Ly6G+ Neutrophils Are Dispensable for Defense against Systemic Listeria monocytogenes Infection

被引:101
作者
Shi, Chao [1 ,2 ]
Hohl, Tobias M. [3 ]
Leiner, Ingrid [1 ]
Equinda, Michele J. [1 ]
Fan, Xiaozhou [1 ,2 ]
Pamer, Eric G. [1 ]
机构
[1] Mem Sloan Kettering Canc Ctr, Infect Dis Serv, Program Immunol, Sloan Kettering Inst,Dept Med, New York, NY 10065 USA
[2] Weill Cornell Grad Sch Med, Program Immunol & Microbial Pathogenesis, New York, NY 10065 USA
[3] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Inst, Seattle, WA 98109 USA
基金
美国国家卫生研究院;
关键词
T-CELL RESPONSES; MONOCLONAL-ANTIBODY; BACTERIAL-INFECTION; DENDRITIC CELLS; BONE-MARROW; INFLAMMATORY MONOCYTES; EXTRACELLULAR TRAPS; CHEMOKINE RECEPTOR; MICE; RESISTANCE;
D O I
10.4049/jimmunol.1101721
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Listeria monocytogenes is a facultative intracellular bacterium that causes systemic infections in immunocompromised hosts. Early recruitment of myeloid cells, including inflammatory monocytes and neutrophils, to sites of L. monocytogenes infection is essential for the control of infection and host survival. Because previous experimental studies used depleting or blocking Abs that affected both inflammatory monocytes and neutrophils, the relative contributions of these cell populations to defense against L. monocytogenes infection remain incompletely defined. In this article, we used highly selective depletion strategies to either deplete inflammatory monocytes or neutrophils from L. monocytogenes-infected mice and demonstrate that neutrophils are dispensable for early and late control of infection. In contrast, inflammatory monocytes are essential for bacterial clearance during the innate and adaptive phases of the immune response to L. monocytogenes infection. The Journal of Immunology, 2011, 187: 5293-5298.
引用
收藏
页码:5293 / 5298
页数:6
相关论文
共 42 条
[1]   Blood Monocytes: Development, Heterogeneity, and Relationship with Dendritic Cells [J].
Auffray, Cedric ;
Sieweke, Michael H. ;
Geissmann, Frederic .
ANNUAL REVIEW OF IMMUNOLOGY, 2009, 27 :669-692
[2]   Cross-talk in the innate immune system: Neutrophils instruct recruitment and activation of dendritic cells during microbial infection [J].
Bennouna, S ;
Bliss, SK ;
Curiel, TJ ;
Denkers, EY .
JOURNAL OF IMMUNOLOGY, 2003, 171 (11) :6052-6058
[3]   Neutrophil extracellular traps kill bacteria [J].
Brinkmann, V ;
Reichard, U ;
Goosmann, C ;
Fauler, B ;
Uhlemann, Y ;
Weiss, DS ;
Weinrauch, Y ;
Zychlinsky, A .
SCIENCE, 2004, 303 (5663) :1532-1535
[4]   The involvement of neutrophils in the resistance to Leishmania major infection in susceptible but not in resistant mice [J].
Chen, L ;
Zhang, ZH ;
Watanabe, T ;
Yamashita, T ;
Kobayakawa, T ;
Kaneko, A ;
Fujiwara, H ;
Sendo, F .
PARASITOLOGY INTERNATIONAL, 2005, 54 (02) :109-118
[5]   Neutrophils play a critical role in the pathogenesis of experimental cerebral malaria [J].
Chen, L ;
Zhang, ZH ;
Sendo, F .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2000, 120 (01) :125-133
[6]  
Chen L, 2001, EUR J IMMUNOL, V31, P265, DOI 10.1002/1521-4141(200101)31:1<265::AID-IMMU265>3.0.CO
[7]  
2-L
[8]   Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood [J].
Clark, Stephen R. ;
Ma, Adrienne C. ;
Tavener, Samantha A. ;
McDonald, Braedon ;
Goodarzi, Zahra ;
Kelly, Margaret M. ;
Patel, Kamala D. ;
Chakrabarti, Subhadeep ;
McAvoy, Erin ;
Sinclair, Gary D. ;
Keys, Elizabeth M. ;
Allen-Vercoe, Emma ;
DeVinney, Rebekah ;
Doig, Christopher J. ;
Green, Francis H. Y. ;
Kubes, Paul .
NATURE MEDICINE, 2007, 13 (04) :463-469
[9]   NEUTROPHILS ARE ESSENTIAL FOR EARLY ANTI-LISTERIA DEFENSE IN THE LIVER, BUT NOT IN THE SPLEEN OR PERITONEAL-CAVITY, AS REVEALED BY A GRANULOCYTE-DEPLETING MONOCLONAL-ANTIBODY [J].
CONLAN, JW ;
NORTH, RJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (01) :259-268
[10]   ADMINISTRATION OF ANTIGRANULOCYTE MONOCLONAL-ANTIBODY RB6-8C5 PREVENTS EXPRESSION OF ACQUIRED-RESISTANCE TO LISTERIA-MONOCYTOGENES INFECTION IN PREVIOUSLY IMMUNIZED MICE [J].
CZUPRYNSKI, CJ ;
BROWN, JF ;
WAGNER, RD ;
STEINBERG, H .
INFECTION AND IMMUNITY, 1994, 62 (11) :5161-5163