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Background   Moraxella catarrhalis , a major nasopharyngeal pathogen of the human respiratory tract, is exposed to rapid downshifts of environmental temperature when humans breathe cold air. It was previously shown that the prevalence of pharyngeal colonization and respiratory tract infections caused by  M. catarrhalis  are greatest in winter. The aim of this study was to investigate how  M. catarrhalis  uses the physiologic exposure to cold air to upregulate pivotal survival systems in the pharynx that may contribute to  M. catarrhalis  virulence.    Results  A 26°C cold shock induces the expression of genes involved in transferrin and lactoferrin acquisition, and enhances binding of these proteins on the surface of  M. catarrhalis . Exposure of  M. catarrhalis  to 26°C upregulates the expression of UspA2, a major outer membrane protein involved in serum resistance, leading to improved binding of vitronectin which neutralizes the lethal effect of human complement. In contrast, cold shock decreases the expression of Hemagglutinin, a major adhesin, which mediates B cell response, and reduces immunoglobulin D-binding on the surface of  M. catarrhalis .    Conclusion  Cold shock of  M. catarrhalis  induces the expression of genes involved in iron acquisition, serum resistance and immune evasion. Thus, cold shock at a physiologically relevant temperature of 26°C induces in  M. catarrhalis  a complex of adaptive mechanisms that enables the bacterium to target their host cellular receptors or soluble effectors and may contribute to enhanced growth, colonization and virulence.

Physiologic cold shock of Moraxella catarrhalisaffects the expression of genes involved in the iron acquisition, serum resistance and immune evasion