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LBP3 enhanced antitumor immune responses partly via

releasing the brakes of immunosuppression in the tumor

microenvironment of H22 tumor-bearing mice

Deng, X.L.

1,2

, Hu,M.H.

1

,Wang, Y.Y.

1

,Ma, F.L.

1

, Luo, X.

2

, Zhou, L.

2

1

InfinitusChineseHerbalImmunityResearchCentre,Guangzhou,China,

2

GuangzhouUniversityofChineseMedicine, Guangzhou, China

Recent studies have shown that targeting of immunosuppressive

cells and immune checkpoints in the tumor microenvironment

is a promising approach to enhance the efficacy for cancer

immunotherapy. Polysaccharide from Lycium barbarum LBP

inhibits tumor growth in vivo at least partly via improving antitumor

immunity. However, themechanismsof howLBPmounts aneffective

antitumor immune response are not well understood. In the present

study, the modulation of a polysaccharide fraction from LBP (LBP3)

on the immune system inH22 tumor-bearingmicewas investigated.

TheresultsshowedthatLBP3couldeffectivelyinhibit the solid tumor

growth of H22 tumor-bearing mice. Thymus indexes, the numbers/

percentages of T cells in peripheral blood and tumor tissues, killing

activities of natural killer (NK) cells, cytotoxic T lymphocytes (CTL)

andperitonealmacrophages againstH22 cellswere also improved in

three LBP3 treated groups. Besides, LBP3 treatment could decrease

the secretion of TGF-β, IL-6, IL-2 and IL-10 levels in serum. The

percentages of regulatory T cells (Tregs) in tumor-draining lymph

nodes (TDLN) and tumor tissues were also significantly decreases

in the all LBP3 treated groups. Furthermore, LBP3 treatment could

effectively down regulate the PD-1 expression on T cells in TDLN

and tumor tissues. Taken together, these findings indicate that LBP3

enhanced antitumor immune responses partly via releasing the

brakes of immunosuppression in the tumor microenvironment of

H22 tumor-bearing mice.

All the authors contributedequally to thismanuscript).

Interaction between breast cancer cells and microglia in the

microenvironment of brain metastasis

Foo,S.L.

1,2

,Lim,H.K.L.

1,2

1

NUSGraduateSchoolforIntegrativeSciencesandEngineering,

NationalUniversityofSingapore,Singapore,Singapore,

2

Inflammation

andCancerLaboratory,ImmunologyProgramme,YongLooLinSchool

ofMedicine,NationalUniversityof Singapore,Physiology,Singapore,

Singapore

The occurrence of breast cancer metastases is preferential to certain

organs, and one of it being the brain. As the brain microenvironment

is continuously monitored by microglia- a major component of the

brain immune system, invasion of metastatic breast cancer cells to

the brain should stimulate an immune response in the microglial

cells. In this study, we use an in vitro model comprising of microglia

and metastatic breast cancer cell lines to investigate microglial

reactionstometastaticbreastcancercells, particularly inmodulating

tumour cell proliferation, cell invasion, immune suppression, and

microenvironment modification. In contrast to macrophages, co-

cultures and insert-cultures of microglia and breast cancer cells

demonstrated that microglia are activated by tumor cell-oriented

factors, resulting in priming or sensitization of microglia to adopt

an M1 (pro-inflammatory), rather than M2 (anti-inflammatory)

phenotype. It is alsoobserved that there are chemoattractant factors

secretedbybreastcancercells thatinducedasignificantchemotactic

activity for microglial cells in vitro, and the recruited microglia have

further been found to reduce cancer cells growth. The findings of

the metastasis-antagonizing role of microglia suggest that there

are possibly differences between tumour associated peripheral

macrophagesandbrainintrinsicmicrogliaintermsoftheirresponses

towards breast cancer cells and that differences may also exist in

microglial reactions toward primary breast cancer cells as compared

to cancer cells that have metastasized to the brain. Therefore, it

wouldbeof interest to investigate the functional aspectsofmicroglia

in invasion, dormancy, and relapse of brainmetastatic breast cancer.

Correlation betwen the metabolome and binder of ST2

receptor in chronic periodontics in elderly

Borges,A.

1

,Carvalho,M.

2

,Venturini,G.

3

,Vieira,C.

4

,Paulino,T.

5

,Botelho

Miguel,C.

6

,Oliveira,C.

6

,Pereira,A.

3

,Binvignat,O.

7

, Rodrigues,W.

4,7,8

1

FaculdadeMineirense-Fama,Odontology,Mineiros-GO,Brazil,

2

FaculdadeMineirense-FAMA,Odontology,Mineiros,Brazil,

3

Heart

Institute (InCor)/Univ of SaoPauloMed Sch, SãoPaulo, Brazil,

4

Federal

University of Uberlandia, Uberlandia, Brazil,

5

FederalUniversityof

GoiasTrianguloMineiro-CEFORES,Uberaba,Brazil,

6

FederalUniversity

ofTrianguloMineiro,Uberaba, Brazil,

7

FaculdadeMineirense-Fama,

Mineiros-GO,Brazil,

8

FederalUniversityofGoiasTrianguloMineiro,

Uberaba,Brazil

Introduction:

High relationship of senescence with the emergence

and/or compromise of disease in oral cavity is a triggering factor

of disease in this age group including chronic periodontal disease

(CPD). Some markers have been associated with disease prognosis,

as well as systemic diseases, such as ST2 binder.

Objectives:

Evaluate the correlation between metabolites and

ST2 receptor binder in crevicular fluid in the elderly.

Methods:

All

procedures were approved by the Ethics Committee in Research

of the Federal University of Triangulo Mineiro, under number:

017430/2014. Twenty individuals were selected after applying the

inclusion and exclusion criteria. They were divided into 2 groups,

CPD (N= 10 - Clinical evaluation+probing depth higher or equal to 3

mm, and at least presence of

marginal bleeding at a site) without disease - Control (n = 10). To

the assessment of metabolites was performed the metabolome

(triplicate - GC/MS Agilent -7890B GC; 5977A MS). The ELISA was

performed for the detection and quantification of IL-33 (R&D

Systems).ThePrismsoftwarewas used for statistical evaluation.

Results:

Wereidentified969metabolites,ofwhich64wereselectedto

analyze. After analysis 5 metabolic (2,3 dihydroxypropyl icosanoate,

glycerol, serine, 5-aminovaleric acid e putrescine) obtained a ratio

CPD/Control greater than 2. The elevation was accompanied of

increase of the ST2-binder, wherewas found a positive correlation.

Conclusion/discussion:

Thedatapointtoarelationshipofmetabolic

activity inducible IL-33/ST2 inCPD in the elderly.