Phosphamide-Based Washing-Durable Flame Retardant for Cotton Fabrics.

A formaldehyde-free reactive flame retardant, an ammonium salt of triethylenetetramine phosphoryl dimethyl ester phosphamide phosphoric acid (ATPEPDPA), was synthesized and characterized using nuclear magnetic resonance (NMR). Fourier transform infrared spectroscopy test (FT-IR), durability test and scanning electron microscopy (SEM) results suggested that ATPEPDPA was successfully grafted on cotton fabrics through a -N-P(=O)-O-C covalent bond. Moreover, the limiting oxygen index (LOI) value of 20 wt% ATPEPDPA-treated cotton was 44.6%, which met stringent washing standard after 50 laundering cycles (LCs). The high washing resistance of the ATPEPDPA-treated cotton was due to the p-π conjugation between the N atom and the P(=O) group in the flame-retardant molecule, which strengthened the stability of the -N-P(=O)-O-C bonds between ATPEPDPA and cellulose, and the -N-P(=O)-(O-CH3)2 groups in the ATPEPDPA. The cone calorimetric test showed that the treated cotton had excellent flame retardance. In addition, the TG and TG-IR tests suggested that ATPEPDPA performed a condensed flame retardance mechanism. Furthermore, the physical properties and hand feel of the treated cotton were well maintained. These results suggested that introducing -N-P(=O)-(O-CH3)2 and -N-P(=O)-(ONH4)2 groups into ATPEPDPA could significantly increase the fire resistance and durability of cotton fabrics.

Evaluating the fire resistance and durability of cotton textiles treated with a phosphoramide phosphorus ester phosphate ammonium flame retardant.

The phosphoramide phosphorus ester phosphate ammonium (PPEPA) flame retardant was synthesized by phosphorus oxychloride and ethanolamine, and its structure was characterized by nuclear magnetic resonance and Fourier transform infrared spectroscopy (FTIR). Cotton textiles treated with 20 wt% PPEPA (CT-PPEPA3) would have high durability and flame retardance. The limiting oxygen index (LOI) of CT-PPEPA3 was found to be 46.5 %, while after undergoing 50 laundering cycles (LCs) following the AATCC 61-2013 3 A standard, the LOI only decreased to 31.4 %. Scanning electron microscopy and X-ray diffraction analyses suggested the penetration of PPEPA molecules into the interior of cotton fibers, resulting in a minor alteration of the cellulose crystal structure. The excellent durability, FTIR, and energy-dispersive X-ray of CT-PPEPA3 provided evidence for the formation of -N-P(=O)-O-C- and -O-P(=O)-O-C- covalent bonds between the PPEPA molecules and cellulose. The -N-P(=O)-O-C- bond exhibited a p-π conjugation effect, leading to enhanced stability and improved durability of the flame-retardant cotton textiles. Vertical flame, thermogravimetric, and cone calorimetry tests demonstrated that the CT-PPEPA3 underwent condensed-phase and synergistic flame retardation. Additionally, these finished cotton textiles retained adequate breaking strength and softness, making them suitable for various applications. In conclusion, the incorporation of the -N-P(=O)-ONH4 group into the phosphorus ester phosphate ammonium flame retardant demonstrated effective enhancement of the fire resistance and durability of treated cotton textiles.

Formaldehyde-free and durable phosphorus-containing cotton flame retardant with -N=P-(N)3- and reactive ammonium phosphoric acid groups.

A flame retardant (FR) hexachlorocyclotriphosphazene diethylenetriamine ammonium phosphoric acid (HDAPA) was synthesized. Vertical flammability test and limiting oxygen index (LOI) results showed that cotton samples finished with HDAPA solutions (15 % and 20 %) could pass vertical flame retardancy test, and LOIs reached 30.1 % and 35.4 % even after 50 laundering cycles according to AATCC 61-2013 3A washing standard (3A), performing flame retardancy and washing durability. Meanwhile, Fourier transform infrared and X-ray photoelectron spectroscopy analyses suggested that HDAPA was grafted on cotton fibers through -P(=O)-O-C covalent bond. Total heat release (1.98 MJ/m2) and char residue (16.2 %) of HDAPA treated cotton were much lower than those (4.26 MJ/m2, 3.2 %) of untreated cotton. Thermogravimetry results showed HDAPA changed thermal decomposition pathway of cotton fabric, which was further supported by thermogravimetric-Fourier infrared spectrometer results, revealing HDAPA performed a condensed phase flame retardancy mechanism. Scanning electron microscopy implied HDAPA entered amorphous region of cotton fibers to react with cellulose. Mechanical properties of HDAPA treated cotton decreased a little. Although the synthesis process used formaldehyde but no free formaldehyde released. In consequence, the aforementioned results indicated that the introduction of -N=P-(N)3- and -P(=O)(O-NH4+)2 groups to FR was an viable method to improve flame retardancy and durability.

A cationic, durable, P/N-containing starch-based flame retardant for cotton fabrics.

A cationic, durable flame retardant for cotton fabrics, 6-(2-(dimethoxy phosphoryl)-2-(trimethyl ammonium)) methoxy-2-methoxy-polysaccharide ammonium phosphate (DTPAP), was synthesized. Its structure was verified by NMR and FTIR spectroscopy. According to the FTIR spectra and X-ray photoelectron spectroscopy (XPS), DTPAP formed P(=O)-O-C bonds with cellulose molecules and firmly grafted to cotton fabrics, giving the fabric a high durability. DTPAP-25-treated fabrics passed the vertical flame test (VFT), and the limiting oxygen index (LOI) was 43.9 %. After 50 laundering cycles (LCs), the DTPAP-25-treated fabrics had an LOI of 29.9 %, passed the VFT, and retained their flame retardancy. EDS data showed that, compared with engrafted cationic ammonium phosphate flame retardants, the DTPAP-treated fabrics contained fewer metal ions. Cone calorimetry data showed that DTPAP-25-treated fabrics did not display concentrated heat release. The results suggested that DTPAP exhibited a condensed-phase flame retardant mechanism, and the introduction of cations into the ammonium phosphate flame retardant reduced ion exchange, which improved the durability.

Synthesis and evaluation of an eco-friendly and durable flame-retardant cotton fabrics based on a high-phosphorous-content.

Cotton fabrics are extremely flammable. Therefore, ammonium salt of dipentaerythritol hexaphosphoric acid (ADPHPA), a novel reactive phosphorus flame retardant without halogen and formaldehyde, was synthesized by solvent-free synthesis method. Surface chemical graft modification was chosen to introduce flame retardant, imparting its flame retardancy and washability. SEM indicated that ADPHPA entered the interior of cotton fiber, which was grafted with OH of control cotton fabrics (CCF) by forming POC covalent bonds to obtain treated cotton fabrics (TCF). There were no apparent differences in the fiber morphology and crystal structure after treatment according to SEM and XRD analysis. TG analysis demonstrated that the decomposition process of TCF was changed compared with CCF, while lower heat release rate and total heat release of TCF indicated its combustion efficiency was also reduced based on cone calorimetry test. Meanwhile, in the durability test, TCF had undergone 50 laundering cycles (LCs) in accordance with AATCC-61-2013 3A standard and had a short vertical combustion charcoal length, which were able to be regard as durable flame-retardant fabrics. The mechanical properties of TCF decreased to a degree, but did not affect the actual use of cotton fabrics. Taken as a whole, ADPHPA has research significance and development potential as a durable phosphorus-based flame retardant.

A novel polymer reactive flame retardant for the preparation of highly durable cotton fabrics.

A novel polymer ammonium salt of polyethyleneimine phosphate phosphonic acid (APEMPPA) flame retardant for cotton fabrics was synthesized and characterized by nuclear magnetic resonance (NMR), in which some ammonium phosphoric acid groups were replaced by phosphate ester groups to decrease the phenomena that the ammonium ions in flame retardant would exchange with metal ions such as Ca2+ and Mg2+ in washing water to keep flame retardance well after washing. Energy dispersive X-ray (EDX), Fourier transform infrared spectroscopy (FTIR) results, and durability of treated cotton fabrics suggested that APEMPPA was grafted onto the cellulose. Limiting oxygen index (LOI) of 40 wt% APEMPPA-treated cotton fabric was 44.5 %, which was still 34.7 % after 50 LCs according to AATCC 61-2013 3A standard. Cone calorimetric and thermogravimetric (TG) results showed the treated cotton fabrics had excellent flame retardancy. TG-FTIR and Raman test results proposed that APEMPPA mainly played a condensed phase flame retardant. EDX results indicated that replacing some ammonium phosphate groups with phosphate ester groups was effective in maintaining flame retardancy during washing. All results showed that increasing the molecular weight and introducing phosphonate group in ammonium phosphorus acid flame retardant can effectively improve flame retardancy and durability. APEMPPA-treated cotton fabrics maintained good tensile strength.

GATA1 controls numbers of hematopoietic progenitors and their response to autoimmune neuroinflammation.

GATA-binding factor 1 (GATA1) is a transcription factor that governs the development and function of multiple hematopoietic cell lineages. GATA1 is expressed in hematopoietic stem and progenitor cells (HSPCs) and is essential for erythroid lineage commitment; however, whether it plays a role in hematopoietic stem cell (HSC) biology and the development of myeloid cells, and what that role might be, remains unclear. We initially set out to test the role of eosinophils in experimental autoimmune encephalomyelitis (EAE), a model of central nervous system autoimmunity, using mice lacking a double GATA-site (ΔdblGATA), which lacks eosinophils due to the deletion of the dblGATA enhancer to Gata1, which alters its expression. ΔdblGATA mice were resistant to EAE, but not because of a lack of eosinophils, suggesting that these mice have an additional defect. ΔdblGATA mice with EAE had fewer inflammatory myeloid cells than the control mice, suggesting that resistance to EAE is caused by a defect in myeloid cells. Naïve ΔdblGATA mice also showed reduced frequency of CD11b+ myeloid cells in the blood, indicating a defect in myeloid cell production. Examination of HSPCs revealed fewer HSCs and myeloid cell progenitors in the ΔdblGATA bone marrow (BM), and competitive BM chimera experiments showed a reduced capacity of the ΔdblGATA BM to reconstitute immune cells, suggesting that reduced numbers of ΔdblGATA HSPCs cause a functional deficit during inflammation. Taken together, our data show that GATA1 regulates the number of HSPCs and that reduced GATA1 expression due to dblGATA deletion results in a diminished immune response following the inflammatory challenge.

A bio-based macromolecular phosphorus-containing active cotton flame retardant synthesized from starch.

A novel phosphorus-containing flame retardant, ammonium starch phosphate (ASTP) based on biomass starch, was synthesized for cotton fabrics, and its structure was characterized by 1D and 2D NMR. The limiting oxygen index (LOI) of the cotton fabric treated with 30 % ASTP reached 45.2 %, and the LOI remained at 32.1 % after 50 laundry cycles, indicating that the cotton fabrics treated with ASTP had a high flame retardancy and semi-permanent wash durability. The semi-permanent wash durability, Fourier transform infrared spectroscopy (FT-IR) and the SEM results suggested ASTP was grafted on the surface of cotton fibers by P-O-C covalent bonds. Vertical flammability, the thermogravimetry (TG) and cone calorimetry results showed that the cotton fabrics treated with ASTP had excellent flame retardancy. There were some reductions in the physical properties of the treated cotton fabric. Overall, these results suggested that starch can replace polyhydric alcohols to prepare a more durable formaldehyde-free P-based flame retardants.

SIRT1 inactivation switches reactive astrocytes to an antiinflammatory phenotype in CNS autoimmunity.

Astrocytes are highly heterogeneous in their phenotype and function, which contributes to CNS disease, repair, and aging; however, the molecular mechanism of their functional states remains largely unknown. Here, we show that activation of sirtuin 1 (SIRT1), a protein deacetylase, played an important role in the detrimental actions of reactive astrocytes, whereas its inactivation conferred these cells with antiinflammatory functions that inhibited the production of proinflammatory mediators by myeloid cells and microglia and promoted the differentiation of oligodendrocyte progenitor cells. Mice with astrocyte-specific Sirt1 knockout (Sirt1-/-) had suppressed progression of experimental autoimmune encephalomyelitis (EAE), an animal model of CNS inflammatory demyelinating disease. Ongoing EAE was also suppressed when Sirt1 expression in astrocytes was diminished by a CRISPR/Cas vector, resulting in reduced demyelination, decreased numbers of T cells, and an increased rate of IL-10-producing macrophages and microglia in the CNS, whereas the peripheral immune response remained unaffected. Mechanistically, Sirt1-/- astrocytes expressed a range of nuclear factor erythroid-derived 2-like 2 (Nfe2l2) target genes, and Nfe2l2 deficiency shifted the beneficial action of Sirt1-/- astrocytes to a detrimental one. These findings identify an approach for switching the functional state of reactive astrocytes that will facilitate the development of astrocyte-targeting therapies for inflammatory neurodegenerative diseases such as multiple sclerosis.

Transcription Factor RUNX3 Mediates Plasticity of ThGM Cells Toward Th1 Phenotype.

GM-CSF-producing T helper (Th) cells play a crucial role in the pathogenesis of autoimmune diseases such as multiple sclerosis (MS). Recent studies have identified a distinct population of GM-CSF-producing Th cells, named ThGM cells, that also express cytokines TNF, IL-2, and IL-3, but lack expression of master transcription factors (TF) and signature cytokines of commonly recognized Th cell lineages. ThGM cells are highly encephalitogenic in a mouse model of MS, experimental autoimmune encephalomyelitis (EAE). Similar to Th17 cells, in response to IL-12, ThGM cells upregulate expression of T-bet and IFN-γ and switch their phenotype to Th1. Here we show that in addition to T-bet, TF RUNX3 also contributes to the Th1 switch of ThGM cells. T-bet-deficient ThGM cells in the CNS of mice with EAE had low expression of RUNX3, and knockdown of RUNX3 expression in ThGM cells abrogated the Th1-inducing effect of IL-12. Comparison of ThGM and Th1 cell transcriptomes showed that ThGM cells expressed a set of TFs known to inhibit the development of other Th lineages. Lack of expression of lineage-specific cytokines and TFs by ThGM cells, together with expression of TFs that inhibit the development of other Th lineages, suggests that ThGM cells are a non-polarized subset of Th cells with lineage characteristics.

CSF-1 maintains pathogenic but not homeostatic myeloid cells in the central nervous system during autoimmune neuroinflammation.

The receptor for colony stimulating factor 1 (CSF-1R) is important for the survival and function of myeloid cells that mediate pathology during experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). CSF-1 and IL-34, the ligands of CSF-1R, have similar bioactivities but distinct tissue and context-dependent expression patterns, suggesting that they have different roles. This could be the case in EAE, given that CSF-1 expression is up-regulated in the CNS, while IL-34 remains constitutively expressed. We found that targeting CSF-1 with neutralizing antibody halted ongoing EAE, with efficacy superior to CSF-1R inhibitor BLZ945, whereas IL-34 neutralization had no effect, suggesting that pathogenic myeloid cells were maintained by CSF-1. Both anti­CSF-1 and BLZ945 treatment greatly reduced the number of monocyte-derived cells and microglia in the CNS. However, anti­CSF-1 selectively depleted inflammatory microglia and monocytes in inflamed CNS areas, whereas BLZ945 depleted virtually all myeloid cells, including quiescent microglia, throughout the CNS. Anti­CSF-1 treatment reduced the size of demyelinated lesions and microglial activation in the gray matter. Lastly, we found that bone marrow­derived immune cells were the major mediators of CSF-1R­dependent pathology, while microglia played a lesser role. Our findings suggest that targeting CSF-1 could be effective in ameliorating MS pathology, while preserving the homeostatic functions of myeloid cells, thereby minimizing risks associated with ablation of CSF-1R­dependent cells.

Corrigendum: Combination therapy with fingolimod and neural stem cells promotes functional myelination in vivo through a non-immunomodulatory mechanism.

[This corrects the article DOI: 10.3389/fncel.2019.00014.].

Oral D-mannose treatment suppresses experimental autoimmune encephalomyelitis via induction of regulatory T cells.

D-mannose (D-m) is a glucose epimer found in natural products, especially fruits. In mouse models of diabetes and airway inflammation, D-m supplementation via drinking water attenuated pathology by modifying cellular energy metabolism, leading to the activation of latent transforming growth factor beta (TGF-ß), which in turn induced T regulatory cells (Tregs). Given that Tregs are important in controlling neuroinflammation in experimental autoimmune encephalomyelitis (EAE) and likely in multiple sclerosis (MS), we hypothesized that D-m could also suppress EAE. We found that D-m delayed disease onset and reduced disease severity in two models of EAE. Importantly, D-m treatment prevented relapses in a relapsing-remitting model of EAE, which mimics the most common clinical manifestation of MS. EAE suppression was accompanied by increased frequency of CD4+FoxP3+ Tregs in the central nervous system, suggesting that EAE suppression resulted from Treg cell induction by D-m. These findings suggest that D-m has the potential to be a safe and low-cost complementary therapy for MS.