Host-Pathogen Interaction in Leishmaniasis: Immune Response and Vaccination Strategies

Copyright: © 2022 by the authors. Licensee MDPI, Basel, Switzerland. Leishmaniasis is a zoonotic and vector-borne infectious disease that is caused by the genus Leishmania belonging to the trypanosomatid family. The protozoan parasite has a digenetic life cycle involving a mammalian host and an insect vector. Leishmaniasisis is a worldwide public health problem falling under the neglected tropical disease category, with over 90 endemic countries, and approximately 1 million new cases and 20,000 deaths annually. Leishmania infection can progress toward the development of species–specific pathologic disorders, ranging in severity from self-healing cutaneous lesions to disseminating muco-cutaneous and fatal visceral manifestations. The severity and the outcome of leishmaniasis is determined by the parasite’s antigenic epitope characteristics, the vector physiology, and most importantly, the immune response and immune status of the host. This review examines the nature of host–pathogen interaction in leishmaniasis, innate and adaptive immune responses, and various strategies that have been employed for vaccine development.Funding: This research received no external funding

Full-length human Surfactant Protein A inhibits Influenza A Virus infection of A549 lung epithelial cells: a recombinant form containing neck and lectin domains promotes infectivity

Hydrophilic lung surfactant proteins have emerged as key immunomodulators aimed at recognition and clearance of pulmonary pathogens. Surfactant protein A (SP-A) is a surfactant-associated innate immune pattern recognition molecule, which is known to interact with a variety of pathogens, and display anti-microbial effects. SP-A, being carbohydrate pattern recognition molecule, has been suggested to have a wide range of innate immune functions against pathogens. In addition, SP-A can work against respiratory pathogens, including influenza A virus (IAV). Some pandemic pH1N1 strains resist neutralization by SP-A due to differences in the N-glycosylation of viral hemagglutinin (HA). Here, we provide evidence, for the first time, that a recombinant form of human SP-A (rfhSP-A) composed of α-helical neck and carbohydrate recognition domains can actually promote the IAV replication, as observed by an upregulation of M1 expression in lung epithelial cell line, A549, when challenged with pH1N1 and H3N2 IAV subtypes. rfhSP-A (10 μg/ml) bound neuraminidase (NA) (˜60 kDa), matrix protein 1 (M1) (˜25 kDa) and M2 (˜17 kDa) in a calcium dependent manner, as revealed by far western blotting, and direct binding ELISA. However, human full length native SP-A downregulated mRNA expression levels of M1 in A549 cells challenged with IAV subtypes. Furthermore, qPCR analysis showed that transcriptional levels of TNF-α, IL-12, IL-6, IFN-α and RANTES were enhanced following rfhSP-A treatment by both IAV subtypes at 6 h post-IAV infection of A549 lung epithelial cells. In the case of full length SP-A treatment, mRNA expression levels of TNF-α, and IL-6 were downregulated during the mid-to-late stage of IAV infection of A549 cells. Multiplex cytokine/chemokine array revealed enhanced levels of both IL-6 and TNF-α due to rfhSP-A treatment in the case of both IAV subtypes tested, while no significant effect was seen in the case of IL-12. Enhancement of IAV infection of pH1N1 and H3N2 subtypes by truncated rfhSP-A, concomitant with infection inhibition by full-length SP-A, appears to suggest that a complete SP-A molecule is required for protection against IAV. This is in contrast to a recombinant form of trimeric lectin domains of human SP-D (rfhSP-D) that acts as an entry inhibitor of IAV.KACST (14-MED258-20

Increased prevalence of rotavirus among children associated gastroenteritis in Riyadh Saudi Arabia

The aim of this study is to assess the epidemiology along with the molecular structure of rotavirus causing pediatric diarrhea among Saudi patients. However, in this report we sited the epidemiological reflect coming from our project

First reported nosocomial outbreak of Serratia marcescens harboring blaIMP-4 and blaVIM-2 in a neonatal intensive care unit in Cairo, Egypt

Doaa Mohammad Ghaith,1 Mai Mahmoud Zafer,2 Dalia Kadry Ismail,1 Mohamed Hamed Al-Agamy,3,4 Marie Fe F Bohol,5 Ahmed Al-Qahtani,5 Mohammed N Al-Ahdal,5 Sherif M Elnagdy,6 Islam Yousif Mostafa7 1Department of Clinical and Chemical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt; 2Department of Microbiology and Immunology, Faculty of Pharmacy, Ahram Canadian University, Giza, Egypt; 3Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia; 4Department of Microbiology and Immunology, Faculty of Pharmacy, Al-Azhar University, Cairo, Egypt; 5Department of Infection and Immunity, Research Center, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia; 6Department of Botany and Microbiology, Faculty of Science, Cairo University, Cairo, Egypt; 7Department of Microbiology, Faculty of Dentistry and Oral Medicine, Future University, Cairo, Egypt Introduction: Serratia marcescens is a significant hospital-acquired pathogen, and many outbreaks of S. marcescens infection have been reported in neonates. We report a sudden breakout of S. marcescens harboring the blaIMP-4 and blaVIM-2 metallo-β-lactamase (MBL) genes that occurred from March to August 2015 in the neonatal intensive care unit of Cairo University Hospital, Cairo, Egypt. Methods: During the study period, 40 nonduplicate clinical isolates of S. marcescens were collected from blood culture samples. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry was used to identify each isolate. Then, minimum inhibitory concentrations of different antibiotics were assessed by the Vitek 2 compact system. Screening of the MBL genes blaIMP, blaVIM, blaSIM-1, blaSPM-1, and blaGIM-1 as well as the carbapenemase genes KPC, NDM, OXA-48, SME-1, and SME-2 were evaluated. Pulsed field gel electrophoresis was preformed to detect the genetic relationship of the isolates. Results: Analysis showed that 37.5% of the S. marcescens clinical isolates were resistant to meropenem (minimum inhibitory concentrations ≥ 2 µg/mL), and blaIMP-4 and blaVIM-2 were the most prevalent MBL genes (42.5% and 37.5%, respectively). None of the other investigated genes were observed. Pulsed field gel electrophoresis typing revealed two discrete clones; 33/40 (82.5%) were pulsotype A and 7/40 (17.5%) were pulsotype B. Conclusion: Here, we report for the first time the detection of MBL-producing S. marcescens isolates, particularly IMP-4 and VIM-2 recovered from inpatients with bacteremias from the intensive care unit at Cairo University Hospital. Keywords: PFGE, outbreak, MALDI-TOFF, SME-1, SME-2, carbapenemases, MBL gene