lipoteichoic-acid and Lung-Neoplasms
lipoteichoic-acid has been researched along with Lung-Neoplasms* in 4 studies
Other Studies
4 other study(ies) available for lipoteichoic-acid and Lung-Neoplasms
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Lipoteichoic acids from Staphylococcus aureus stimulate proliferation of human non-small-cell lung cancer cells in vitro.
Pulmonary infections are frequent complications in lung cancer and may worsen its outcome and survival. Inflammatory mediators are suspected to promote tumor growth in non-small-cell lung cancer (NSCLC). Hence, bacterial pathogens may affect lung cancer growth by activation of inflammatory signalling. Against this background, we investigated the effect of purified lipoteichoic acids (LTA) of Staphylococcus aureus (S. aureus) on cellular proliferation and liberation of interleukin (IL)-8 in the NSCLC cell lines A549 and H226. A549 as well as H226 cells constitutively expressed TLR-2 mRNA. Even in low concentrations, LTA induced a prominent increase in cellular proliferation of A549 cells as quantified by automatic cell counting. In parallel, metabolic activity of A549 cells was enhanced. The increase in proliferation was accompanied by an increase in IL-8 mRNA expression and a dose- and time-dependent release of IL-8. Cellular proliferation as well as the release of IL-8 was dependent on specific ligation of TLR-2. Interestingly, targeting IL-8 by neutralizing antibodies completely abolished the LTA-induced proliferation of A549 cells. The pro-proliferative effect of LTA could also be reproduced in the squamous NSCLC cell line H226. In summary, LTA of S. aureus induced proliferation of NSCLC cell lines of adeno- and squamous cell carcinoma origin. Ligation of TLR-2 followed by auto- or paracrine signalling by endogenously synthesized IL-8 is centrally involved in LTA-induced tumor cell proliferation. Therefore, pulmonary infections may exert a direct pro-proliferative effect on lung cancer growth. Topics: Carcinoma, Non-Small-Cell Lung; Carcinoma, Squamous Cell; Cell Proliferation; Humans; In Vitro Techniques; Interleukin-8; Lipopolysaccharides; Lung Neoplasms; Staphylococcus aureus; Teichoic Acids; Toll-Like Receptor 2; Tumor Cells, Cultured | 2017 |
Amplification of lipopolysaccharide-induced cytokine synthesis in non-small cell lung cancer/neutrophil cocultures.
Proinflammatory cytokines are centrally involved in tumor progression and survival in non-small cell lung cancer, and both the presence of infiltrating neutrophils and bacterial infection in the lung may indicate a poor prognosis. Against this background, we investigated the effect of the bacterial cell wall component lipopolysaccharide (LPS) on interleukin (IL)-6 and IL-8 synthesis in the non-small cell lung cancer line A549 and in A549-neutrophil cocultures. The LPS induced a dose-dependent and time-dependent release of IL-8 from A549 cells, whereas IL-6 could not be detected. Interestingly, in A549-neutrophil cocultures, IL-8 synthesis was massively amplified and IL-6 was also released, compared with the respective monocultures. The A549 cells were identified as the primary cellular source of these cytokines, as enhanced cytokine mRNA transcription was detected in this cell type, although not in neutrophils in the coculture system. Experiments done in transwells indicated that direct cell-cell contact was a prerequisite for the increased cytokine generation. Inhibition of tumor necrosis factor-alpha bioactivity by neutralizing antibodies and blocking cyclooxygenase-2 activity blunted the enhanced cytokine generation in the coculture system. Amplification of LPS-induced cytokine secretion could be reproduced when the small cell lung cancer cell line H69 was cocultured with neutrophils. When the Gram-positive cell wall component lipoteichoic acid was used instead of LPS, cytokine synthesis was also amplified in A549-neutrophil cocultures, to a similar extent to that observed with LPS. These data indicate that interaction between bacterial pathogens, neutrophils, and tumor cells might amplify the release of proinflammatory cytokines which may promote tumor growth in vivo. Topics: Carcinoma, Non-Small-Cell Lung; Cell Communication; Cell Line, Tumor; Cells, Cultured; Chemotaxis, Leukocyte; Coculture Techniques; Cyclooxygenase 2 Inhibitors; Cytokines; Disease Progression; Dose-Response Relationship, Drug; Humans; Inflammation; Inflammation Mediators; Interleukin-6; Interleukin-8; Lipopolysaccharides; Lung Neoplasms; Neutrophils; Pneumonia, Bacterial; RNA, Messenger; Teichoic Acids; Time Factors; Transcriptional Activation | 2009 |
Severe impairment of anti-cancer effect of lipoteichoic acid-related molecule isolated from a penicillin-killed Streptococcus pyogenes in toll-like receptor 4-deficient mice.
A lipoteichoic acid-related molecule (OK-PSA) isolated from OK-432, a penicillin-killed Streptococcus pyogenes, is a potent inducer of Th1 cytokines, and elicits anti-cancer effect in tumor-bearing mice. Toll-like receptor (TLR) 4 is a member of the recently identified toll-like receptor family of proteins that has been implicated in lipopolysaccharide-induced cell signaling. In the present study, we have examined the role of TLR4 for OK-PSA-induced Th1-cytokine production and anti-tumor effect by using C3H/HeJ mice in which TLR4 function is impaired. Although OK-PSA strikingly induced Th1 cytokines [interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-2, IL-12 and IL-18] in the splenocytes derived from control animals (C3H/HeN), OK-PSA did not induce the cytokines in the splenocytes from C3H/HeJ. Furthermore, C3H/HeJ-derived splenocytes acquired the responsiveness to OK-PSA stimulation by overexpression of TLR4 gene. Finally, OK-PSA administration significantly inhibited the tumor growth and lung metastasis of syngeneic squamous cell carcinoma cells in C3H/HeN; however, no effect of OK-PSA was observed in C3H/HeJ. These findings strongly suggest that TLR4 signaling is involved in regulating OK-PSA-induced anti-cancer immunity. Topics: Animals; Antineoplastic Agents; Carcinoma, Squamous Cell; Cell Line; Culture Media; Drosophila Proteins; Lipopolysaccharides; Lung Neoplasms; Membrane Glycoproteins; Mice; Mice, Inbred C3H; Mice, Knockout; Mutation; Penicillins; Picibanil; Receptors, Cell Surface; Spleen; Streptococcus pyogenes; Teichoic Acids; Toll-Like Receptor 4; Toll-Like Receptors; Transfection; Tumor Cells, Cultured | 2001 |
Immunostimulating staphylococcal lipoteichoic acid prevents pulmonary tumor colonization in BALB/c-mice.
Immunostimulating and antineoplastic activities of staphylococcal lipoteichoic acid (LTA) were studied in Balb/c-mice. Systemic administration of LTA (1 mg or 2 mg i. p., 7 and 4 days prior to challenge) significantly enhanced chemiluminescence response of peritoneal macrophages (p less than 0.0125) and induced enlargement of the spleen (p less than 0.025) as compared to non-treated controls. In vivo the number of lung colonies was significantly lower (p less than 0.0125) in LTA-treated mice 14 days after challenge with L-1 sarcoma cells. Topics: Adjuvants, Immunologic; Animals; Lipopolysaccharides; Lung Neoplasms; Macrophages; Male; Mice; Mice, Inbred BALB C; Sarcoma, Experimental; Spleen; Staphylococcus; Teichoic Acids | 1988 |