Labor resembles an inflammatory response that includes secretion of cytokines/chemokines by resident and infiltrating immune cells into reproductive tissues and the maternal/fetal interface. Untimely activation of these inflammatory pathways leads to preterm labor, which can result in preterm birth. Preterm birth is a major determinant of neonatal mortality and morbidity; therefore, the elucidation of the process of labor at a cellular and molecular level is essential for understanding the pathophysiology of preterm labor. Here, we summarize the role of innate and adaptive immune cells in the physiological or pathological activation of labor. We review published literature regarding the role of innate and adaptive immune cells in the cervix, myometrium, fetal membranes, decidua and the fetus in late pregnancy and labor at term and preterm. Accumulating evidence suggests that innate immune cells (neutrophils, macrophages and mast cells) mediate the process of labor by releasing pro-inflammatory factors such as cytokines, chemokines and matrix metalloproteinases. Adaptive immune cells (T-cell subsets and B cells) participate in the maintenance of fetomaternal tolerance during pregnancy, and an alteration in their function or abundance may lead to labor at term or preterm. Also, immune cells that bridge the innate and adaptive immune systems (natural killer T (NKT) cells and dendritic cells (DCs)) seem to participate in the pathophysiology of preterm labor. In conclusion, a balance between innate and adaptive immune cells is required in order to sustain pregnancy; an alteration of this balance will lead to labor at term or preterm.

Soil fungi play a major role in terrestrial ecosystem functioning through interactions with soil structure, plants, micro-and mesofauna, and nutrient cycling through predation, pathogenesis, mutualistic, and saprotrophic roles. The diversity of soil fungi was assessed by sequencing their 28S rRNA gene in Alaskan permafrost and Oklahoma tallgrass prairie soils at experimental sites where the effect of climate warming is under investigation. A total of 226,695 reads were classified into 1,063 genera, covering 62% of the reference data set. Using the Bayesian Classifier offered by the Ribosomal Database Project (RDP) with 50% bootstrapping classification confidence, approximately 70% of sequences were returned as "unclassified" at the genus level, although the majority (ϳ65%) were classified at the class level, which provided insight into these lesser-known fungal lineages. Those unclassified at the genus level were subjected to BLAST analysis against the ARB-SILVA database, where ϳ50% most closely matched nonfungal taxa. Compared to the more abundant sequences, a higher proportion of rare operational taxonomic units (OTU) were successfully classified to genera at 50% bootstrap confidence, indicating that the fungal rare biosphere in these sites is not composed of sequencing artifacts. There was no significant effect after 1 year of warming on the fungal community structure at both sites, except perhaps for a few minor members, but there was a significant effect of sample depth in the permafrost soils. Despite overall significant community structure differences driven by variations in OTU dominance, the prairie and permafrost soils shared 90% and 63% of all fungal sequences, respectively, indicating a fungal "seed bank" common between both sites.

Objective: Maternal-fetal tolerance involves a tight balance between the innate and adaptive immunity, which avoids rejection of the semi-allogeneic embryo. The innate and adaptive limbs of the immune response are bridged by iNKT cells; therefore, we hypothesized that an alteration in their number and/or activation breaks maternal-fetal tolerance, leading to premature delivery. Methods: Pregnant mice were injected on E16.5 with either α-galactosylceramide (an iNKT activator; 2 μg) or PBS as a control (n=19 each). Gestational length and the rates of stillbirth and long-term pup survival were recorded. Peripheral blood, decidua, liver, spleen and lymph nodes were collected just prior to delivery from additional treated and control mice (n=8-9 each). In tissue cell suspensions, iNKT phenotype and activation were analyzed by flow cytometry. Results: 1) iNKT activator treatment promoted premature delivery (E18.09±0.60; controls delivered on E19.51±0.78); 2) iNKT activator treatment increased the rate of stillbirth (63.63 vs. 21.94%); 3) iNKT activator treatment did not reduce long-term pup survival; 4) iNKT activator treatment caused an expansion of iNKT cells (CD1d tetramer+NK1.1+CD49b+) in peripheral blood, liver and decidua, but not in spleen and lymph nodes; 5) iNKT cell activation was unchanged by iNKT activator treatment. Conclusion: Treatment with α-galactosylceramide causes an expansion of systemic and local iNKT cells leading to premature delivery in mice.

Objective: Endotoxin treatment causes preterm delivery in mice, and this is associated with an expansion of regulatory T cells (Tregs) in primary lymphoid organs (Arenas-Hernandez et al. unpublished data). Our aim was to determine whether this expansion causes a pro-inflammatory state and/or macrophage M2-M1 polarization at the maternal-fetal interface. Methods: Pregnant C57BL/6 mice were injected with either 15 μg of LPS (E. coli 0111:B4) or 200 μl PBS as a control (n=9-11 each). Mice were euthanized just prior to preterm delivery. Uterine and decidual cell suspensions were prepared and analyzed by flow cytometry to identify CD4+ and CD8+ Tregs, Th9 cells, Th17 cells, T-bet+ T cells, neutrophils, macrophages, IL4- and IFNγ-producing T cells, and M1 and M2 macrophages. Results: 1) Uterine, but not decidual, CD4+ Tregs were fewer in LPS treated mice than in controls (p=0.019); 2) Uterine and decidual macrophages were fewer in LPS treated mice than in controls (p=0.025 and 0.036); 3) Uterine and decidual neutrophils were greater in LPS treated mice than in controls (p=0.002 and 0.0001); 4) Decidual IFNγ-producing T cells were fewer in LPS treated mice than in controls (p=0.036); 5) M1 and M2 macrophage populations did not change with LPS treatment. Conclusions: Endotoxin treatment of pregnant mice promotes a pro-inflammatory stage, which includes abundant neutrophils and scarce regulatory T cells and macrophages (M1 and M2) at the maternal-fetal interface.