Bombesin Affects Mucosal Immunity and Gut-Associated Lymphoid Tissue in Intravenously Fed Mice

Li, Jian; Kudsk, Kenneth A.; Hamidian, Masoud; Gocinski, Barbara L.

doi:10.1001/archsurg.1995.01430110022005

Cited by 68 publications

(32 citation statements)

References 29 publications

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“…44,45 Both bombesin and gastrin-releasing peptide have been shown to play roles in lung morphogenesis 46,47 and in maintenance of mucosal immunity in both the gastrointestinal and respiratory tracts. 48,49 Two other possibilities are growth hormone (somatotropin) and insulin, possibly mediated by gastrin-releasing peptide. All operate within liver feedback systems and can be tissue-specific; in fact, glucose levels have been shown to regulate the effect of both bombesin and gastrin-releasing peptide.…”

Section: Discussionmentioning

confidence: 99%

Hyalinosis and Ym1/Ym2 Gene Expression in the Stomach and Respiratory Tract of 129S4/SvJae and Wild-Type and CYP1A2-Null B6,129 Mice

Ward

Yoon

Anver

et al. 2001

The American Journal of Pathology

125

129

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The C57BL/6, 129, and B6,129 mouse strains or stocks have been commonly used to generate targeted mutant mice. The pathology of these mice is not well characterized. In studies of these aging mice, we found high incidences of hyalinosis (eosinophilic cytoplasmic change) in the glandular stomach, respiratory tract, bile duct, and gall bladder of B6,129 CYP1A2-null and wild-type mice as well as in both sexes of the background 129S4/SvJae strain. The gastric lesions of the glandular stomach were found in 95.7% of female CYP1A2-null mice as well as in 45.7% of female 129S4/SvJae animals. The eosinophilic protein isolated from characteristic hyaline gastric lesions was identified as Ym2, a member of the chitinase family. Immunohistochemistry, using rabbit polyclonal antibodies to oligopeptides derived from the Ym1 sequence, detected focal to diffuse reactivity within both normal and abnormal nasal olfactory and respiratory epithelium, pulmonary alveolar macrophages, bone marrow myeloid cells, and the squamous epithelium of the forestomach and epithelium of the glandular stomach. Alveolar macrophages in acidophilic pneumonia, a major cause of death of aging 129 mice, and in mice with the me mutation also were highly immunoreactive. CYP1A2 carries out oxidation and N-hydroxylation of arylamine carcinogens and heterocyclic amine food mutagens which, when followed by O-esterification by acetate or sulfate transferases, results in unstable electrophilic derivatives that can cause cell toxicity, cell death, or cell transformation. 1-3 CYP1A2 catalyzes caffeine 3-demethylation and metabolically activates aflatoxin B 1 to its ultimate carcinogenic intermediate 4 and paradoxically catalyzing the hydroxylation of aflatoxin B 1 to aflatoxin M 1 in a detoxification pathway. 5 In addition, CYP1A2 was found to be involved in both hamster and human catechol estrogen metabolism. 6 Although CYP1A2 is constitutively expressed in the liver of mice, rats, and humans and is inducible by ligands of the aryl hydrocarbon receptor (Ahr) in all mammalian species analyzed, no expression has been demonstrated in the stomach, even after treating animals with known inducers of this enzyme. 7 However, the mechanisms involved in CYP1A2 gene regulation are less well established than CYP1A1 because it is difficult to induce expression in vitro and the sensitivities of current methodologies may simply be too low under normal in vivo conditions. The mammalian conservation of the CYP1A subfamily argues for an essential function in metabolism not limited to activation and detoxification of exogenous chemicals and toxins. As with most of the cytochromes P-450, determination of function has primarily been a consequence of exposures to man-made compounds, but it must be remembered that their evolution predates industrialization. The genes of the two recognized members of the CYP1A subfamily,

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Section: Discussionmentioning

confidence: 99%

Hyalinosis and Ym1/Ym2 Gene Expression in the Stomach and Respiratory Tract of 129S4/SvJae and Wild-Type and CYP1A2-Null B6,129 Mice

Ward

Yoon

Anver

et al. 2001

The American Journal of Pathology

125

129

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“…As previous reports have demonstrated, lack of glutamine in PN solutions, less secretion of neuropeptides and IL-7 during PN, and other factors contribute to impairment of gut immunity. [42][43][44][45][46][47] The present study may add another important piece of knowledge-that PQQ is an important factor for the maintenance of gut immunity. We believe that the present results provide an important clue for developing a new PN formula preserving gut and systemic mucosal immunity.…”

Section: Discussionmentioning

confidence: 69%

Influence of Adding Pyrroloquinoline Quinone to Parenteral Nutrition on Gut‐Associated Lymphoid Tissue

Omata

Fukatsu

Murakoshi

et al. 2011

J Parenter Enteral Nutr

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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.

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“…13,14,18 -20 The GALT is exquisitely sensitive to route and type of nutrition as well as to specific nutrients, such as glutamine, and neuropeptides found within the enteric nervous system. 21,22 The enteric nervous system forms a vast network of neurons throughout the gastrointestinal tract. It is estimated that every cubic millimeter of intestinal tissue is innervated with 2 meters of nerve tissue.…”

Section: Resultsmentioning

confidence: 99%

Bombesin Recovers Gut-Associated Lymphoid Tissue and Preserves Immunity to Bacterial Pneumonia in Mice Receiving Total Parenteral Nutrition

DeWitt

Renegar

et al. 2000

Annals of Surgery

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ObjectiveTo study the ability of bombesin (BBS) to recover gut-associated lymphoid tissue (GALT) and preserve immunity in a lethal model of Pseudomonas aeruginosa (Ps) pneumonia in mice receiving total parenteral nutrition (TPN). Summary Background DataTPN causes depression of mucosal immunity compared with enterally fed animals, which may explain the increased incidence of pneumonia in parenterally fed trauma patients. BBS prevents this TPN-induced GALT atrophy, depressed gastrointestinal and respiratory tract IgA levels, and impaired antiviral IgA-mediated mucosal immunity. The authors examined whether some supplement could be added to TPN to avoid this GALT atrophy and lower the incidence of infectious complications in the parenterally fed animal. MethodsMale mice were randomized to chow or intravenous (IV) TPN. After 5 days of IV TPN, mice received 0, 1, 2, or 3 days of BBS IV three times a day and then were killed to harvest Peyer's patch, intraepithelium, and lamina propria for cell yields. Gastrointestinal and respiratory tract IgA levels were analyzed by enzyme-linked immunosorbent assay. Next, mice underwent intranasal inoculation with liposomes alone (nonimmune) or liposome-containing Ps polysaccharide. Ps immune mice were catheterized and randomized to chow, IV TPN, or IV TPN ϩ BBS. The liposome group received chow but no IV catheter. These mice were given an LD 90 dose of intratracheal Ps, and death rates were recorded. ResultsGALT and gastrointestinal and respiratory tract IgA levels improved to those in chow-fed mice after 3 days of BBS. Immunization reduced the death rate from 92% in chow-fed liposome-only animals to 20% in immunized animals. TPN-fed animals lost their mucosal immunity, with a death rate of 86% compared with 21% in the TPN ϩ BBS group. ConclusionThe results demonstrate that BBS reverses TPN-induced changes in GALT and preserves mucosal immunity. Ps immunization reduces the death rate in a gram-negative pneumonia model and maintains gastrointestinal and respiratory immunity in Ps immune mice receiving IV TPN.Nosocomial pneumonia accounts for approximately 15% of hospital-acquired infections 1 and 18 pneumonias per 1,000 ventilator days in the adult intensive care unit.2 The overwhelming majority of bacterial isolates in these cases are aerobic gram-negative bacilli. Pseudomonas aeruginosa (Ps) was identified as the causative agent in 17% to 31% [3][4][5] of the cases, with a subsequent death rate of 40% to 70%. 6,7 Although many etiologic factors, such as prolonged mechanical ventilation, acute pulmonary injury, and aspiration, influence the risk of pneumonia, nutrition also appears to play an important role. In clinical studies of trauma patients, those fed intravenously have a significantly higher incidence of pneumonia and intraabdominal abscess than those fed enterally. 8 -10 Although the mechanism for this increased susceptibility to infection is unclear, our work suggests that enteral feeding improves the function of the major source of mucosal immunity-the gut-associated ly...

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Bombesin Affects Mucosal Immunity and Gut-Associated Lymphoid Tissue in Intravenously Fed Mice

Abstract: Bombesin prevents the TPN-associated atrophy and dysfunction of gut-associated lymphoid tissue, supporting the concept of close neuroimmunologic interaction.

Cited by 68 publications

References 29 publications

Hyalinosis and Ym1/Ym2 Gene Expression in the Stomach and Respiratory Tract of 129S4/SvJae and Wild-Type and CYP1A2-Null B6,129 Mice

Hyalinosis and Ym1/Ym2 Gene Expression in the Stomach and Respiratory Tract of 129S4/SvJae and Wild-Type and CYP1A2-Null B6,129 Mice

Influence of Adding Pyrroloquinoline Quinone to Parenteral Nutrition on Gut‐Associated Lymphoid Tissue

Bombesin Recovers Gut-Associated Lymphoid Tissue and Preserves Immunity to Bacterial Pneumonia in Mice Receiving Total Parenteral Nutrition

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