Antimicrobial Peptides Protect against Ocular Fungal Infection
Complications of ocular trauma and contact lens wear include vision-threatening corneal infection (microbial keratitis), which may be caused by various pathogens, including fungi. Antimicrobial peptides (AMPs) are endogenous, multifunctional molecules with antimicrobial activity and immunomodulatory effects. Kolar et al. (p. 2669–2677) use knockout and knockdown mice to investigate the role of AMPs in defense against keratitis caused by Fusarium solani. They show that murine β-defensins 3 and 4 and cathelicidin CRAMP play a vital role in attenuating disease severity. This discovery raises the possibility of using AMPs as therapeutics for fungal keratitis.
Haemophilus ducreyi Infection Induces Inflammasome Activation in Nonpolarized Human Macrophages
Recognition of microbial infection by pattern recognition receptors leads to inflammasome formation, which activates caspase-1 and leads to cleavage and secretion of interleukin-1 beta (IL-1β). Inflammasome activation helps control bacterial pathogens but also can contribute to immunopathology. Li et al. (p. 2997–3008) demonstrate that Haemophilus ducreyi infection enhances expression of inflammasome-related transcripts in experimentally infected human skin. H. ducreyi induces NLRP3 inflammasome-dependent IL-1β secretion in nonpolarized monocyte-derived macrophages (MDM) but not in classically activated or alternatively activated MDM. Since lesional macrophages express markers of classically activated or alternatively activated polarization, macrophage heterogeneity may modulate inflammasome activation at sites of human infection.
Perforin-2 Kills Chlamydia trachomatis in Macrophages but Is Suppressed in Epithelial Cells
In the molecular arsenal of host immunity, the putative pore former perforin-2 has recently been described as an ancient and effective component of innate resistance to bacterial infection (R. McCormack, L. R. de Armas, M. Shiratsuchi, J. E. Ramos, and E. R. Podack, J. Innate Immun. 5:185–194, 2013). Like other successful pathogens, Chlamydia trachomatis must contend with perforin-2 to cause disease. Fields et al. (p. 3045–3054) report that while chlamydiae are susceptible to perforin-2-mediated killing in professional phagocytes, resistance in epithelial cells is achieved by active suppression of perforin-2 expression. These findings correlate with productive infection of cell types and suggest a newly appreciated paradigm in the host response to bacterial invaders.
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