Lutzomyia longipalpis salivary gland homogenate impairs cytokine production and costimulatory molecule expression on human monocytes and dendritic cells

被引:44
作者
Costa, DJ
Favali, C
Clarêncio, J
Afonso, L
Conceiçao, V
Miranda, JC
Titus, RG
Valenzuela, J
Barral-Netto, M
Barral, A
Brodskyn, CI
机构
[1] Ctr Pesquisa Goncalo Moniz, FIOCRUZ, Lab Imunoparasitol, BR-40295001 Salvador, BA, Brazil
[2] Univ Fed Bahia, Inst Ciencias Saude, Salvador, BA, Brazil
[3] Univ Fed Bahia, Fac Med, Salvador, BA, Brazil
[4] Immunol Invest Inst Salvador, Salvador, BA, Brazil
[5] Colorado State Univ, Coll Vet Med & Biomed Sci, Dept Microbiol Immunol & Pathol, Ft Collins, CO 80523 USA
[6] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA
关键词
D O I
10.1128/IAI.72.3.1298-1305.2004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
In this report, we describe an investigation of the effects of Lutzomyia longipalpis sand fly salivary gland homogenates (SGH) on cytokine production and expression of costimulatory molecules on human monocytes, macrophages (Mphis), and dendritic cells (DCs). SGH of L. longipalpis induced an increase in interleukin-6 (IL-6), IL-8 and IL-12p40 production but a decrease in tumor necrosis factor alpha and IL-10 production by lipopolysaccharida (LPS)-stimulated monocytes. We also examined the expression of costimulatory molecules on the surface of monocytes, Mphis, and DCs. Whereas SGH affected the expression of these molecules on monocytes and Mphis, it had little effect on these molecules on DCs. However, when DCs were generated from human monocytes in the presence of SGH, SGH inhibited the expression of costimulatory molecules. In addition, a decrease in the maturation of DCs induced by CD40L was observed in the presence of SGH. Finally, preincubating SGH with human sera containing anti-SGH-specific antibodies abolished the effects of SGH on cytokine production by LPS-stimulated monocytes.
引用
收藏
页码:1298 / 1305
页数:8
相关论文
共 46 条
[1]
Inhibition of the spontaneous apoptosis of neutrophil granulocytes by the intracellular parasite Leishmania major [J].
Aga, E ;
Katschinski, DM ;
van Zandbergen, G ;
Laufs, H ;
Hansen, B ;
Müller, K ;
Solbach, W ;
Laskay, T .
JOURNAL OF IMMUNOLOGY, 2002, 169 (02) :898-905
[2]
Leishmania major: Infection of human monocytes induces expression of IL-8 and MCAF [J].
Badolato, R ;
Sacks, DL ;
Savoia, D ;
Musso, T .
EXPERIMENTAL PARASITOLOGY, 1996, 82 (01) :21-26
[3]
Human immune response to sand fly salivary gland antigens: A useful epidemiological marker? [J].
Barral, A ;
Honda, E ;
Caldas, A ;
Costa, J ;
Vinhas, V ;
Rowton, ED ;
Valenzuela, JG ;
Charlab, R ;
Barral-Netto, M ;
Ribeiro, JMC .
AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE, 2000, 62 (06) :740-745
[4]
Delayed-type hypersensitivity to Phlebotomus papatasi sand fly bite:: An adaptive response induced by the fly? [J].
Belkaid, Y ;
Valenzuela, JG ;
Kamhawi, S ;
Rowton, E ;
Sacks, DL ;
Ribeiro, JMC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (12) :6704-6709
[5]
Development of a natural model of cutaneous leishmaniasis:: Powerful effects of vector saliva and saliva preexposure on the long-term outcome of Leishmania major infection in the mouse ear dermis [J].
Belkaid, Y ;
Kamhawi, S ;
Modi, G ;
Valenzuela, J ;
Noben-Trauth, N ;
Rowton, E ;
Ribeiro, J ;
Sacks, DL .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (10) :1941-1953
[6]
The role of interleukin (IL)-10 in the persistence of Leishmania major in the skin after healing and the therapeutic potential of anti-IL-10 receptor antibody for sterile cure [J].
Belkaid, Y ;
Hoffmann, KF ;
Mendez, S ;
Kamhawi, S ;
Udey, MC ;
Wynn, TA ;
Sacks, DL .
JOURNAL OF EXPERIMENTAL MEDICINE, 2001, 194 (10) :1497-1506
[7]
Bozza M, 1998, EUR J IMMUNOL, V28, P3120, DOI 10.1002/(SICI)1521-4141(199810)28:10<3120::AID-IMMU3120>3.0.CO
[8]
2-3
[9]
Blockade of CD86 ameliorates Leishmania major infection by down-regulating the Th2 response [J].
Brown, JA ;
Titus, RG ;
Nabavi, N ;
Glimcher, LH .
JOURNAL OF INFECTIOUS DISEASES, 1996, 174 (06) :1303-1308
[10]
TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA) AND TNF-BETA AND THEIR RECEPTORS IN EXPERIMENTAL CUTANEOUS LEISHMANIASIS [J].
DEKOSSODO, S ;
GRAU, GE ;
LOUIS, JA ;
MULLER, I .
INFECTION AND IMMUNITY, 1994, 62 (04) :1414-1420