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Infection and Immunity, March 2009, p. 933-934, Vol. 77, No. 3
0019-9567/09/$08.00+0 doi:10.1128/IAI.00046-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
Major Surface Protein LipL32 Is Not Necessary for Leptospira interrogans Growth or VirulenceLeptospira interrogans is responsible for leptospirosis, a zoonosis which occurs worldwide. LipL32 is the major surface protein of pathogenic leptospires. Murray et al. (p. 952-958) constructed a lipL32 mutant. The mutant had no obvious phenotypic defects and, very surprisingly, retained virulence in both acute and chronic models of infection. This finding is remarkable considering the abundance and conservation of LipL32 among all pathogenic Leptospira spp. This raises an intriguing question: why does L. interrogans produce LipL32 at up to 50% of the total cell protein when this protein is unnecessary for in vivo or in vitro growth?
Neutrophils Protect against Bordetella pertussis Infection in Immune Mice but Not in Naïve Mice
Neutrophils are important cells of innate immune defense against bacterial infections. Bordetella pertussis infects the airways and inhibits early neutrophil recruitment through the activity of pertussis toxin (PT) in a mouse model of infection. Andreasen and Carbonetti (p. 1182-1188) show that, surprisingly, neutrophils play little or no role in the protection or clearance of B. pertussis infection in naïve mice, probably because of the overlapping inhibitory activities of PT and adenylate cyclase toxin (ACT) and the absence of opsonizing antibodies. However, in immune mice, the depletion of neutrophils enhanced infection, and the data indicate that neutrophils are the main target cells for ACT, but not for PT, in promoting infection. This work illustrates how virulence factors and immune status can impact a host-pathogen interaction and may help to elucidate the mechanisms of pathogenesis of this potentially fatal disease.
Toxoplasma gondii Infection of NK Cells: a Novel Immunoevasion Strategy?
The obligate intracellular parasite Toxoplasma gondii causes chronic infections in up to one-third of the human population as well as in animals. In the early stages of infection, antigen-presenting cells, such as macrophages and dendritic cells, are infected by the parasite. However, among the lymphocyte population, natural killer (NK) cells are the primary type of infected cell. Persson et al. (p. 970-976) show that infection of NK cells was largely dependent on NK cell-mediated killing of infected antigen-presenting cells. Interestingly, infected NK cells were not sensitive to NK cell fratricide. Therefore, sequestration in NK cells may constitute an immunoevasion strategy utilized by Toxoplasma to avoid clearance.
Proof-of-Principle Study of Nonhuman Primates Predicts Efficacy of a Capsule Conjugate Vaccine against Campylobacter jejuni
Campylobacter jejuni is an encapsulated human enteric pathogen that is also associated with serious sequelae, including Guillain-Barré and irritable bowel syndromes. Monteiro et al. (p. 1128-1136) synthesized two vaccines by conjugation of polysaccharide capsules from strains of C. jejuni to the carrier protein CRM197, and both vaccines elicited robust immune responses in mice. One vaccine, which was used to immunize Aotus nancymaae monkeys, was 100% efficacious against diarrheal disease following challenge with the homologous strain. These data suggest that a multivalent capsule conjugate vaccine could reduce the disease burden caused by C. jejuni.
Leptospira Species Acquire C4b-Binding Protein for Immune Evasion
Leptospira, the causative agent of leptospirosis, is a highly invasive spirochete that efficiently colonizes target organs after penetrating the host. Barbosa et al. (p. 1137-1143) present evidence regarding strategies employed by this pathogen to evade the protective function of the complement system. They show that pathogenic leptospiral strains efficiently acquire C4b-binding protein (C4BP) from human serum, whereas a nonpathogenic strain binds negligible amounts of this complement regulator to its surface. Surface-bound C4BP remains functionally active, since it promotes factor I-mediated cleavage of C4b. This interaction may contribute to the serum resistance of pathogenic leptospiral strains.
NADPH Phagocyte Oxidase Is Essential for Host Defense against Respiratory Acinetobacter baumannii Infection
Multidrug-resistant Acinetobacter baumannii is responsible for an increasing number of cases of nosocomial pneumonia, with high mortality. Yet, host defense mechanisms remain unknown. Using a mouse model of respiratory A. baumannii infection, Qiu et al. (p. 1015-1021) showed that mice deficient in NADPH phagocyte oxidase (gp91phox–/– mice) were 
100-fold-more susceptible to infection than immunocompetent mice and that gp91phox–/– mice suffered uncontrolled bacterial replication and dissemination and 100% mortality. Although gp91phox–/– mice mounted strong inflammatory responses after infection, their neutrophils failed to kill bacteria effectively. Thus, NADPH phagocyte oxidase plays a crucial role in host defense against A. baumannii.
Infection and Immunity, March 2009, p. 933-934, Vol. 77, No. 3
0019-9567/09/$08.00+0 doi:10.1128/IAI.00046-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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