Aras Kadioglu

Role of inflammatory mediators in resistance and susceptibility to pneumococcal infection.

Upper and lower respiratory tract infection by Streptococcus pneumoniae is affected by pneumolysin deficiency and differences in capsule type.

Pneumococcal behavior and host responses during bronchopneumonia are affected differently by the cytolytic and complement-activating activities of pneumolysin.

The MicAB two-component signaling system is involved in virulence of Streptococcus pneumoniae.

Binding and agglutination of Streptococcus pneumoniae by human surfactant protein D (SP-D) vary between strains, but SP-D fails to enhance killing by neutrophils.

The innate immune response to pneumococcal lung infection: the untold story.

Protein serine/threonine kinase StkP positively controls virulence and competence in Streptococcus pneumoniae.

CD4-T-lymphocyte interactions with pneumolysin and pneumococci suggest a crucial protective role in the host response to pneumococcal infection.

Identification of a detrimental role for NK cells in pneumococcal pneumonia and sepsis in immunocompromised hosts.

Susceptibility and resistance to pneumococcal disease in mice.

Pneumococcal neuraminidases A and B both have essential roles during infection of the respiratory tract and sepsis.

Switch from planktonic to sessile life: a major event in pneumococcal pathogenesis.

The cathepsin B inhibitor, z-FA-FMK, inhibits human T cell proliferation in vitro and modulates host response to pneumococcal infection in vivo.

MobilomeFINDER: web-based tools for in silico and experimental discovery of bacterial genomic islands.

The ability to utilize mucin affects the regulation of virulence gene expression in Streptococcus pneumoniae.

The role of Streptococcus pneumoniae virulence factors in host respiratory colonization and disease.

Increased TNF expression in CD43++ murine blood monocytes.

Sialic acid: a preventable signal for pneumococcal biofilm formation, colonization, and invasion of the host.

Macrophages from BALB/c and CBA/Ca mice differ in their cellular responses to Streptococcus pneumoniae.

The immunising effect of pneumococcal nasopharyngeal colonisation; protection against future colonisation and fatal invasive disease.

Pathogenicity islands PAPI-1 and PAPI-2 contribute individually and synergistically to the virulence of Pseudomonas aeruginosa strain PA14.

Human lung mast cells mediate pneumococcal cell death in response to activation by pneumolysin.

A subtype of a Pseudomonas aeruginosa cystic fibrosis epidemic strain exhibits enhanced virulence in a murine model of acute respiratory infection.

Pneumolysin activates the NLRP3 inflammasome and promotes proinflammatory cytokines independently of TLR4.

The integrins Mac-1 and alpha4beta1 perform crucial roles in neutrophil and T cell recruitment to lungs during Streptococcus pneumoniae infection.

Streptococcus pyogenes antigen I/II-family polypeptide AspA shows differential ligand-binding properties and mediates biofilm formation.

Sex-based differences in susceptibility to respiratory and systemic pneumococcal disease in mice.

Absence of the lectin activation pathway of complement does not increase susceptibility to Pseudomonas aeruginosa infections.

Persistence of pneumolysin in the cerebrospinal fluid of patients with pneumococcal meningitis is associated with mortality.

Capsule type of Streptococcus pneumoniae determines growth phenotype.

P4-mediated antibody therapy in an acute model of invasive pneumococcal disease.

T regulatory cells control susceptibility to invasive pneumococcal pneumonia in mice.

Nicotinamide nucleotide transhydrogenase (NNT) acts as a novel modulator of macrophage inflammatory responses.

Gene expression in fungi.

The lectin pathway of complement activation is a critical component of the innate immune response to pneumococcal infection.

Nasopharyngeal carriage with Streptococcus pneumoniae augments the immunizing effect of pneumolysin toxoid B.

Controlled Human Infection and Re-Challenge with Streptococcus Pneumoniae Reveals the Protective Efficacy of Carriage in Healthy Adults.