Leukocytes of the intestinal muscularis: their phenotype and isolation

Kalff, Jörg C.; Schwarz, Nicolas T.; Walgenbach, K.-J.; Schraut, Wolfgang H.; Bauer, Anthony J.

doi:10.1002/jlb.63.6.683

Cited by 111 publications

(100 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our group has previously demonstrated that prostanoids produced by COX-2 and NO produced by iNOS have potent inhibitory effects on intestinal smooth muscle contractility and that inhibition of the COX-2 enzyme or the selective knockout of the leukocyte-derived iNOS gene averts the development of postoperative ileus (27,49). Additionally, CO treatment before intestinal manipulation decreased iNOS gene expression and NO production in mice (37).…”

Section: Discussionmentioning

confidence: 99%

Biliverdin protects against polymicrobial sepsis by modulating inflammatory mediators

Overhaus¹,

Moore²,

Barbato³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

Self Cite

View full text Add to dashboard Cite

Highly inducible heme oxygenase (HO)-1 is protective against acute and chronic inflammation. HO-1 generates carbon monoxide (CO), ferrous iron, and biliverdin. The aim of this study was to investigate the protective effects of biliverdin against sepsis-induced inflammation and intestinal dysmotility. Cecal ligation and puncture (CLP) was performed on Sprague-Dawley rats under isoflurane anesthesia with and without intraperitoneal biliverdin injections, which were done before, at the time of CLP, and after CLP. In vivo gastrointestinal transit was carried out with fluorescein-labeled dextran. Jejunal circular muscle contractility was quantified in vitro using organ bath-generated bethanechol dose-response curves. Neutrophilic infiltration into the muscularis externa was quantified. The jejunal muscularis was studied for cytokine mRNA expressions [interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, inducible nitric oxide synthase, cyclooxygenase-2, biliverdin, IL-10, and HO-1] using real-time RT-PCR. Biliverdin treatment prevented the sepsis-induced suppression of gastrointestinal muscle contractility in vivo and in vitro and significantly decreased neutrophilic infiltration into the jejunal muscularis. Inflammatory mRNA expressions for small bowel IL-6 and MCP-1 were significantly reduced after biliverdin treatment in CLP-induced septic animals compared with untreated septic animals. The anti-inflammatory mediator expression of small bowel IL-10 was significantly augmented after CLP at 3 h compared with untreated septic animals. These findings demonstrate that biliverdin attenuates sepsis-induced morbidity to the intestine by selectively modulating the inflammatory cascade and its subsequent sequelae on intestinal muscularis function.

show abstract

Section: Discussionmentioning

confidence: 99%

Biliverdin protects against polymicrobial sepsis by modulating inflammatory mediators

Overhaus¹,

Moore²,

Barbato³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

Self Cite

View full text Add to dashboard Cite

show abstract

“…Histochemical and immunohistochemical analysis was performed on whole mounts of the intestinal muscularis as described previously (N = 5-7) (20,23). Myeloperoxidase (MPO)-positive cells were detected using HankerYates reagent (Polysciences Europe GmbH, Eppelheim, Germany).…”

Section: Histochemistry and Immunohistochemistrymentioning

confidence: 99%

Resident Macrophages are Involved in Intestinal Transplantation-Associated Inflammation and Motoric Dysfunction of the Graft Muscularis

Schaefer

Tahara

Schmidt

et al. 2007

American Journal of Transplantation

View full text Add to dashboard Cite

Gut manipulation and ischemia/reperfusion evoke an inflammatory response within the intestinal muscularis that contributes to dysmotility. We hypothesize that resident macrophages play a key role in initiating the inflammatory cascade. Isogenic small bowel transplantation was performed in Lewis rats. The impact of recovery of organs on muscularis inflammation was investigated by comparing cold whole-body perfusion after versus prior to recovery. The role of macrophages was investigated by transplantation of macrophage-depleted gut. Leukocytes were counted using muscularis whole mounts. Mediator expression was determined by real-time RT-PCR. Contractility was assessed in a standard organ bath. Both organ recovery and ischemia/reperfusion induced leukocyte recruitment and a significant upregulation in IL-6, MCP-1, ICAM-1 and iNOS mRNAs. Although organ recovery in cold ischemia prevented early gene expression, peak expression was not changed by modification of the recovery technique. Compared to controls, transplanted animals showed a 65% decrease in smooth muscle contractility. In contrast, transplanted macrophagedepleted isografts exhibited significant less leukocyte infiltration and only a 19% decrease in contractile activity. In summary, intestinal manipulation during recovery of organs initiates a functionally relevant inflammatory response within the intestinal muscularis that is massively intensified by the ischemia reperfusion injury. Resident muscularis macrophages participate in initiating this inflammatory response.

show abstract

“…The functional, molecular, and cellular mechanisms determining POI are to be found within the intestinal muscularis. The changes within intestinal mucosa do not influence the cellular and molecular mechanisms of POI (35,37,39,41,42,67,80,82). Previously, we could show a recruitment of CD11bϩCD103ϩ dendritic cells into the intestinal muscularis, but not into the colonic muscularis after IM, which induced a T H 1 response by producing IL-12 at the manipulated site.…”

Section: Discussionmentioning

confidence: 74%

“…Specimens for histochemical analysis were prepared 24 h after surgical procedure and performed on whole mounts of the distal jejunum and the colon (n ϭ 5-7 each group) as described before (41). Freshly prepared whole mounts were stained with Hanker-Yates reagent as described previously (88).…”

Section: Myeloperoxidase Stainingmentioning

confidence: 99%

“…Both the neuronal activation by intestinal manipulation (IM) and inflammatory cell infiltrates in the intestinal muscularis compromise gastrointestinal motility. These detrimental alterations are emphasized as major factors in the development of POI (4,8,9,15,16,[35][36][37][38][40][41][42]. We reported a time-and trauma-degree-dependent inflammatory cascade (35, 36); infiltration of leukocytes (40 -42, 72, 83), macrophages (21,22,37,87), and immunologically competent cells (35,36,40,67,69,72,81,83); and an upregulation of proinflammatory cytokines within the intestinal muscularis (36, 38 -40, 66, 68, 71, 80 -82, 84, 88).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Impact of CCR7 on the gastrointestinal field effect

Koscielny

Engel

Maurer

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

.2010.-Standardized intestinal manipulation (IM) leads to local bowel wall inflammation subsequently spreading over the entire gastrointestinal tract. Previously, we demonstrated that this so-called gastrointestinal field effect (FE) is immune mediated. This study aimed to investigate the role of CCR7 in IM-induced FE. Since CCR7 is expressed on activated dendritic cells and T cells and is well known to control their migration, we hypothesized that lack of CCR7 reduces or abolishes FE. Small bowel muscularis and colonic muscularis from CCR7Ϫ/Ϫ and wild-type (WT) mice were obtained after IM of the jejunum or sham operation. FE was analyzed by measuring gastrointestinal transit time of orally given fluorescent dextran (geometric center), colonic transit time, infiltration of MPO-positive cells, and circular smooth muscle contractility. Furthermore, mRNA levels of the inflammatory cytokine IL-6 were determined by RT-PCR. The number of dendritic cells and CD3ϩCD25ϩ T cells separately isolated from jejunum and colon was determined in mice after IM and sham operation. There was no significant difference in IL-6 mRNA upregulation in colonic muscularis between sham-operated WT and CCR7 Ϫ/Ϫ mice after IM. Contractility of circular muscularis strips of the colon was significantly improved in CCR7 Ϫ/Ϫ animals following IM and did not vary significantly from sham-operated animals. Additionally, inflammation of the colon determined by the number of MPO-positive cells and colonic transit time was significantly reduced in CCR7 Ϫ/Ϫ mice. In contrast, jejunal contractility and jejunal inflammation of transgenic mice did not differ significantly from WT mice after IM. These data are supported by a significant increase of CD3ϩCD25ϩ T cells in the colonic muscularis of WT mice after IM, which could not be observed in CCR7Ϫ/Ϫ mice. These data demonstrate that CCR7 is required for FE and postoperative ileus. CCR7 indirectly affects FE by inhibiting migration of activated dendritic cells and of T cells from the jejunum to the colon. These findings support the critical role of the adaptive immune system in FE. postoperative ileus; chemokine receptor 7 POSTOPERATIVE ILEUS (POI) is an inevitable sequela of abdominal surgery or trauma with a variably gradual manifestation. It leads to postoperative discomfort, prolonged hospitalization, and increased patient morbidity and has a high impact on socioeconomic costs (27,43,49,63). The pathophysiology of POI and postoperative gastrointestinal dysmotility, respectively, has been elucidated in recent years. POI is marked by a neurogenic phase and a clinically relevant prolonged inflammatory phase. Both the neuronal activation by intestinal manipulation (IM) and inflammatory cell infiltrates in the intestinal muscularis compromise gastrointestinal motility. These detrimental alterations are emphasized as major factors in the development of POI (4,8,9,15,16,[35][36][37][38][40][41][42]. We reported a time-and trauma-degree-dependent inflammatory cascade (35, 36); infiltration of leukocytes (40 -42...

show abstract

Leukocytes of the intestinal muscularis: their phenotype and isolation

Cited by 111 publications

References 0 publications

Biliverdin protects against polymicrobial sepsis by modulating inflammatory mediators

Biliverdin protects against polymicrobial sepsis by modulating inflammatory mediators

Resident Macrophages are Involved in Intestinal Transplantation-Associated Inflammation and Motoric Dysfunction of the Graft Muscularis

Impact of CCR7 on the gastrointestinal field effect

Contact Info

Product

Resources

About