title: Mitigation of colitis with NovaSil clay therapy.
abstract: OBJECTIVE
  Five million people currently live with Crohn's disease (CD) or ulcerative colitis, the two major forms of inflammatory bowel disease. Available treatments frequently result in side effects that compromise the immune health of the patient. Consequently, alternative therapies that cause fewer systemic effects are needed. Dioctahedral smectite clays have been utilized to treat medical conditions, including diarrheal and enteric disease. Herein, we report the ability of a refined dioctahedral smectite (NovaSil, NS) to sorb inflammatory proteins and reduce inflammation in a TNBS (2,4,6-trinitrobenzenesulfonic acid) mouse model of CD. We also investigated whether NS could rescue gut microbial diversity in TNBS-induced mice.
  
  
  METHODS
  ELISA, X-ray diffraction, and transmission electron microscopy were employed to characterize the NS-cytokine interaction in vitro. A TNBS mouse colitis model was utilized to study the efficacy of NS supplementation for 4 weeks. The three treatment groups included control, TNBS, and TNBS + NS. DNA was extracted from feces and sorted for bacterial phylogenetic analysis.
  
  
  RESULTS
  Results suggest that NS binds TNFα in vitro. In TNBS-treated mice, supplementation with NS significantly reduced weight loss, and serum proinflammatory cytokine levels (IL-2, IL-6, and IL-12, TNFα, IFNγ) compared with the TNBS group. TNBS-treated mice demonstrated a significant reduction in gut microbiota species richness when compared with the TNBS + NS group and control group.
  
  
  CONCLUSIONS
  NovaSil mitigated the effects of TNBS-induced colitis based on reduction in systemic markers of inflammation, significant improvement in weight gain, and intestinal microbial profile.
authors.affiliation: College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, TAMU 4458, College Station, TX, 77843-4458, USA, kzychowski@cvm.tamu.edu.
authors.forename: Katherine E
authors.initials: KE
authors.lastname: Zychowski
authors.forename: Sarah E
authors.initials: SE
authors.lastname: Elmore
authors.forename: Kristal A
authors.initials: KA
authors.lastname: Rychlik
authors.forename: Hoai J
authors.initials: HJ
authors.lastname: Ly
authors.forename: Felipe
authors.initials: F
authors.lastname: Pierezan
authors.forename: Anitha
authors.initials: A
authors.lastname: Isaiah
authors.forename: Jan S
authors.initials: JS
authors.lastname: Suchodolski
authors.forename: Aline Rodrigues
authors.initials: AR
authors.lastname: Hoffmann
authors.forename: Amelia A
authors.initials: AA
authors.lastname: Romoser
authors.forename: Timothy D
authors.initials: TD
authors.lastname: Phillips
mesh_terms: D000538:Aluminum Silicates / Q000737:chemistry / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000737:chemistry / Q000494:pharmacology*; D001419:Bacteria / Q000145:classification / Q000302:isolation & purification; D000077215:Clay; D003092:Colitis / Q000097:blood / Q000139:chemically induced / Q000382:microbiology / Q000517:prevention & control*; D003106:Colon / Q000187:drug effects* / Q000378:metabolism / Q000382:microbiology; D018360:Crystallography, X-Ray; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D005243:Feces / Q000382:microbiology; D005260:Female; D005765:Gastrointestinal Agents / Q000737:chemistry / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000097:blood; D008807:Mice, Inbred BALB C; D046529:Microscopy, Electron, Transmission; D033362:Powder Diffraction; D021521:Ribotyping; D017640:Silicates / Q000737:chemistry / Q000494:pharmacology*; D013997:Time Factors; D014302:Trinitrobenzenesulfonic Acid; D015430:Weight Gain / Q000187:drug effects
chemical_list: D000538:Aluminum Silicates; D000893:Anti-Inflammatory Agents; D016207:Cytokines; D005765:Gastrointestinal Agents; D018836:Inflammation Mediators; D017640:Silicates; C016752:smecta; D014302:Trinitrobenzenesulfonic Acid; D000077215:Clay