Goblet Cell Depletion: CD4+ T Cells Protect against Citrobacter rodentium Infection by Modulating the Phenotype and Turnover of the Intestinal Epithelium
Rapid turnover and dramatic reorganization of the intestinal epithelium are observed in many gastrointestinal diseases. Infection of mice with Citrobacter rodentium increases intestinal epithelial cell (IEC) proliferation and causes widespread goblet cell depletion, but the underlying mechanisms and impact on host defense are unknown. Adoptive transfer experiments by Chan et al. (p. 4649–4658) demonstrate that CD4+ T cells and gamma interferon are essential in driving goblet cell depletion and IEC proliferation while reducing mortality in infected mice. The importance of this response suggests that immunomodulation of goblet cell numbers, mucus secretion, and IEC turnover may reflect a generalized host response against mucosal pathogens.
Knock, Knock, Who's There? Staphylococcus aureus Biofilms Discriminate between Leukocyte Subsets To Alter Their Transcriptional Profiles
Staphylococcus aureus frequently establishes biofilms on native tissues and medical devices. Recent studies demonstrate that S. aureus biofilms skew innate immune responses to subvert clearance; however, the specific changes occurring within S. aureus biofilms after leukocyte exposure remain unknown. Utilizing transcriptional profiling, Scherr et al. (p. 4363–4376) identify genes differentially expressed in S. aureus biofilms following macrophage or neutrophil exposure. Interestingly, macrophages induce global suppression of the biofilm transcriptome whereas minimal changes result from neutrophil challenge. This suggests that S. aureus biofilms differentially modify their transcriptional profile in response to distinct leukocyte subsets, presumably to avoid detection and promote biofilm persistence.
Mitochondrial Protein Fus1 Highlights a Crucial Role of Mitochondria in the Antibacterial Defense
Recent studies suggest that mitochondria may facilitate antibacterial immunity by generating reactive oxygen species (ROS) and contribute to the activation of neutrophils and macrophages following cellular damage and stress. Consistent with these novel mitochondrial roles, Hood et al. (p. 4461–4469) show that loss of the regulator of mitochondrial homeostasis Fus1 results in significantly increased resistance of mice to Acinetobacter baumannii pneumonia due to earlier and robust recruitment of neutrophils and macrophages to the lungs and more-rapid bacterial clearance. Mechanisms of such resistance include early activation of molecular proinflammatory pathways due to increased mitochondrial ROS and membrane potential, highlighting a crucial role of mitochondria in systemic antibacterial response.
Effective Population Size Limits Within-Host Selection of Streptococcus pneumoniae
Antimicrobials and host immunity exert selection on the population of pneumococci colonizing the nasopharynx. The dynamics of selection will be influenced by the effective population size (Ne) of the selected population, which affects the relative role of stochastic versus selective factors in changing variant frequencies. Li et al. (p. 4534–4543) determine pneumococcal Ne during mouse colonization and find it is much smaller than the census population. Their mathematical model explains the observed Ne patterns, predicts that selection coefficients may be difficult to measure in vivo, and suggests that noise in the outcome of competition experiments may be unavoidable.
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- Goblet Cell Depletion: CD4+ T Cells Protect against Citrobacter rodentium Infection by Modulating the Phenotype and Turnover of the Intestinal Epithelium
- Knock, Knock, Who's There? Staphylococcus aureus Biofilms Discriminate between Leukocyte Subsets To Alter Their Transcriptional Profiles
- Mitochondrial Protein Fus1 Highlights a Crucial Role of Mitochondria in the Antibacterial Defense
- Effective Population Size Limits Within-Host Selection of Streptococcus pneumoniae
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