Colonization by M. catarrhalis is more frequent than is determined by surface culture, because the organism resides both within and beneath the epithelium and invades host cells.

Colonization of the human nasopharynx exposes Moraxella catarrhalis, a common cause of otitis media in children and exacerbations of chronic obstructive pulmonary disease in adults, to sudden downshifts in temperature, occurring when the host breathes cold air. We investigated whether in vitro cold shock influences the expressions of the outer membrane adhesins UspA1 and hemagglutinin, which are considered virulence factors, and of an M. catarrhalis homolog of recA, a housekeeping gene, which in Escherichia coli is induced by cold shock. Quantitative real-time reverse transcriptase PCR was used for measuring mRNA copy number. A screening experiment revealed that a cold shock at 26°C maximally induced the copy number of uspA1. In comparison with 37°C conditions, a 1-hour cold shock at 26°C increased copy numbers of uspA1 and recA by 2.5-fold (11.2 ؎ 1.8 versus 4.5 ؎ 0.8 copies/CFU) and 2.7-fold (0.30 ؎ 0.10 versus 0.11 ؎ 0.06), respectively, but did not induce transcription of hag. Exposure to 26°C increased surface expression of UspA1, as assessed by fluorescence-activated cell sorter analysis, and resulted in a significant increase in adherence of strain O35E to Chang human conjunctival cells (97.1% ؎ 2.0% versus 48.3% ؎ 9.2% at 37°C; P ‫؍‬ 0.01). Cold shock induction of uspA1 and recA was detected in strains belonging to either phylogenetic subpopulation of M. catarrhalis (16S rRNA types 1 and 2/3) and was most pronounced in type 2/3 strains (4-to 25-fold for uspA1), which do not express detectable amounts of UspA1 protein at 37°C. These data indicate that cold shock at a physiologically relevant temperature of 26°C induces the expression of at least one virulence factor (UspA1). To our knowledge, no similar data are available for other nasopharyngeal pathogens.Moraxella catarrhalis is exclusively a pathogen of primates. No other host organisms or environmental reservoirs have been identified (7,35). Intimate adaptation to the primate host is illustrated by, for instance, the specificity of M. catarrhalis transferrin-binding proteins for transferrin of primate origin (14) and by the organism's capacity to grow with iron-loaded human transferrin or lactoferrin as the sole source of iron (9).M. catarrhalis colonizes the mucosal surface of the nasopharynx and causes upper and lower respiratory tract infections (28,35). Colonization rates exceeding 50% in infants and young children (12, 39) indicate efficient person-to-person transmission and successful adaptation to environmental conditions found in the upper respiratory tract. Temperature is one of the key environmental variables with which microorganisms are confronted. Temperature determines molecular dynamics and diffusion rates, enzyme kinetics, and secondary structures of macromolecules and is thus a fundamental determinant of cellular function (40). Despite its close association with a single colonization site in a single warm-blooded host, M. catarrhalis is exposed to brisk fluctuations of temperature. Breathing cold air reduces nasopharyngeal temperature...

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The antiinflammatory agent curcumin (diferuloylmethane) has a potential to mitigate cancer therapy-induced mucositis. We assessed the in vitro extent of its bactericidal activity and determined the kinetics of its antiinflammatory effect on pharyngeal cells. Bactericidal activity was assessed using the LIVE/DEAD® Kit after 4 h of exposure to curcumin (50-200 μM) in 18 oropharyngeal species commonly associated with bacteremia in febrile neutropenia. Moraxella catarrhalis or its outer membrane vesicles were used to determine the inhibitory effect of curcumin on bacteria-induced proinflammatory activity as determined by cytokine release into the supernatant of Detroit 562 pharyngeal cells using the Luminex® xMAP® technology. Curcumin exerted a concentration-dependent bactericidal effect on all 18 species tested. After 4 h at 200 μM, 12 species tested were completely killed. Preincubation of Detroit cells with 200 μM curcumin for 5 to 60 min resulted in complete suppression of the release of tumor necrosis factor-α, interleukin (IL)-6, IL-8, monocyte chemoattractant protein 1, granulocyte macrophage-colony stimulating factor, and vascular endothelial growth factor. Fibroblast growth factor-2 and interferon-γ were not affected. Repetitive exposure to curcumin resulted in repetitive suppression of cytokine/chemokine expression lasting from 4 to 6 h. Through reduction of oral microbial density as well as suppression of inflammation cascades curcumin may prevent cancer therapy-induced oral mucositis, e.g., when applied as multiple daily mouth washes.