nontuberculous mycobacterium, is increasingly prevalent in chronic lung disease, including cystic fibrosis, and infections are characterized by neutrophil-dominated environments. However, mechanisms of immune control are poorly understood. Azithromycin, a macrolide antibiotic with immunomodulatory effects, is used to treat M. abscessusinfections. Recently, inhibition of macrophage bactericidal autophagy was described for azithromycin, which could be detrimental to the host.

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results