title: Influence of adding pyrroloquinoline quinone to parenteral nutrition on gut-associated lymphoid tissue.
abstract: BACKGROUND
  Experimental intravenous (IV) parenteral nutrition (PN) diminishes gut-associated lymphoid tissue (GALT) cell number and function. PN solution cannot maintain GALT at the same level as a normal diet, even when delivered intragastrically (IG). Previous studies demonstrated pyrroloquinoline quinone (PQQ)-deficient mice to be less immunologically responsive. Because standard (STD) PN solution lacks PQQ, PQQ supplementation may prevent PN-induced GALT changes. This study was designed to determine the influence of adding PQQ to PN on GALT.
  
  
  METHODS
  In experiment 1, mice (n = 32) were randomized to chow, IV-STD-PN, and IV-PQQ-PN groups. The chow group was fed chow with the same caloric content as PN. The IV-STD-PN group received STD-PN solution, whereas the IV-PQQ-PN group was given PQQ (3 mcg/d)-enriched PN by the IV route. After 5 days of feeding, lymphocytes were isolated from the Peyer's patch (PPs), intraepithelial space (IE), and lamina propria (LP) of the small intestine. GALT lymphocyte number and phenotype (αβTCR+, γδTCR+, CD4+, CD8+, B220+ cells) and intestinal immunoglobulin A (IgA) level were determined. In experiment 2, mice (n = 28) were randomized to IG-STD-PN or IG-PQQ-PN group. After IG nutrition supports, GALT mass and function were determined as in experiment 1.
  
  
  RESULTS
  The IV-PQQ-PN group showed increased PP lymphocyte number and PP CD8+ cell number compared with the IV-STD PN group. The IG-PQQ-PN group had significantly greater PP lymphocyte number and PP CD4+ cell numbers than the IG-STD-PN group. Neither IV nor IG PQQ treatment raised IgA level.
  
  
  CONCLUSIONS
  PQQ added to PN partly restores GALT mass, although its effects on GALT function remain unclear.
authors.affiliation: Department of Surgery, National Defense Medical College, Tokorozawa, Japan.
authors.forename: Jiro
authors.initials: J
authors.lastname: Omata
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Fukatsu
authors.forename: Satoshi
authors.initials: S
authors.lastname: Murakoshi
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Moriya
authors.forename: Chikara
authors.initials: C
authors.lastname: Ueno
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Maeshima
authors.forename: Koichi
authors.initials: K
authors.lastname: Okamoto
authors.forename: Daizoh
authors.initials: D
authors.lastname: Saitoh
authors.forename: Junji
authors.initials: J
authors.lastname: Yamamoto
authors.forename: Kazuo
authors.initials: K
authors.lastname: Hase
mesh_terms: D000818:Animals; D005753:Gastric Mucosa / Q000166:cytology / Q000187:drug effects*; D007070:Immunoglobulin A / Q000032:analysis; D007413:Intestinal Mucosa / Q000166:cytology / Q000187:drug effects*; D007421:Intestine, Small / Q000187:drug effects; D018655:Lymphocyte Count; D008214:Lymphocytes / Q000166:cytology / Q000187:drug effects; D008297:Male; D051379:Mice; D045542:PQQ Cofactor / Q000494:pharmacology*; D010288:Parenteral Nutrition; D010581:Peyer's Patches / Q000166:cytology / Q000187:drug effects*; D010641:Phenotype; D011897:Random Allocation
chemical_list: D007070:Immunoglobulin A; D045542:PQQ Cofactor