Professor, Pediatrics, UCLA School of Medicine
Pediatric Infectious Disease
Dr. Moshe Arditi, MD
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Moshe Arditi, MD practices Pediatric Infectious Disease. He received awards:"Super Doctor". Moshe Arditi is a published MD as well. He has 22 publications published. The latest was: IL-1 Signaling Is Critically Required in Stromal Cells in Kawasaki Disease Vasculitis Mouse Model: Role of Both IL-1 and IL-1.
Publications
- TIR Domain-Containing Adapter-Inducing Beta Interferon (TRIF) Mediates Immunological Memory against Bacterial Pathogens.
- IL-1 Signaling Is Critically Required in Stromal Cells in Kawasaki Disease Vasculitis Mouse Model: Role of Both IL-1α and IL-1β.
- POPsicle for Fever! Cooling Down the Inflammasome.
- Inflammation and Pyroptosis Mediate Muscle Expansion in an Interleukin-1β (IL-1β)-dependent Manner.
- A single infection with Chlamydia pneumoniae is sufficient to exacerbate atherosclerosis in ApoE deficient mice.
- Mast Cells Play an Important Role in Chlamydia pneumoniae Lung Infection by Facilitating Immune Cell Recruitment into the Airway.
- Alternatively spliced myeloid differentiation protein-2 inhibits TLR4-mediated lung inflammation.
- ApoB-100-Related Peptide Vaccine Protects Against Angiotensin II-Induced Aortic Aneurysm Formation and Rupture.
- The NLRP3 Inflammasome is Required for the Development of Hypoxemia in LPS/Mechanical Ventilation Acute Lung Injury.
- Validation of a bedside, on-line/smartphone algorithm to differentiate Kawasaki Disease from other febrile illnesses.
- Regulation of Toll-like receptor 2 interaction with Ecgp96 controls Escherichia coli K1 invasion of brain endothelial cells.
- Plasmacytoid Dendritic Cells Play a Role for Effective Innate Immune Responses during Chlamydia pneumoniae Infection in Mice.
- Innate immune responses to Chlamydia pneumoniae infection: role of TLRs, NLRs, and the inflammasome.
- Marked Acceleration of Atherosclerosis After Lactobacillus casei-Induced Coronary Arteritis in a Mouse Model of Kawasaki Disease.
- Oxidized Mitochondrial DNA Activates the NLRP3 Inflammasome during Apoptosis.
- The NOD/RIP2 pathway is essential for host defenses against Chlamydophila pneumoniae lung infection.
- Chlamydia pneumoniae-induced foam cell formation requires MyD88-dependent and -independent signaling and is reciprocally modulated by liver X receptor activation.
- TLR/MyD88 and liver X receptor alpha signaling pathways reciprocally control Chlamydia pneumoniae-induced acceleration of atherosclerosis.
- Nicotinamide exacerbates hypoxemia in ventilator-induced lung injury independent of neutrophil infiltration.
- Deficiency of CCAAT/Enhancer Binding Protein-Epsilon Reduces Atherosclerotic Lesions in LDLR-/- Mice.
- Chlamydia pneumoniae Infection in Mice Induces Chronic Lung Inflammation, iBALT Formation, and Fibrosis.
Schools
Istanbul University Cerrahpasa Medical Faculty
University of Chicago
Chldns Meml Hospital Northwestern University
Doctors Specialties
- Pediatric Infectious Disease Medicine
- Pediatric Infectious Disease
Accepted Insurances
- Aetna HMO
- Choice Plus POS II
- Blue Card PPO
- CaliforniaCare HMO
- Advantage Preferred DirectAccess Plus PPO
- Blue Cross Blue Shield of California PPO
- Pathway X Direct Access PPO
- Pathway X Tiered Direct Access
- Select Plus HMO
- Access Plus Savenet
- Basic PPO
- First Health (Coventry Health Care) PPO
- Covered California - Bronze PPO
- Employer Group HMO
- Health Net PPO
- Individual and Family PPO
- Kaiser PHCS Network PPO
- MultiPlan PPO
- PHCS Network PPO
- Heritage Signature
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
- PacifiCare HMO
Awards
- Super Doctor
Education
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McGaw Medical Center of Northwestern University -
University of Chicago -
Istanbul University Faculty of Medicine
Hospital
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Ronald Reagan UCLA Medical Center -
Cedars-Sinai Medical Center
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