Display options
Cite
Jukosky J, Gosselin BJ, Foley L, et al. In vivo Cigarette Smoke Exposure Decreases CCL20, SLPI, and BD-1 Secretion by Human Primary Nasal Epithelial Cells. Front Psychiatry. 2016;6:185doi: 10.3389/fpsyt.2015.00185.
Jukosky, J., Gosselin, B. J., Foley, L., Dechen, T., Fiering, S., & Crane-Godreau, M. A. (2015). In vivo Cigarette Smoke Exposure Decreases CCL20, SLPI, and BD-1 Secretion by Human Primary Nasal Epithelial Cells. Frontiers in psychiatry, 6185. https://doi.org/10.3389/fpsyt.2015.00185
Jukosky, James, et al. "In vivo Cigarette Smoke Exposure Decreases CCL20, SLPI, and BD-1 Secretion by Human Primary Nasal Epithelial Cells." Frontiers in psychiatry vol. 6 (2015): 185. doi: https://doi.org/10.3389/fpsyt.2015.00185
Jukosky J, Gosselin BJ, Foley L, Dechen T, Fiering S, Crane-Godreau MA. In vivo Cigarette Smoke Exposure Decreases CCL20, SLPI, and BD-1 Secretion by Human Primary Nasal Epithelial Cells. Front Psychiatry. 2016 Jan 13;6:185. doi: 10.3389/fpsyt.2015.00185. eCollection 2015. PMID: 26793127; PMCID: PMC4710704.
Copy Download .nbib Format: NLM
Share it on

Front Psychiatry. 2016 Jan 13;6:185. doi: 10.3389/fpsyt.2015.00185. eCollection 2015.

In vivo Cigarette Smoke Exposure Decreases CCL20, SLPI, and BD-1 Secretion by Human Primary Nasal Epithelial Cells.

Frontiers in psychiatry

James Jukosky, Benoit J Gosselin, Leah Foley, Tenzin Dechen, Steven Fiering, Mardi A Crane-Godreau

Affiliations

  1. Department of Natural Science, Colby-Sawyer College , New London, NH , USA.
  2. Department of Otolaryngology, Dartmouth Hitchcock Medical Center , Lebanon, NH , USA.
  3. Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth , Lebanon, NH , USA.

PMID: 26793127 PMCID: PMC4710704 DOI: 10.3389/fpsyt.2015.00185

Abstract

Smokers and individuals exposed to second-hand cigarette smoke have a higher risk of developing chronic sinus and bronchial infections. This suggests that cigarette smoke (CS) has adverse effects on immune defenses against pathogens. Epithelial cells are important in airway innate immunity and are the first line of defense against infection. Airway epithelial cells not only form a physical barrier but also respond to the presence of microbes by secreting antimicrobials, cytokines, and chemokines. These molecules can lyse infectious microorganisms and/or provide signals critical to the initiation of adaptive immune responses. We examined the effects of CS on antimicrobial secretions of primary human nasal epithelial cells (PHNECs). Compared to non-CS-exposed individuals, PHNEC from in vivo CS-exposed individuals secreted less chemokine ligand (C-C motif) 20 (CCL20), Beta-defensin 1 (BD-1), and SLPI apically, less BD-1 and SLPI basolaterally, and more CCL20 basolaterally. Cigarette smoke extract (CSE) exposure in vitro decreased the apical secretion of CCL20 and beta-defensin 1 by PHNEC from non-CS-exposed individuals. Exposing PHNEC from non-CS exposed to CSE also significantly decreased the levels of many mRNA transcripts that are involved in immune signaling. Our results show that in vivo or in vitro exposure to CS alters the secretion of key antimicrobial peptides from PHNEC, but that in vivo CS exposure is a much more important modifier of antimicrobial peptide secretion. Based on the gene expression data, it appears that CSE disrupts multiple immune signaling pathways in PHNEC. Our results provide mechanistic insight into how CS exposure alters the innate immune response and increases an individual's susceptibility to pathogen infection.

Keywords: CCL20; SLPI; antimicrobial peptides; beta defensing-1; cigarette smoke exposure; innate immune response; nasal epithelial cell culture; primary nasal epithelium

References

  1. Laryngorhinootologie. 2000 Jul;79(7):400-3 - PubMed
  2. Nucleic Acids Res. 2000 Jan 1;28(1):27-30 - PubMed
  3. J Leukoc Biol. 2006 Mar;79(3):417-24 - PubMed
  4. Acta Otolaryngol. 2000 Jan;120(1):58-61 - PubMed
  5. Am J Rhinol. 2001 May-Jun;15(3):175-9 - PubMed
  6. Chest. 2005 Jun;127(6):2072-5 - PubMed
  7. Mucosal Immunol. 2011 Sep;4(5):484-95 - PubMed
  8. J Asthma. 2005 Sep;42(7):543-7 - PubMed
  9. J Infect Dis. 1998 Jul;178(1):266-9 - PubMed
  10. Sex Transm Dis. 2003 May;30(5):405-10 - PubMed
  11. FEMS Immunol Med Microbiol. 1999 Aug 1;25(1-2):145-54 - PubMed
  12. Adv Exp Med Biol. 1998;437:279-89 - PubMed
  13. Science. 2003 Jun 6;300(5625):1524-5 - PubMed
  14. J Immunol. 2005 Nov 1;175(9):6058-64 - PubMed
  15. Annu Rev Physiol. 2002;64:709-48 - PubMed
  16. Int J Pediatr Otorhinolaryngol. 1999 Oct 5;49 Suppl 1:S275-8 - PubMed
  17. Respir Res. 2006 Jan 05;7:3 - PubMed
  18. Am J Respir Cell Mol Biol. 2010 Sep;43(3):368-75 - PubMed
  19. Eur Respir J. 2006 Oct;28(4):721-9 - PubMed
  20. Scand J Immunol. 2002 Sep;56(3):294-302 - PubMed
  21. Arch Intern Med. 2004 Nov 8;164(20):2206-16 - PubMed
  22. Open Immunol J. 2009 Jan 1;2:86-93 - PubMed
  23. FEMS Immunol Med Microbiol. 1999 Jan;23(1):27-36 - PubMed
  24. Pediatr Infect Dis J. 1994 Jan;13(1 Suppl 1):S5-9; discussion S20-2 - PubMed
  25. J Allergy Clin Immunol. 2007 Feb;119(2):457-63 - PubMed
  26. Am J Respir Cell Mol Biol. 2004 Sep;31(3):358-64 - PubMed
  27. In Vitro Cell Dev Biol Anim. 2010 Jul;46(7):606-12 - PubMed
  28. J Asthma. 2004 Feb;41(1):91-8 - PubMed
  29. J Biol Chem. 1998 Feb 20;273(8):4530-8 - PubMed
  30. J Acquir Immune Defic Syndr Hum Retrovirol. 1997 Apr 1;14(4):338-42 - PubMed
  31. Laryngoscope. 2003 Jul;113(7):1199-205 - PubMed
  32. J Acquir Immune Defic Syndr Hum Retrovirol. 1996 Dec 1;13(4):374-83 - PubMed
  33. Rhinology. 1989 Jun;27(2):97-103 - PubMed
  34. Otolaryngol Head Neck Surg. 1992 Feb;106(2):181-8 - PubMed
  35. Am J Respir Crit Care Med. 2001 Aug 15;164(4):542-5 - PubMed
  36. Am J Respir Cell Mol Biol. 2011 Feb;44(2):155-65 - PubMed
  37. Acta Otolaryngol. 1994 Mar;114(2):199-202 - PubMed
  38. Immunol Lett. 2006 Mar 15;103(2):167-76 - PubMed
  39. Am J Respir Crit Care Med. 2004 Dec 1;170(11):1164-71 - PubMed

Publication Types

Grant support