The course of autoimmune inflammatory diseases of the central nervous system (CNS) can be influenced by infections. Here we assessed the disease-modulating effects of the most frequent respiratory pathogen Streptococcus pneumonia on the course of experimental autoimmune encephalomyelitis (EAE). Mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG 35-55 ) peptide, challenged intraperitoneally with live S. pneumoniae type 3, and then treated with ceftriaxone. EAE was monitored by a clinical score for 35 days after immunization. EAE was unaltered in mice infected with S. pneumoniae 2 days before and 21 days after the first MOG 35-55 injection but was more severe in animals infected 7 days after the first MOG 35-55 injection. The antigen-driven systemic T-cell response was unaltered, and the intraspinal Th1 cytokine mRNA concentrations at the peak of disease were unchanged. The composition of CNS-infiltrating cells and subsequent tissue destruction were only slightly increased after S. pneumoniae infection. In contrast, the serum levels of tumor necrosis factor alpha and interleukin-6 and spinal interleukin-6 levels were elevated, and the expression of major histocompatibility complex class II molecules, CD80, and CD86 on splenic dendritic cells were enhanced early after infection. Serum cytokine concentrations were not elevated, and EAE was not aggravated by S. pneumoniae infection in Toll-like receptor 2 (TLR2)-deficient mice. In conclusion, infection with S. pneumoniae worsens EAE probably by elevation of proinflammatory cytokines and activation of dendritic cells in the systemic circulation via TLR2 and cross talk through the blood-brain barrier.

Although statistically significant (P = 0.04), a delay of 1 day in the onset of symptoms of EAE after minocycline treatment is of minor clinical relevance. These data do not support the hypothesis of superiority of a bacterial protein synthesis inhibitor over a beta-lactam antibiotic for the treatment of concomitant infections during the latent phase of EAE or MS.

In the present work, an electrospun nanofibrous textile composed of polyurethane (PU), sodium bicarbonate (NaHCO 3) and pantothenic acid (PA) is developed for treating chronic wounds. Wounds are a common health problem and in particular, the chronic wounds such as vascular ulcers, diabetic ulcers and pressure ulcers cause a large number of morbidity and mortality. The main problems of the chronic wounds are prolonged inflammation phase and presence of acidic environment. These events deactivate the operation of growth factors and also the progression of natural healing mechanism. Hence, various types of advanced textile-based dressings are developed to address the clinical complications associated with chronic wound management. The prepared electrospun scaffolds were characterized to study their physicochemical and haemocompatible properties. The scanning electron microscopy micrographs depicted continuous, smooth-interconnected nanofibrous morphology of PU-NaHCO 3-PA scaffolds. The Fourier transform infrared spectroscopy spectra indicated the addition of NaHCO 3 and PA-based hydrophilic chemical groups, which significantly enhanced the wettability of the composites. Further, the PU-NaHCO 3-PA composite membrane inferred to have a highly porous structure with the mean porosity of 79.4 ± 4.8%, which may provide a conducive environment for adherence and proliferation of skin cells. The composite scaffold also offers a highly haemocompatible surface by delaying coagulation of blood through contact activation pathways and by limiting red blood cells damage. Therefore, the excellent physicochemical properties, blood compatibility and the delivery of PA are anticipated to speed up the impaired healing process of chronic wounds.