A5014119951- Oral microbiology and periodontitis research
- Oral Health Pathology and Treatment
- Immune Response and Inflammation
- Immunodeficiency and Autoimmune Disorders
- HIV/AIDS oral health manifestations
- Endodontics and Root Canal Treatments
- Protease and Inhibitor Mechanisms
- Oral and gingival health research
- NF-κB Signaling Pathways
- Streptococcal Infections and Treatments
- Psoriasis: Treatment and Pathogenesis
- Immunotherapy and Immune Responses
- Proteoglycans and glycosaminoglycans research
- Salivary Gland Disorders and Functions
- Autoimmune Bullous Skin Diseases
- T-cell and B-cell Immunology
- Gut microbiota and health
- Bone Metabolism and Diseases
- Diabetes and associated disorders
- Blood disorders and treatments
- Sinusitis and nasal conditions
- Oral and Maxillofacial Pathology
- Inflammatory mediators and NSAID effects
- Immune Cell Function and Interaction
- Pediatric health and respiratory diseases
University of Chile
2013-2024
National Institute of Dental and Craniofacial Research
2014-2021
National Institutes of Health
2014-2021
Universidad Andrés Bello
2012
Viña del Mar University
2012
British Society of Periodontology
2006
Periodontitis is one of the most common human inflammatory diseases, yet mechanisms that drive immunopathology and could be therapeutically targeted are not well defined. Here, we demonstrate an expansion resident memory T helper 17 (TH17) cells in periodontitis. Phenocopying humans, TH17 expanded murine experimental periodontitis through local proliferation. Unlike homeostatic oral cells, which accumulate a commensal-independent interleukin-6 (IL-6)-dependent manner,...
Inflammatory bone loss from periodontal infections in leukocyte adhesion deficiency disease can be reversed by treatment with antibodies to IL-17 or IL-23.
Immuno-surveillance networks operating at barrier sites are tuned by local tissue cues to ensure effective immunity. Site-specific commensal bacteria provide key signals ensuring host defense in the skin and gut. However, how oral microbiome tissue-specific balance immunity regulation gingiva, a barrier, remains minimally explored. In contrast gut, we demonstrate that gingiva-resident T helper 17 (Th17) cells developed via colonization-independent mechanism. Accumulation of Th17 gingiva was...
Human monogenic disorders have revealed the critical contribution of type 17 responses in mucosal fungal surveillance. We unexpectedly found that certain settings, enhanced 1 immunity rather than defective can promote infection susceptibility. Notably, mice and humans with
Tissue-specific cues are critical for homeostasis at mucosal barriers. Here, we report that the clotting factor fibrin is a regulator of neutrophil function oral barrier. We demonstrate commensal microbiota trigger extravascular deposition in mucosa. Fibrin engages neutrophils through α
Abstract Background and Aims: Interleukin‐17 (IL‐17) is a T‐cell‐derived cytokine that may play an important role in the initiation or maintenance of pro‐inflammatory response has recently been found to stimulate osteoclastic resorption. The purpose present study was determine presence IL‐17 gingival crevicular fluid (GCF) samples culture supernatants cells from patients with chronic periodontitis. Method: GCF were collected during 30 s two sites 16 periodontally affected (probing depth 5...
Abstract Aim: T regulatory (Treg) cells have been detected in periodontitis lesions, and forkhead box P3 (Foxp3) expression has negatively correlated to receptor activator of nuclear factor‐ κ B ligand (RANKL). The aim this study was correlate T‐helper type 1 (Th1), Th2, Th17 Treg transcription factor expressions, gingival tissues from patients undergoing active periodontal tissue destruction, with bone loss‐associated cytokines. Materials Methods: In 10 chronic disease progression, the mRNA...
Periodontitis is an infection with episodic nature of tissue support destruction. The aim this work was to determine the levels chemokines, cytokines, matrix metalloproteinase-13, periodontal pathogens and inflammatory cells in sites characterized by active connective destruction.Fifty-six patients moderate or advanced severity chronic periodontitis were selected. at least six probing depth > =5 mm, clinical attachment level =3 mm radiographic bone loss. progression determined tolerance...
A patient with leukocyte adhesion deficiency type 1 (LAD1) had severe periodontitis and an intractable, deep, nonhealing sacral wound. We previously found a dominant interleukin-23-interleukin-17 signature at inflamed sites in humans LAD1 mouse models of the disorder. Blockade this pathway has resulted resolution immunopathologic condition. treated our ustekinumab, antibody that binds p40 subunit interleukin-23 interleukin-12 thereby blocks activity these cytokines, inhibiting...
Background: Matrix metalloproteinase (MMP)‐8 is a central mediator in chronic periodontitis. MMP‐8 can be activated by the cooperative action of other MMPs such as MMP‐14, reactive oxygen species, and microbial proteases. The aim this study to associate levels, molecular forms, isoenzyme distribution, degree activation ‐14, myeloperoxidase (MPO), tissue inhibitor MMP (TIMP)‐1 gingival crevicular fluid (GCF) from patients with progressive periodontitis at baseline after periodontal therapy....
Background: Periodontitis is an infection with episodic pattern of tissue‐support destruction. During the generation a primary CD4 + T helper 1 (Th1) response, interferon‐gamma (IFN‐γ) acts as positive regulator by selectively inducing Th1 differentiation through increased transcription T‐bet. The aims this work were to determine IFN‐γ levels in samples gingival crevicular fluid (GCF) and factor T‐bet expression tissue from patients undergoing progression chronic periodontitis. Methods: One...
Abstract Aim: Matrix metalloproteinases (MMP)‐13 can initiate bone resorption and activate proMMP‐9 in vitro, both these MMPs have been widely implicated tissue destruction associated with chronic periodontitis. We studied whether MMP‐13 activity TIMP‐1 levels gingival crevicular fluid (GCF) progression of periodontitis assessed clinically by measuring carboxy‐terminal telopeptide collagen I (ICTP) levels. additionally addressed could potentiate gelatinase activation diseased tissue....
Leukocyte Adhesion Deficiency I (LAD-I) is a primary immunodeficiency caused by single gene mutations in the CD18 subunit of β2 integrins which result defective transmigration neutrophils into tissues. Affected patients suffer from recurrent life threatening infections and severe oral disease (periodontitis). Microbial communities local environment (subgingival plaque) are thought to be triggers for inflammatory periodontitis, yet little known regarding microbial associated with LAD-I...
The cytokine receptor activator of nuclear factor kappaB-ligand (RANKL) has been involved in both the physiological and pathological regulation osteoclast life span bone metabolism. Periapical granuloma is a periradicular lesion characterized by periapical destruction. aims this study were to associate RANKL mRNA levels granulomas using real-time reverse transcriptase-polymerase chain reaction (RT-PCR) technique determine specific cell synthesis.In eight periodontal ligament samples from...
Interleukin-21 (IL-21) controls the differentiation of T-helper Th17 cells and induces production IL-17 in this T-cell subtype. The aim study is to determine relative expression IL-21 gingival tissues chronic periodontitis patients correlate/associate with proinflammatory cytokines clinical parameters disease.Samples biopsies were collected from (n = 10) 8). mRNA expressions IL-21, IL-1β, IL-6, IL-17, IL-23, IL-10, transforming growth factor-β1 (TGF-β1) quantified using real-time reverse...
Chronic periodontitis is an infectious disease characterized by alveolar bone destruction and teeth loss. Receptor activator of nuclear factor-kappa B ligand (RANKL) osteoclastogenic cytokine, a central regulatory factor in the osteoclast's lifespan, participant physiological pathological resorption. Gingival T cells synthesize RANKL, contributing to molecular local imbalance that entails resorption seen periodontitis. Our study was aimed at associating levels RANKL with CD4(+) T-cell...
Commensal microbiomes exert critical functions at barrier sites. In particular, establishment of the commensal microbiome after birth dictates immune functionality and tissue homeostasis mucosal surfaces. To investigate stability oral in mice, we evaluated communities shortly birth, through adulthood, up to 1 y life a controlled manner, using sequential samples from same mice over time. We further transmissibility parents during cohousing experiments susceptibility inflammatory disease...
Immune cell networks in tissues play a vital role mediating local immunity and maintaining tissue homeostasis, yet little is known of the resident immune populations oral mucosa gingiva. We have established technique for isolation study cells from murine gingival tissues, an area constant microbial exposure vulnerable site to common inflammatory disease, periodontitis. Our protocol allows detailed phenotypic characterization gingiva, even at steady state. procedure also yields sufficient...