immunology of infectious and parasitic diseases - XXXVII Congress ...

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susceptible to the infection and produced higher amounts of IFN- . Conclusion: Our data show that the IL-6 production induced during T. gondii infection subverts Treg cell population resulting in the susceptibility to the intestinal inflammation induced by the parasite. Financial support: FAPESP, CNPq, INCTV.
PPAR-α AGONIST GEMFIBROZIL DECREASES SPLEEN TREG CELLS AND AUGMENT MICE SUSCEPTIBILITY TO Toxoplasma gondii INFECTION GIULIANO BONFÁ (1) ; LUCIANA BENEVIDES (1) ; MONIQUE THAÍS COSTA FONSECA (1) ; FRANCIELLE RODRIGUES GUIMARÃES (2) ; DENISE MORAIS FONSECA (1) ; NEIDE MARIA SILVA (3) , JOÃO SANTANA SILVA (1) ; CRISTINA RIBEIRO DE BARROS CARDOSO (2) (1) Department of Biochemistry and Immunology - School of Medicine of Ribeirao Preto - FMRP/USP - SP - Brazil; (2) Department of Clinical Analyses, Toxicology and Food Sciences - School of Pharmaceutical Sciences of Ribeirao Preto - FCFRP/USP - SP - Brazil; (3) Biomedical Science Institute - Federal University of Uberlândia - ICB/UFU - MG - Brazil. E-mail: giubonfa@usp.br Introduction: Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors of which PPARα is the most studied. PPARs function as lipid sensors, regulating metabolism and immune response by acting as transcription factor resulting in the inhibition of pro-inflammatory cytokines. Toxoplasma gondii infection induces a robust Th1 inflammatory response similar to Inflammatory Bowel Disease (IBD) with excessive IFN-γ, TNF and nitric oxide (NO) production. The role of PPAR in the gut inflammation caused by T. gondii in some mice lineages and its possible association with regulation of immune response is still unclear. Then, the aim of this work was to evaluate the role of activated PPAR-α in the susceptibility to T. gondii infection. Methods and Results: C57BL/6 mice were orally infected with cysts of T. gondii, ME-49 strain. The transcripts of PPAR-α were evaluated at 0, 4, 6 and 8 days post-infection (p.i.) by real time PCR (qPCR) of ileum and liver on mice inoculated with 40 cysts. One group of animals infected with 5 cysts was treated with PPAR-α agonist (Gemfibrozil, GEM) for mortality assessment, ileum and liver histological evaluation. Spleen cells were phenotyped by flow cytometry. PPAR-α expression was downregulated in ileum and liver at day 8 p.i. when compared to the previous periods evaluated. Interestingly, when mice were treated with GEM at 10mg/Kg/day for 7 days p.i. there was an increase in mortality. Infection increased inflammatory infiltrate in the ileum associated with visible edema at the villi in vehicle and GEM treated mice. However, GEM group presented an intense inflammation with reduced length and larger villi. Liver inflammatory infiltrate was also increased and more diffuse in GEM treated mice. In addition, there was an increased in NK and NKT cells frequency and decreased number of T CD8 and T regulatory cells (CD4 + CD25 + Foxp3 + ) in the spleen of GEM treated mice. Conclusion: These data indicate that PPAR-α is modulated by T. gondii infection in susceptible mice. Besides its known anti-inflammatory function, activation of this nuclear receptor led to increased susceptibility to parasite induced intestinal damage associated to decreased splenic Treg cells. These
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IMMUNOLOGY OF INFECTIOUS AND PARASI
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profiles appear to be dependent on
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INVOLVEMENT OF TNF RECEPTORS IN APO
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Effects of bioactive Cryptococcus n
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DCs expressing Indoleamine 2,3-diox
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DETECTION OF GITR ON PATIENT CERVIX
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DETECTION OF GITR AND IL-10 ON CERV
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VACCINATION WITH SM10.3 ANTIGEN, A
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Financial support: FAPESP, CAPES an
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clearance that follows Sylvio X10/4
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EhMSP-1 - AN ENTAMOEBA HISTOLYTICA
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THERAPY WITH SCFV TRANSFECTED-DENDR
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etween the groups. The results show
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Financial support: FIOCRUZ, CNPq.
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elease of NETs from human neutrophi
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ROLE OF CD18 IN ACTIVATION OF M1 MA
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IDENTIFICATION, PURIFICATION AND CH
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with hemin showed higher levels of
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SEPTIC ARTHRITIS TRIGGERED BY S. au
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eing higher levels induced by a vir
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parasite load skin. The TGF-β was
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cultures, both treatments decreased
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observed a tendency to lower parasi
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SERUM COMPONENTS AND MONONUCLEAR CE
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VIABILITY OF LEISHMANIA (L.) CHAGAS
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EVALUATION OF THE INTERFERENCE OF S
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IMMUNODETECTION OF THE TGF- β IN L
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DIFFERENT LEVELS OF NKT AND NK CELL
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Funding: CNPQ; FAPESPA; SESPA; UFPA
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saliva that exacerbated leishmania
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BACTERIAL FILAMENTATION: SUPER-RESI
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IMMUNOLOGICAL PARAMETERS ASSOCIATED
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supernatant. BMDC stimulation with
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such as number of eosinophils, prot
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EVALUATION OF THE PRODUCTION OF TNF
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Critical motifs of the Anaplasma ma
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SCHISTOSOMA SPP ANTIGENS IMPAIR THE
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DOWN-REGULATION OF IFN-g RECEPTOR A
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MONOCYTES SUBSETS IN SCHISTOSOMIASI
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THE IN VITRO ANALYSIS OF iNOS-KO MO
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CCR7 IS CRITICAL FOR RESISTANCE AGA
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EVALUATION OF THE IMMUNE RESPONSE A
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our data suggest that monocyte secr
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DIVERGENT OUTCOMES OF THE INTERACTI
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they can deactivate immune effector
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Conclusions: We observed a signific
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TLR2 AND TLR4 EXPRESSION AND NUTRIT
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DEVELOPMENT OF MURINE PLACENTAL MAL
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INDUCTION OF TH17 LYMPHOCYTES CONTR
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Leishmania amazonensis INCREASES EC
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TYPE II GRANULOMA INDUCED BY SCHIST
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The Role of Eosinophils in Aspergil
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compared to baseline (p
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disordered loop and NcSAG2A present
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Conclusion: We demonstrate the exis
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WT. By contrast, uninfected AhR -/-
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in the synthesis of proinflammatory
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PRODUCTION AND EVALUATION OF CHICKE
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allow a conclusion about the differ
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contributes to parasite control and
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Financial support: FAPESP, CNPq, an
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MILTEFOSINE EXERTS ITS LEISHMANICID
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IMMUNOMODULATORY ACTIVITIES OF Β-G
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REGULATION OF IMMUNE RESPONSE AGAIN
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THE ROLE OF REACTIVE OXIGEN SPECIES
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INNATE AND ADAPTIVE IMMUNE REPONSE
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KINETIC OF THE SPECIFIC HUMMORAL IM
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PURINERGIC RECEPTOR P2Y12 ACTIVATIO
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Evaluation of cytokine and chemokin
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Financial support: This research wa
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COMPARISON OF VIRULENCE AND IMMUNE
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THE IMPACT OF TUBERCULOSIS IN THE I
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GALACTOMANNAN ANTIGENEMIA SCREENING
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NATURAL ISOTYPIC RESPONSE AGAINST P
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Characterization of costimulatory m
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P2X7 RECEPTOR ACTIVATION IS REQUIRE
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CASPASE-1 AND NLRP3 CONTRIBUTE TO T
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circulating Treg cells expressing C
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PBMC, none of the treatments alter
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CHARACTERIZATION OF MONOCYTE SUBSET
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EFFECT OF OUABAIN IN MACROPHAGES IN
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OspC1 AND OspF: VIRULENCE FACTORS I
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Conclusion: Taken together, these r
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FIB produced higher proportion of f
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MØ phenotype M2, resulting in decr
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Financial support FAPESP, CAPES, CN
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ALTERATION IN THE DISTRIBUTION OF P
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BENEFICIAL EFFECTS OF PENTOXIFYLLIN
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MODULATION OF IMMUNE RESPONSE AND C
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FAS/FASL AND TRAIL CAUSE APOPTOSIS
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actin were more frequently detected
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NEUTROPHILS AND MACROPHAGES ARE INV
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EXPLORING THE INFLAMMATORY ROLE OF
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CERVICAL LEVELS OF INTERLEUKIN-1 BE
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Title: IDENTIFICATION BY PHAGE DISP
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PROFILE OF PRO- AND ANTI-INFLAMMATO
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IMMUNOMODULATORY MECHANISMS OF SOLU
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EVALUATION OF THE TH1, TH2 AND TH17
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production, as the blockade of PD-L
Page 199 and 200: CHARACTERIZATION OF POLYMORPHISM TN
Page 201 and 202: seems to be dependent on M. leprae
Page 203 and 204: 7 with tendency to normalization on
Page 205 and 206: CHARACTERIZATION OF THE CONSERVATIO
Page 207 and 208: ASC INFLAMMASOME IS NECESSARY TO AC
Page 209 and 210: CASPASE-1 IS REQUIRED TO CONTROL OF
Page 211 and 212: The role of CD4 + T lymphocytes dur
Page 213 and 214: CRITICAL ROLE OF MYD88 EXPRESSION I
Page 215 and 216: on ROS, cathepsin B and Syk kinase
Page 217 and 218: Financial Support: FAPESP and CNPq.
Page 219 and 220: 80% in symptomatic group; 45% in as
Page 221 and 222: of cells undergoing apoptosis in DT
Page 223 and 224: Financial support: FAPESP/LIM-56/HC
Page 225 and 226: identify the active components and
Page 227 and 228: EVALUATION OF HUMORAL AND CELULLAR
Page 229 and 230: Financial support: CNPq-PIBIC, FAPE
Page 231 and 232: addition, significant expression of
Page 233 and 234: THE ROLE OF K + TRANSPORTERS IN THE
Page 235 and 236: Conclusion: In this study, we estab
Page 237 and 238: Heme activates oxidative mechanisms
Page 239 and 240: ROLE OF ADENOSINE AND PROSTAGLANDIN
Page 241 and 242: Taken together, our results indicat
Page 243 and 244: Conclusion: Our findings suggest th
Page 245 and 246: Financial support: CNPq, CAPES, IOC
Page 247 and 248: number of circulating parasites in
Page 249: CRITICAL ROLE OF IL-6 IN REGULATORY
Page 253 and 254: Cutaneous Leishmaniasis in Amazonas
Page 255 and 256: CYTOTOXICITY IN IMMUNOPATHOGENESIS
Page 257 and 258: ROS production and TLR2 and 4 expre
Page 259 and 260: ROLE OF IL-4 IN THE INTESTINAL INFL
Page 261 and 262: In vitro CULTURE SYSTEM FOR Plasmod
Page 263 and 264: interactions, Tandem Affinity Purif
Page 265 and 266: in the course of human infection wi
Page 267 and 268: findings suggest that IL-17 and IL-
Page 269 and 270: 23 contribute to immunological cont
Page 271 and 272: not produced during infection by C.
Page 273 and 274: Conclusion: The production of cytok
Page 275 and 276: CONCLUSION: It is likely, in this p
Page 277 and 278: expression in CCC myocardium was 64
Page 279 and 280: that mononuclear cells derived from
Page 281 and 282: Conclusion: Altogether, our data sh
Page 283 and 284: PARACOCCIDIOIDES BRASILIENSIS INHIB
Page 285 and 286: CANINE VISCERAL LEISHMANIASIS AND S
Page 287 and 288: IMMUNOMODULATORY EFFECTS OF BIOTHER
Page 289 and 290: Leishmania EFFECT ON HEME CYTOTOXIC
Page 291 and 292: ROLE OF STRONGYLOIDES VENEZUELENSIS
Page 293 and 294: TREATMENT WITH Harpagophytum procum
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