ISSN: 2375-3005
American Journal of Microbiology and Biotechnology  
Manuscript Information
 
 
THP-1 Macrophage Cells as a Model to Study Intrinsic Adjuvant Properties of Vibrio cholerae Bacterial Ghosts during Chlamydia Infection
American Journal of Microbiology and Biotechnology
Vol.1 , No. 1, Publication Date: Aug. 14, 2014, Page: 1-8
1574 Views Since August 14, 2014, 786 Downloads Since Apr. 14, 2015
 
 
Authors
 
[1]    

M. Stevens, Department of Biological Sciences, Clark Atlanta University, Atlanta, GA, United States.

[2]    

D. McKeithen, Department of Biological Sciences, Clark Atlanta University, Atlanta, GA, United States; Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, GA, United States.

[3]    

O-R Martinez, Department of Biological Sciences, Clark Atlanta University, Atlanta, GA, United States.

[4]    

J. U. Igietseme, Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, GA, United States; National Center for Infectious Disease, Centers for Disease Control and Prevention, Atlanta, GA, United States.

[5]    

C. Black, National Center for Infectious Disease, Centers for Disease Control and Prevention, Atlanta, GA, United States.

[6]    

Q. He, Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, GA, United States.

[7]    

G. A. Ananaba, Department of Biological Sciences, Clark Atlanta University, Atlanta, GA, United States.

 
Abstract
 

Chlamydia trachomatis is an obligatory intracellular human pathogen responsible for the most common sexually transmitted infections (STIs) worldwide. Chlamydia primarily infects the urogenital tract. In men the infections are usually symptomatic versus in women whereby the infections are usually asymptomatic causing severe complications including pelvic inflammatory disease (PID), ectopic pregnancy and infertility. We tested the hypothesis that intrinsic adjuvant properties of Vibrio cholerae ghosts (VCG) induce an enhanced immune response to infections. The human monocytic leukemia cell line THP-1, has been established as a useful tool for studying the role of monocytes in the human immune response (1) and for their phagocytosis capacity (2). THP-1 monocytes (Mn) or macrophages (MФ) were pulsed with VCG with or without interleukin (IL)-10 for 24 hours. IL-10 inhibits nuclear factor kappa B (NF-κB) translocation into the nucleus by blocking inhibitor of kappa B (IκB) kinase activity (3). IL-10 also inhibits NF-κB already found in the nucleus blocking DNA-binding (4) and gene transcription (5). After stimulation, cellular supernatants were assayed for Th1 and Th2 cytokine secretion. Mn secretion of Th1cytokine tumor necrosis factor-alpha (TNFα) was greater (2200.0 pg/mL) than when cells were primed with IL-10 (1356.0 pg/mL) or secretion by macrophages (1917.0 pg/mL). We concluded that this secretion was significant enough to compliment that which would be secreted when THP-1 Mn or Mϕ are pulsed with Chlamydia elementary bodies alone (6), enhancing the innate immune response during infection. Cellular supernatants containing Th1or Th2 cytokines were also used to culture Chlamydia-infected HeLa cells. Cell viability against the secretory factors contained in the supernatant was measured to determine the effects of the secretory factors on the Chlamydia-infected HeLa cells. Cells infected with serovar F and cultured in VCG-pulsed THP-1 Mϕ soup were only 8.7% viable after 8 h. This suggests that the immune factors elicited by the VCG signaling pathway are toxic to Chlamydia-infected HeLa cells.


Keywords
 

Chlamydia trachomatis, Bacterial Ghosts, Adjuvant, Monocytes, Macrophages, T Helper Cytokines


Reference
 
[01]    

Tsuchiya, S. et al., Int. J. Cancer: 26, 171-176 (1980).

[02]    

Santegoets, SJAM, et al., Journal of Leukocyte Biology Vol. 84 No. 6, 1364-1373 (2008).

[03]    

Vey, E. et al., J. of Immunol. Vol. 149 No.6, 2040-2046 (1992).

[04]    

Driessler F. et al., Clin Exp Immunol 135, 64-73 (2004).

[05]    

Wang P. et al., J. Biol.Chemistry Vol. 270 No. 6, 9558-9563 (1995).

[06]    

Gervassi, A et al., Infection and Immunity 7231-7239 (2004).

[07]    

Brunham RC et al., Nat Rev Immunol. (2), 149-61 (2005).

[08]    

Frankhauser SC et al., J Immunol. 192(3), 1079-90 (2014).

[09]    

Eko FO et al., Vaccine 29, 1472-1480 (2011).

[10]    

Ifere GO et al., J Microbiol Immunol Infect. 40(3), 188-200 (2007).

[11]    

Jalava K. et al., Expert Rev Vaccines 2(1), 45-51 (2003).

[12]    

Haidinger W. et al., Appl Environ Microbiol 69(1), 468-74 (2003).

[13]    

Tabrizi CA. et al., Curr Opin Biotechnol 15(6), 530-7 (2004).

[14]    

Igietseme JU. et al., Expert Rev Vaccines 5(6),739-45 (2006).

[15]    

Araujo FG. et al., Antimicrob Agents Chemother. 46(10), 3327–3330 (2002).

[16]    

Kakizaki Y. et al., Endocr J. 46(4), 487-96 (1999).

[17]    

Xiong Y. et al., Endocrinology 133(6), 2568-73 (1993).

[18]    

Wang JE. et al., Infect. Immun. vol. 68 no. 7, 3965-3970 (2002).

[19]    

Moore KW. et al., Annu Rev Immunol. 11, 165-90 (1993).

[20]    

He Q. et al., J Immunol 174(8), 4860-9 (2005).

[21]    

Yang, X. et al., J. Immunol. 156:4338 (2006).

[22]    

Cohen, CR. AIDS 25:327 (1999).

[23]    

Eko FO. et al., Vaccine 21(15), 1694-703 (2003).

[24]    

Igietseme JU. et al., Immunology 98(4), 510-9(1999).

[25]    

Gracey, E. et al., Nature Reviews Rheumatology 8, 55-59 (2012)

[26]    

Langowski JN. et al., Nature 442 (7101), 461–5 (2006).

[27]    

Kikly K. et al., Curr. Opin. Immunol. 18 (6), 670–5 (2006).

[28]    

Belland RJ. et al., PNAS Vol. 98 No. 24, 13984-13989 (2001)

[29]    

Cocchiaro JL. et al., Cell Microbiol. 11(11), 1571-1578 (2009).

[30]    

Al-Moslih MI et al., J. gen. Virol. 18, 189-193 (1973).





 
  Join Us
 
  Join as Reviewer
 
  Join Editorial Board
 
share:
 
 
Submission
 
 
Membership