Human Polymorphonuclear Neutrophil Responses to Burkholderia pseudomallei in Healthy and Diabetic Subjects

被引:103
作者
Chanchamroen, Sujin [1 ]
Kewcharoenwong, Chidchamai [1 ]
Susaengrat, Wattanachai [2 ]
Ato, Manabu [3 ]
Lertmemongkolchai, Ganjana [1 ]
机构
[1] Khon Kaen Univ, Fac Associated Med Sci, Ctr Res & Dev Med Diagnost Labs, Khon Kaen, Thailand
[2] Khon Kaen Hosp, Dept Med, Minist Publ Hlth, Khon Kaen, Thailand
[3] Natl Inst Infect Dis, Dept Immunol, Tokyo, Japan
关键词
COLONY-STIMULATING FACTOR; WHOLE-BLOOD; YERSINIA-ENTEROCOLITICA; PSEUDOMONAS-PSEUDOMALLEI; SPONTANEOUS APOPTOSIS; BACTERIAL PATHOGENS; FLOW-CYTOMETRY; RISK-FACTORS; HOST-CELLS; MELIOIDOSIS;
D O I
10.1128/IAI.00503-08
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The major predisposing factor for melioidosis is diabetes mellitus, but no immunological mechanisms have been investigated to explain this. In this study, polymorphonuclear neutrophil (PMN) responses to Burkholderia pseudomallei, the causative agent of melioidosis, in healthy and diabetic Thai subjects were determined by flow cytometry. The results showed that B. pseudomallei displayed reduced uptake by PMNs compared to Salmonella enterica serovar Typhimurium and Escherichia coli. Additionally, intracellular survival of B. pseudomallei was detected throughout a 24-h period, indicating the intrinsic resistance of B. pseudomallei to killing by PMNs. Moreover, PMNs from diabetic subjects displayed impaired phagocytosis of B. pseudomallei, reduced migration in response to interleukin-8, and an inability to delay apoptosis. These data show that B. pseudomallei is intrinsically resistant to phagocytosis and killing by PMNs. These observations, together with the impaired migration and apoptosis in diabetes mellitus, may explain host susceptibility in melioidosis.
引用
收藏
页码:456 / 463
页数:8
相关论文
共 45 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]   Neutrophil function and metabolism in individuals with diabetes mellitus [J].
Alba-Loureiro, T. C. ;
Munhoz, C. D. ;
Martins, J. O. ;
Cerchiaro, G. A. ;
Scavone, C. ;
Curi, R. ;
Sannomiya, P. .
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH, 2007, 40 (08) :1037-1044
[3]   Diabetes causes marked changes in function and metabolism of rat neutrophils [J].
Alba-Loureiro, TC ;
Hirabara, SM ;
Mendonça, JR ;
Curi, R ;
Pithon-Curi, TC .
JOURNAL OF ENDOCRINOLOGY, 2006, 188 (02) :295-303
[4]   Granulocyte colony-stimulating factor and an in vitro whole blood model of melioidosis [J].
Cheng, AC ;
Dasari, P ;
Currie, BJ .
EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES, 2004, 23 (03) :205-207
[5]   Melioidosis: Epidemiology, pathophysiology, and management [J].
Cheng, AC ;
Currie, BJ .
CLINICAL MICROBIOLOGY REVIEWS, 2005, 18 (02) :383-+
[6]   Randomized controlled trial of granulocyte colony-stimulating factor for the treatment of severe sepsis due to melioidosis in Thailand [J].
Cheng, Allen C. ;
Limmathurotsakul, Direk ;
Chierakul, Wirongrong ;
Getchalarat, Nongluk ;
Wuthiekanun, Vanaporn ;
Stephens, Dianne P. ;
Day, Nicholas P. J. ;
White, Nicholas J. ;
Chaowagul, Wipada ;
Currie, Bart J. ;
Peacock, Sharon J. .
CLINICAL INFECTIOUS DISEASES, 2007, 45 (03) :308-314
[7]   ROLE OF YADA IN RESISTANCE OF YERSINIA-ENTEROCOLITICA TO PHAGOCYTOSIS BY HUMAN POLYMORPHONUCLEAR LEUKOCYTES [J].
CHINA, B ;
NGUYEN, BT ;
DEBRUYERE, M ;
CORNELIS, GR .
INFECTION AND IMMUNITY, 1994, 62 (04) :1275-1281
[8]   Anaplasma phagocytophilum delay of neutrophil apoptosis through the p38 mitogen-activated protein kinase signal pathway [J].
Choi, KS ;
Park, JT ;
Dumler, JS .
INFECTION AND IMMUNITY, 2005, 73 (12) :8209-8218
[9]   A critical role for neutrophils in resistance to experimental infection with Burkholderia pseudomallei [J].
Easton, Anna ;
Haque, Ashraful ;
Chu, Karen ;
Lukaszewski, Roman ;
Bancroft, Gregory J. .
JOURNAL OF INFECTIOUS DISEASES, 2007, 195 (01) :99-107
[10]   Specific C-terminal cleavage and inactivation of interleukin-8 by invasive disease isolates of Streptococcus pyogenes [J].
Edwards, RJ ;
Taylor, GW ;
Ferguson, M ;
Murray, S ;
Rendell, N ;
Wrigley, A ;
Bai, ZH ;
Boyle, J ;
Finney, SJ ;
Jones, A ;
Russell, HH ;
Turner, C ;
Cohen, J ;
Faulkner, L ;
Sriskandan, S .
JOURNAL OF INFECTIOUS DISEASES, 2005, 192 (05) :783-790