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In this Issue

2014; Elsevier BV; Volume: 7; Issue: 5 Linguagem: Inglês

10.1038/mi.2014.76

1935-3456

Chrissy M. Leopold Wager, Floyd L. Wormley,

Pediatric health and respiratory diseases

Chrissy Leopold Wager and Floyd Wormley Jr discuss the roles of macrophage activation states in fungal infections using Cryptococcus neoformans and Pneumocystis model systems. Disease resolution of these two opportunistic fungal pathogens is linked to classically or alternatively activated macrophages. See page 1023 Ying-Ying Wang and colleagues demonstrate how anti–herpes simplex virus serotype 1 (HSV-1) immunoglobulin G (IgG) acts in mucosal surfaces to trap HSV within mucus, thereby blocking infection. See page 1036 Lisa Korn and co-workers report that conventional CD4+ T cells regulate the number and function of innate lymphoid cells (ILCs), as well as production of the antimicrobial peptides Reg3γ and Reg3β. See page 1045 A study by Kylie Webster and associates shows that interleukin-7 (IL-7) is essential for survival and homeostasis of IL-17-producing natural killer T (NKT) cells. See page 1058 Henry McSorley and colleagues found that secreted products from the nematode Heligmosomoides polygyrus strongly induced interleukin-33 release and inhibited type 2 innate lymphoid cell (ILC2) responses in a model of airway allergy. See page 1068 Rodrigo Guabiraba and colleagues demonstrate that interleukin-33 (IL-33) mediates the severe intestinal mucositis that develops in mice treated with irinotecan (CPT-11), a commonly used cancer chemotherapeutic agent, and that blocking IL-33 attenuates mucosal injury. See page 1079 Rowann Bowcutt and co-workers show the importance of Nod2 signaling in colonic epithelial cells in driving chemokine-mediated dendritic cell (DC) recruitment and T-cell responses following Trichuris muris infection in the colon. See page 1094 Yi Wang and colleagues show that infiltrating neutrophils contribute to colitis-associated tumorigenesis by producing interleukin-1β (IL-1β), which triggers IL-6 production by mononuclear phagocytes. See page 1106 Kondwani Jambo and coauthors observed that during human infection, HIV preferentially infects small alveolar macrophages and impairs their phagocytic function. See page 1116 Raza Zaheer et al. provide evidence for a role of interferonstimulated gene of 15 kD (ISG15) in modulating epithelial cell antiviral immunity during human rhinovirus infection. See page 1127 Findings by Jinyu Zhang and co-workers support a primary role for inflammasome-induced interleukin-1β (IL-1β) production in the development of colitis in IL-10 knockout mice. See page 1139 Annabelle Jayaraman et al. report that interleukin-15 (IL-15) complexes induce natural killer (NK)- and T-cell responses independent of type I interferon signaling during rhinovirus infection. See page 1151 Using ex vivo human ectocervical tissue models, Christiane Rollenhagen and colleagues determined that herpes simplex virus type 2 (HSV-2) infection stimulates HIV-1 replication in cervical tissues. See page 1165 Nipasiri Voraphani and coauthors demonstrate that nitrative stress in airway epithelial cells, which has been associated with severe asthma, is mediated by inducible nitric oxide synthase, dual oxidase-2, and thyroid peroxidase, and is regulated by interferon-γ and interleukin-13. See page 1175 Michelle Manni and colleagues investigated the relationship of airway inflammation to lung function in mice and humans with allergic airway inflammation. They found that lung compliance may be linked with cellular inflammation in the airspace, whereas T cell– driven airway hyperresponsiveness may be associated with tissue inflammation and other pulmonary factors. See page 1186 Lucas Faustino et al. report that resolution of established allergic lung inflammation by chronic allergen administration to mice is due to tumor necrosis factor– related apoptosis-inducing ligand (TRAIL)- mediated apoptosis of lung inflammatory cells. They also show that intranasal TRAIL administration results in increased resolution of T helper type 2 cell– mediated inflammation. See page 1199 Tatiana Akimova and co-workers show that sirtuin-1 is important for induction of Foxp3+ regulatory T cells and can be targeted for treatment of colitis in mouse models. See page 1209 intestinal barrier function Dominique Weber and associates show that junctional adhesion molecule– like protein (JAML) is cleaved from the neutrophil surface during transepithelial migration and can bind to the epithelial tight-junction protein coxsackieadenovirus receptor, resulting in compromised barrier and inhibition of wound repair, through decreased epithelial proliferation. See page 1221 Liyen Loh and co-workers demonstrate that fetal invariant natural killer T (iNKT) cells can differentiate and acquire potent effector functions in utero before the commensal microflora has been established. See page 1233 infection Koji Yamamoto and colleagues determined that anti- CXCL13 antibody can inhibit the formation of gastric lymphoid follicles induced by Helicobacter pylori infection. See page 1244 Wendy Goodman et al. demonstrate that estrogens can induce protection from colitis in SAMP1/YitFc male, but not female, mice. They also found that female mice develop more severe colitis, consistent with a loss of estrogen conditioning. See page 1255 Mary Morgan and colleagues provide data indicating that Toll-like receptor 6 (TLR6) stimulation supports responses by T helper types 1 and 17 cells in the gut-associated lymphoid tissue (GALT). See page 1266 Classical versus alternative macrophage activation: the Ying and the Yang in host defense against pulmonary fungal infectionsMucosal ImmunologyVol. 7Issue 5PreviewMacrophages are innate immune cells that possess unique abilities to polarize toward different phenotypes. Classically activated macrophages are known to have major roles in host defense against various microbial pathogens, including fungi, while alternatively activated macrophages are instrumental in immune-regulation and wound healing. Macrophages in the lungs are often the first responders to pulmonary fungal pathogens, and the macrophage polarization state has the potential to be a deciding factor in disease progression or resolution. Full-Text PDF Open Archive