Source: http://www.asmscience.org/content/concept/Entity/ASM/Microbiology/Cell_and_Molecular_Microbiology/Proteins/Complement_System?page=4
Timestamp: 2019-04-18 20:40:49+00:00

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The low frequency of symptomatic cryptococcal infections, despite the presumably high frequency of exposure, suggests that physical barriers and nonspecific immunity provide adequate defenses to protect the host against infection. This chapter describes physical barriers such as skin, nasal passages, and eye, and humoral and cellular nonspecific defense mechanisms such as polymorphonuclear cells (PMNs), natural killer (NK) cells and macrophages that are believed to provide the first line of defense against cryptococcal infection. Antibody-mediated phagocytosis occurs through Fc receptors, which are constitutively expressed in macrophages, but it should be emphasized that opsonic capsule-binding antibody is not consistently present during human and animal infections. In human macrophages, complement-mediated binding is an energy-dependent process that requires three C3 complement receptors (CR1, CR3, and CR4) and actin but does not necessarily lead to phagocytosis. In summary, there is considerable evidence that macrophages from patients with AIDS are less effective against Cryptococcus neoformans than are those from HIV-seronegative individuals. The relative importance of oxidative and nonoxidative antimicrobial mechanisms of host effector cells in inhibiting and killing C. neoformans is uncertain. In vivo, it is likely that the oxidative and nonoxidative antimicrobial mechanisms cooperate to produce the antifungal effects described for host effector cells.
This chapter focuses on the different molecular mechanisms two model luminous bacteria, Vibrio fischeri (a symbiont) and V. harveyi (a free-living microbe), use for regulating lux expression. Expression of luminescence in most bacteria is tightly regulated by the density of the population. In V. fischeri, the regulatory genes involved in density-dependent control of luminescence are adjacent to the luxCDABEG operon encoding the luciferase enzymes. The regulatory genes that control luminescence in V. harveyi are different from those of V. fischeri. One complementation group of V. harveyi dim mutants could be restored to full light production by a family of recombinant cosmids containing a subset of common restriction fragments. Initial HAI-1 and HAI-2 signal recognition by LuxN and LuxQ could activate a series of phosphotransfer reactions. Two-component circuits have been characterized in which a single protein contains both a sensor kinase and a response regulator domain (similar to LuxN and LuxQ) and a second protein contains both a response regulator domain and a DNA binding motif (similar to LuxO). The differences between the regulatory circuits controlling density-dependent expression of luminescence in V. fischeri and V. harveyi are striking. Subsequent mutations and gene duplications and rearrangements generated new and multiple autoinducers, receptivities, and regulatory connections, finally resulting in a bacterium with the properties of V. harveyi.

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