These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The contribution of endotoxins present in the respiratory tract to overproduction of nitric oxide associated with impaired interleukin 6 release in bronchoalveolar leukocytes from lung cancer patients.
    Author: Cembrzyńska-Nowak M, Bieńkowska M, Weryńska B, Dyła T, Jankowska R.
    Journal: Arch Immunol Ther Exp (Warsz); 2000; 48(2):119-25. PubMed ID: 10807053.
    Abstract:
    The purpose of the study was to assess the relation between the levels of endotoxins circulating in airways of patients with lung cancer and the ability of bronchoalveolar lavage (BAL) leukocytes for ex vivo release of nitric oxide (NO) and interleukin 6 (IL-6) and for in vitro lipopolysaccharide (LPS)-induced production of the mediators. Leukocytes isolated from the BAL of 11 patients and from 5 healthy individuals were cultured in the absence or presence of LPS(E. coli). The levels of endotoxins in the BAL fluids (BALF) and the amounts of NO released ex vivo from unstimulated cells from the patients were highly (p = 0.0025) elevated in comparison with those from healthy individuals. The release of NO was significantly correlated (R(S) = 0.638, p = 0.047) with the levels of endotoxins in BALF. In contrast, production of IL-6 remained very low and a negative correlation (R(S) = -0.623, p = 0.0542) was observed between the amounts of NO and IL-6. It was also found that, in response to LPS, bronchoalveolar leukocytes from patients with lung cancer express a reduced capacity for in vitro production of NO and IL-6. Our data suggest that, in patients with lung cancer, the activation of BAL cells by endotoxins circulating in the airways may contribute, at least in part, to overproduction of spontaneous NO and, subsequently, the NO may reduce IL-6 production. Moreover, the exposure in vivo of the BAL cells to LPS renders them unable to respond to the second signals.
    [Abstract] [Full Text] [Related] [New Search]