The C‐Terminal Heptapeptide of Bombesin Reduces the Deleterious Effect of Total Parenteral Nutrition (TPN) on Gut‐Associated Lymphoid Tissue (GALT) Mass but Not Intestinal Immunoglobulin A In Vivo

Abstract

The C-terminal heptapeptide of bombesin prevented the TPN-induced decrease in intestinal lymphocyte populations but not the reduction in intestinal IgA levels.

Insights into bombesin receptors and ligands: Highlighting recent advances

“…One area that has received particularly attention is the ability of Bn/GRP to improve side effects of total parenteral nutrition (TPN). These including reversing TPN’s impairment of upper respiratory tract immunity [126]; preventing the atrophy of Peyer’s patches and dysfunction of M cells [86]; preventing the decrease in salivary gland adaptive immunity; [269]; preventing the decrease in intestinal lymphocyte population and reversing decreases in CD4+ and CD8+ T cells as well as small intestinal IgA levels [176]: reversing the decrease in both respiratory and intestinal IgA levels as well as maintaining lamina propria IL-4 levels and memory B cells [89,141,392] and preserving immunity to bacterial pneumonia [69]. At present there are no controlled studies, which have established the clinical value of altering BnR activity in any human inflammatory disease.…”

Alterations of gut barrier and gut microbiota in food restriction, food deprivation and protein-energy wasting

“…Bombesin, an analog to mammalian gastrin-releasing peptide, decreased intestinal permeability in burned rats [100] and increased the number of GALT lymphocytes and intestinal IgA levels in mice [101]. Other neuropeptides and gastro-intestinal hormones can also enhance epithelial gut barrier in vitro or in animal models, as NPY [102], cholecystokinin [103] and ghrelin [104].…”

Parenteral‐nutrition‐associated liver disease after intestinal perforation in extremely low‐birthweight infants: Consequent lethal portal hypertension

“…Although the detailed mechanism of abrupt exacerbation of PNALD followed by liver cirrhosis and consequent portal hypertension is to be solved, the resumption of EN after long‐term PN must be involved in the pathogenesis. The authors speculate that intestinal perforation followed by PN without enteral nutrition caused PN‐associated intrahepatic cholestasis, and might have caused the atrophy of intestinal mucosa, decrease in immunoglobulin A level and gut‐associated lymphoid tissue . Consequently the small intestine became susceptible to impaired intestinal microflora or bacterial overgrowth, and the resumption of enteral feeding after long‐term sole PN might have caused impaired intestinal microflora or bacterial overgrowth followed by bacterial translocation, consequent sepsis and marked hepatic injury synergistically with PNALD.…”

“…The authors speculate that intestinal perforation followed by PN without enteral nutrition caused PN-associated intrahepatic cholestasis, and might have caused the atrophy of intestinal mucosa, decrease in immunoglobulin A level 18 and gut-associated lymphoid tissue. 19 Consequently the small intestine became susceptible to impaired intestinal microflora or bacterial overgrowth, and the resumption of enteral feeding after long-term sole PN might have caused impaired intestinal microflora or bacterial overgrowth followed by bacterial translocation, 20 consequent sepsis and marked hepatic injury synergistically with PNALD. The histopathological findings of the liver in all three cases demonstrated massive hepatocyte necrosis, extensive destruction of hepatic lobuli, severe fibrosis and ductular proliferation in addition to cholestasis, which strongly suggested the hepatic change was caused by hematogenous mediators, probably portal endotoxemia secondary to translocation of endotoxin.…”