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To determine whether Pseudomonas aeruginosa, a common cholesteatoma pathogen, known to form biofilms in other chronic infections, is capable of contributing to biofilm formation in cholesteatoma. Design: We tested 12 OPPA isolates for several aspects of biofilm formation, including adherence to human keratinocytes, expression of quorum-sensing genes, twitching motility, and production of extracellular matrix as determined by both crystal violet staining and carbazole reaction. Results: Ten OPPA strains demonstrated increased adherence (1.5-to 12-fold) to human keratinocytes relative to PAO1, a laboratory strain. Expression of las and rhl quorum-sensing products were detected in 11 OPPA strains. By crystal violet staining, we found biofilm formation in all OPPA strains equal to or greater than that found in PAO1 (2-to 18-fold). In addition, OPPA strains demonstrated mucoid characteristics, including downregulation of twitching motility and increased alginate production. Conclusions: Strains of OPPA isolated from cholesteatoma are strongly adherent to keratinocytes and capable of forming biofilm. In addition, OPPA strains have mucoid characteristics in vitro. When these bacteria assume a biofilm phenotype, they are highly resistant to antibiotics and host defenses. These data suggest that OPPA can contribute to biofilm formation in cholesteatoma, leading to the persistence of this infection.

P. aeruginosa LPS acts indirectly through osteoblasts to induce bone resorption. Optimal osteoclastogenesis in vitro required functional TLR4 expression in both BMMs and osteoblasts.

Several lines of evidence suggest that the progression of head-and-neck squamous-cell carcinoma (HNSCC) involves inactivation of at least one and possibly several tumorsuppressor genes on the long arm of chromosome 13. The fact that neither Rb1 nor BRCA2 appears to be inactivated in the majority of head-and-neck cancers suggests that novel tumor-suppressor genes are involved. We have used microsatellite repeat polymorphisms and PCR to detect several distinct minimal regions of deletion on 13q in supraglottic and oral squamous-cell carcinomas. One region maps to 13q34, the second to 13q14.3 and a potential third region, not reported in previous studies, maps to 13q12.1. Overall, 69% of the 145 tumors examined demonstrated allelic loss at one or more loci on 13q. We investigated whether a novel suppressor candidate mapping to 13q14.3-q21, leukemia-associated gene 1, might also be involved in the progression of squamouscell carcinomas. Multiplexed PCR revealed homozygous deletion of leu1 in one oral cavity tumor. This suggests that this gene or one nearby may be the actual target of deletions in this region of the chromosome arm. Int. J. Cancer (Pred. Oncol.) 84:453-457, 1999. Wiley-Liss, Inc.Deletion of portions of chromosome arm 13q or mutation of genes located on this arm frequently contribute to the development of a wide variety of human cancers, including those of liver (Zhang et al

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