Sitafloxacin (STFX) is a new generation of broad-spectrum oral fluoroquinolones. STFX has significantly enhanced antibacterial activity than most similar drugs. Clinically, this drug is mainly used to treat respiratory and urinary tract infections and other serious bacterial infections. In this study, the interaction between sitafloxacin and human serum albumin (HSA) was investigated by spectroscopic methods and molecular simulations. Fluorescence quenching experiments showed that the interaction mechanism between STFX and HSA was static quenching, which was confirmed by time-resolved fluorescence. Thermodynamic parameters and docking results indicated that hydrophobic and electrostatic forces played a key role in this mechanism. Probe experiments and molecular docking results indicated that the major binding of STFX was at site I. 3D fluorescence showed that the insertion of STFX had minimal impact on the microenvironment. Analysis of the protein secondary structure showed that the insertion of STFX had little effect on the secondary structure of the protein. Hydrophobicity experiments showed the slight decrease in the overall hydrophobicity index of the system. Molecular dynamics simulations further validated the stability of the HSA-STFX complex. This study are useful for further drug development, in vivo toxicity studies, and can provide guidance for the clinical application of STFX to study its pharmacokinetic properties.

Trichodysplasia spinulosa polyomavirus causes trichodysplasia spinulosa, a skin infection, in immunocompromised persons, but the virus is rarely detected in respiratory samples. Using PCR, we detected persistent virus in respiratory and skin samples from an immunocompromised boy with respiratory signs but no characteristic skin spicules. This virus may play a role in respiratory illness.

Influenza is an infectious disease that is a common cause of infection among children. The main reason for it is the extremely low percentage of vaccinated people in Poland. In the 2016/2017 epidemic season more than 3,000 tests from children up to age 14 were examined. The dominance of subtype A/H3N2/ (40.9%) was confirmed. The evaluation was stratified by three age groups (0-4, 5-9, and 10-14 years), which revealed significant differences. The highest number of samples was available in the 0-4 years group. The highest percentage of positive samples was present in the 10-14 years group. Influenza-like viral infections, among them the respiratory syncytial virus, were also observed. Children due to immature immunity are at particular risk for influenza. A lack of proper vaccination coverage strongly increases the chance of serious complications of the infection.

Respiratory syncytial virus is one of the major causes of respiratory tract infections during infancy with high rates of hospitalization and mortality during the first years of life. It is the most common cause of acute bronchiolitis and viral pneumonia in children below two years of age and second the most common cause of postneonatal infant mortality all around the world following malaria. In addition, the virus has been causally linked to recurrent wheezing and associated with pediatric asthma. The respiratory syncytial virus infections tend to be severe in high risk patients such as patients below six months of age, with prematurity, congenital heart diseases, neuromuscular diseases and immune deficiencies. No specific treatment is available for respiratory syncytial virus infections to date. Severe cases require supportive therapy, mainly oxygen supplementation and hydration, and less frequently, ventilatory support. Because there is no vaccine to prevent respiratory syncytial virus infections or clinically effective treatment to administer to children with respiratory syncytial virus infection, immunoprophylaxis with palivizumab is currently the only method for reducing morbidity associated with severe respiratory syncytial virus in high-risk infants.

BPZE1 is a live attenuated Bordetella pertussis vaccine for nasal administration to mimic the natural route of infection. Here, we studied the mechanism of BPZE1-induced immunity in the murine nasal cavity in contrast to acellular vaccine (aPV), although both vaccines protected against lung colonization. Transfer of splenocytes or serum from BPZE1-vaccinated or aPV-vaccinated mice protected naïve mice against lung colonization but not against nasal colonization. However, transfer of nasal washes from BPZE1-vaccinated mice resulted in protection against nasal colonization, which was lost in IgA-deficient or poly-Ig receptor-deficient mice, indicating that it depends on secretory IgA (SIgA) induction induced in the nose. BPZE1-induced protection against nasal colonization was long-lived despite the relatively rapid decay of SIgA, indicating a potent BPZE1-induced local memory response, likely due to CD4+ tissue-resident memory T cells induced in the nose by BPZE1. These cells produced interleukin-17 (IL-17), known to be important for SIgA secretion. Furthermore, BPZE1 failed to protect Il17-/- mice against nasal colonization by B. pertussis and induced only background levels of nasal SIgA. Thus, our results show important differences in the protective mechanism between the upper and the lower murine respiratory tract and demonstrate an IL-17-dependent SIgA-mediated mechanism of BPZE1-induced protection against B. pertussis nasopharyngeal colonization.