Infection and Immunity, April 2007, p. 1543-1544, Vol. 75, No. 4
0019-9567/07/$08.00+0 doi:10.1128/IAI.00242-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
Neutrophils Enhance the Lethality of Serotype 8 Pneumococcal Pneumonia in MiceNeutrophils are considered to be the key cells in host defense against pneumococcal pneumonia. However, neutrophils can also damage host tissues in the course of inflammatory responses. Marks et al. (p. 1586-1597) investigated the effect of peripheral neutrophil depletion on the pathogenesis of lethal serotype 8 pneumococcal pneumonia in mice. They found that neutropenia enhanced mouse survival without affecting lung bacterial clearance and was associated with the formation of unique lung inflammatory lesions, with markedly decreased apoptosis compared to that in controls. These findings suggest that the long held view that neutrophils are essential for host defense against pneumococcal pneumonia may require reexamination.
Parasites and AIDS Virus Coinfection in a Primate Model: Double Jeopardy
Helminth infections induce a T helper type 2 (Th2) immune environment and have been suggested to accelerate immunodeficiency virus replication. Ayash-Rashkovsky et al. (p. 1751-1756) demonstrate that when rhesus monkeys with chronic, stable R5 simian-human immunodeficiency virus clade C infection are coinfected with Schistosoma mansoni, viral RNA levels peak coincident with the acute phase of schistosomiasis, which is characterized by elevated interleukin-4 mRNA levels and eosinophilia. With resolution of these Th2-type responses, viral RNA loads return to control levels. These results strengthen the argument for treating helminth infections in human immunodeficiency virus type 1-positive persons.
Pertussis Toxin Targets Airway Macrophages To Promote Bordetella pertussis Respiratory Infection
The role of pertussis toxin (PT) in Bordetella pertussis infection has been enigmatic. Using a mouse respiratory infection model, Carbonetti et al. (p. 1713-1720) provide evidence that airway macrophages (AM) are the primary target for PT. When mice were depleted of AM, a PT-deficient mutant strain achieved the same high level of infection as the wild-type strain, and PT caused a long-lived modification of target G proteins in AM recovered from treated mice. Understanding the role of PT in pertussis infection may lead to novel therapies to combat this increasingly reported disease.
Native Flora of Drosophila melanogaster and Its Use To Study Gastrointestinal Tract Colonization
Progress in understanding microbe-microbe and microbe-host interactions in the gastrointestinal (GI) tract has been hampered by the complexity of the GI tract consortium and because of age, diet, and genetics-based animal-to-animal variation. Cox and Gilmore (p. 1565-1576) characterized the native flora of laboratory-reared Drosophila and Drosophila captured from the wild. It was found that the Drosophila GI tract consortium is only 1/10 as complex at that of humans. Moreover, enterococci were an invariant part of the native GI tract consortium of Drosophila, with the leading species being Enterococcus faecalis. Drosophila was reassociated, via feeding, with isogenic enterococcus strains that varied in expression of the E. faecalis cytolysin toxin. Cytolytic E. faecalis, when acquired orally, led to a significant increase in mortality.
Chronic Helminth Infection Induces Programmed Cell Death of the Intestinal Epithelium
Over 1 billion people harbor chronic intestinal nematode infection, although little is known about how the host responds to infection. Often thought of as benign, gut-dwelling helminths cause dysregulation of the intestinal epithelium, primarily through an immune response-driven elevation in proliferation. Cliffe et al. (p. 1556-1564) demonstrate that infection also induces increased apoptosis within the stem cell compartment of the gut, which is a consequence of the immune response rather than direct damage by the worm. In this way, apoptosis induction acts as a homeostatic regulator, curbing the severity of hyperplasia. This phenomenon is ultimately of benefit to both parasite and host.
Cystic Fibrosis Transmembrane Conductance Regulator-Dependent Rapid Release of Interleukin-1 from Airway Epithelia Mediates NF-
B Nuclear Translocation and Effective Innate Immunity to Pseudomonas aeruginosa
Pseudomonas aeruginosa clearance from lungs is impaired in cystic fibrosis (CF) due to lack of a functional CF transmembrane conductance regulator (CFTR). CFTR binds to this pathogen, initiating effective innate immunity. To understand how bacterium-CFTR interactions activate innate immunity, Reiniger et al. (p. 1598-1608) determined that both MyD88-deficient and interleukin-1 receptor (IL-1R)-deficient mice failed to rapidly translocate NF-B to nuclei in response to P. aeruginosa, whereas Toll-like receptors 2, 4, and 5 were not involved. Wild-type CFTR was needed for rapid release of IL-1ß. Chronic P. aeruginosa lung infections, mimicking the early stages of disease and analogous to those achievable in CFTR-deficient mice, could be established in IL-1R knockout mice. Rapid release of IL-1 and signaling through IL-1R and MyD-88 are key steps in the CFTR-dependent innate immune response to P. aeruginosa infection.
Infection and Immunity, April 2007, p. 1543-1544, Vol. 75, No. 4
0019-9567/07/$08.00+0 doi:10.1128/IAI.00242-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
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