Abstract

The emergence of nosocomial infections and sepsis epitomizes the gravest obstruction in survival and timely recovery to best functionality. It is without exaggeration to state that timely targeted sepsis management, particularly when concomitant with ischemia-reperfusion injury, is one of the most burning, complex matters in critical care. Currently, besides antibiotic therapy, cytokine filtration and sophisticated organ support, alternative methods are sparse in clinical practice. Sepsis is a concern in specialized university settings and community hospitals, likewise. The new definition of sepsis tilts the emphasis towards the issue of the dysregulated immune response. Here I will narrate the phenotypes and dynamics of sepsis and provide an overview of literature-based search on experimental therapies, emphasizing the topic of monoclonal antibodies for intensivists.

Keywords:Sepsis; Polyclonal antibodies; Monoclonal neutralizing antibodies; Phagocytosis; Hyperinflammation; Immunosupression

Abbreviations: ICU: Intensive Care Unit; IVIG: Intravenous Immunoglobulin; CAP: Community Acquired Pneumonia; FDA: Food and Drug Administration; CRP: C-Reactive Protein; PCT: Procalcitonin, MAB: Monoclonal Antibodies; MAC: Membrane Attack Complex; ADCC: Antibody Dependent Cytotoxicity; CMV: Cytomegalovirus; HSV: Herpes Simplex Virus; RSV: Respiratory Syncytial Virus; ADE: Antibody Mediated Disease Enhancement; TLR: Toll-Like Receptor; CR: Complement Receptor; ROS: Reactive Oxygen Species; PAL: Peptidoglycan Associated Lipoprotein; LPS: Lipopolysaccharide; NK: Natural Killercell; cDC- Conventional Dendritic Cell: NADPH: Nicotinamide Dinucleotide Phosphate; MHC: Major Histocompatibility Complex; CTLA4: Cytotoxic T-Lymphocyte Associated Protein 4; PD-1(L): Programmed Death1(Ligand)