Carlos J. Orihuela

Organ-specific models of Streptococcus pneumoniae disease.

Microarray analysis of pneumococcal gene expression during invasive disease.

Tissue-specific contributions of pneumococcal virulence factors to pathogenesis.

Virulence in mice of pneumococcal clonal types with known invasive disease potential in humans.

beta-Arrestin 1 participates in platelet-activating factor receptor-mediated endocytosis of Streptococcus pneumoniae.

Cell wall-mediated neuronal damage in early sepsis.

Identification of a Candidate Streptococcus pneumoniae core genome and regions of diversity correlated with invasive pneumococcal disease.

Platelet-activating factor receptor and innate immunity: uptake of gram-positive bacterial cell wall into host cells and cell-specific pathophysiology.

Induction of pro- and anti-inflammatory molecules in a mouse model of pneumococcal pneumonia after influenza.

Regions of Diversity 8, 9 and 13 contribute to Streptococcus pneumoniae virulence.

Assessment of molecular typing methods to determine invasiveness and to differentiate clones of Streptococcus pneumoniae.

Antibodies against PsrP, a novel Streptococcus pneumoniae adhesin, block adhesion and protect mice against pneumococcal challenge.

Laminin receptor initiates bacterial contact with the blood brain barrier in experimental meningitis models.

Age-associated inflammation and toll-like receptor dysfunction prime the lungs for pneumococcal pneumonia.

The Streptococcus pneumoniae adhesin PsrP binds to Keratin 10 on lung cells.

Emu-BCL10 mice exhibit constitutive activation of both canonical and noncanonical NF-kappaB pathways generating marginal zone (MZ) B-cell expansion as a precursor to splenic MZ lymphoma.

Role played by psrP-secY2A2 (accessory region 34) in the invasive disease potential of Streptococcus pneumoniae.

Statins protect against fulminant pneumococcal infection and cytolysin toxicity in a mouse model of sickle cell disease.

Early biofilm formation on microtiter plates is not correlated with the invasive disease potential of Streptococcus pneumoniae.

Pneumococcal microbial surface components recognizing adhesive matrix molecules targeting of the extracellular matrix.

Pneumococci: immunology of the innate host response.

The pneumococcal serine-rich repeat protein is an intra-species bacterial adhesin that promotes bacterial aggregation in vivo and in biofilms.

PsrP, a protective pneumococcal antigen, is highly prevalent in children with pneumonia and is strongly associated with clonal type.

Rapamycin, but not resveratrol or simvastatin, extends life span of genetically heterogeneous mice.

Incidence of cardiovascular events after hospital admission for pneumonia.

Cellular senescence increases expression of bacterial ligands in the lungs and is positively correlated with increased susceptibility to pneumococcal pneumonia.

Changes in capsular serotype alter the surface exposure of pneumococcal adhesins and impact virulence.

Biofilm and planktonic pneumococci demonstrate disparate immunoreactivity to human convalescent sera.

Streptococcus pneumoniae in biofilms are unable to cause invasive disease due to altered virulence determinant production.

Pneumococcal gene complex involved in resistance to extracellular oxidative stress.

Dysregulated inflammation as a risk factor for pneumonia in the elderly.

Future perspective on host-pathogen interactions during bacterial biofilm formation within the nasopharynx.

Age-related defects in TLR2 signaling diminish the cytokine response by alveolar macrophages during murine pneumococcal pneumonia.

Impact of oral simvastatin therapy on acute lung injury in mice during pneumococcal pneumonia.

Prevalence and clonal distribution of pcpA, psrP and Pilus-1 among pediatric isolates of Streptococcus pneumoniae.

Enteric-delivered rapamycin enhances resistance of aged mice to pneumococcal pneumonia through reduced cellular senescence.

Interactions between blood-borne Streptococcus pneumoniae and the blood-brain barrier preceding meningitis.

Streptococcus pneumoniae biofilm formation is strain dependent, multifactorial, and associated with reduced invasiveness and immunoreactivity during colonization.

Elevated A20 contributes to age-dependent macrophage dysfunction in the lungs.

Streptococcus pneumoniae translocates into the myocardium and forms unique microlesions that disrupt cardiac function.

Pneumococci in biofilms are non-invasive: implications on nasopharyngeal colonization.

Requirement for Serratia marcescens cytolysin in a murine model of hemorrhagic pneumonia.

Senescent Cells Contribute to the Physiological Remodeling of Aged Lungs.

Cardiotoxicity during Invasive Pneumococcal Disease.