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Serum Derived Transfer Factor Stimulates the Innate Immune System to Improve Survival Traits in High Risk Pathogen Scenarios
Author(s) -
Willeford Bridget V.,
ShapiroDunlap Trudy,
Willeford Kenneth O.
Publication year - 2017
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.21392
Subject(s) - cytokine , biology , immune system , immunology , innate immune system , population , placebo , pathogen , transfer factor , pharmacology , medicine , pathology , alternative medicine , environmental health
ABSTRACTPreclinical ResearchTransfer Factors (TFs) are low molecular weight (<5,000 daltons) biological response mediators. In the present study, a serum derived TF improved the ability of the recipient animal to survive high‐risk infectious challenges (salmonellosis and canine parvoviral enteritis (CPV)) by altering the host's cytokine response profile. Mice mortally challenged with 5,000 colony‐forming units of Salmonella experienced a group mortality of 73% while mice treated with a single 5 mg dose of the TF demonstrated a significant decrease in morbidity (7%, p ≤ 0.01). The splenic bacterial load in untreated mice was over 10,000 times higher than that in the TF treated mice. Twenty‐four hours post‐administration, the treated murine population expressed a rapid temporal increase in serum IL‐6 (26‐fold) and INF‐γ (77‐fold) concentrations. IL‐6 can act as a critical signal regulating action against bacterial pathogens. A comparative double‐blind study performed using dogs confirmed to be undergoing a canine parvovirus challenge showed that when conventional supportive therapy was supplemented with a single 5 mg TF dose there was a reduction ( p ≤ 0.01) in group mortality (68% of the TF treated group survived versus 32% of the placebo group), an observation consistent with the observed increase in INF‐γ, a cytokine associated with promoting antiviral activity. Drug Dev Res 78 : 189–195, 2017. © 2017 Wiley Periodicals, Inc.