Article

Microcirculatory detection of Toll-like receptor 4 in rat pancreas and intestine.

Institute of Digestive Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
Clinical hemorheology and microcirculation (impact factor: 3.4). 02/2006; 34(1-2):213-9. pp.213-9
Source: PubMed

ABSTRACT This paper was aimed to detect Toll-like receptor 4 (TLR4) microcirculatory expression and localization in rat pancreas and intestine. Acute pancreatitis (AP) was induced by twice injections of cerulein (20 mug in total) and acute necrotizing pancreatitis (ANP) was induced by intraductal injection of 5% taurocholate (1 ml/kg.bw). Reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) were used to detect and localize TLR4 in the pancreas and intestine. Results showed that RT-PCR of RNA isolated from pancreatic and intestinal tissue yielded the predicted amplicon for TLR4; IHC analysis localized TLR4 expression to the endothelium of pancreatic arteriole, venule, acinar capillary network and sinusoidal capillary of endocrine islet; TLR4 expression in intestine was principally in the microvascular endothelium and leucocytes within the mucosa lamina propria. TLR4 staining in intestine was more intense in taurocholate-induced pancreatitis (TIP) than that in cerulein-induced pancreatitis (CIP). In conclusion, TLR4 could be detected in the pancreatic and intestinal microcirculation, suggesting TLR4 involved in the microcirculatory impairment in AP; the more intense intestinal TLR4 expression in TIP suggests a potential risk for secondary infection.

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    Article: Proposed protective mechanism of the pancreas in the rat.
    Jakob Bf Axelsson, Hamid Akbarshahi, Katarzyna Said, Anders Malmström, Roland Andersson
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    ABSTRACT: Heparan sulphate is known to have various functions in the animal body, including surveillance of tissue integrity. Administered intraperitoneally, it induces a systemic inflammatory response syndrome and when given locally in the pancreas it initiates a protective inflammatory response. The aim of the present study was to investigate the underlying mechanisms behind cell recruitment following intra-ductal infusion of heparan sulphate. Rats were subjected to intraductal-infusion of heparan sulphate, lipopolysaccharide and phosphate buffered saline into the pancreas. Pancreatic tissue was harvested 1, 3, 6, 9 or 48 hours after infusion and stained immunohistochemically for myeloperoxidase, ED-1, CINC-1 and MCP-1, as well as using eosin hematoxylin staining. Furthermore, MPO activity and MCP-1 and CINC-1 concentrations of tissue homogenates were measured. All differences were analyzed statistically using the Mann-Whitney U-test. During HS infusion, a rapid influx of macrophages/monocytes, as visualized as ED-1 positive cells, was seen reaching a maximum at 6 hours. After 48 hours, the same levels of ED-1 positive cells were noted in the pancreatic tissue, but with different location and morphology. Increased neutrophil numbers of heparan sulphate treated animals compared to control could be detected only 9 hours after infusion. The number of neutrophils was lower than the number of ED-1 positive cells. On the contrary, LPS infusion caused increased neutrophil numbers to a larger extent than heparan sulphate. Furthermore, this accumulation of neutrophils preceded the infiltration of ED-1 positive cells. Chemokine expression correlates very well to the cell infiltrate. MCP-1 was evident in the ductal cells of both groups early on. MCP-1 preceded monocyte infiltration in both groups, while the CINC-1 increase was only noticeable in the LPS group. Our data suggest that heparan and LPS both induce host defense reactions, though by using different mechanisms of cell-recruitment. This implies that the etiology of pancreatic inflammation may influence how the subsequent events will develop.
    Journal of Inflammation 01/2010; 7:24. · 2.26 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

5% taurocholate
 
acinar capillary network
 
acute necrotizing pancreatitis
 
Acute pancreatitis
 
cerulein-induced pancreatitis
 
endocrine islet
 
IHC analysis localized TLR4 expression
 
intense intestinal TLR4 expression
 
intestinal microcirculation
 
localize TLR4
 
microcirculatory impairment
 
mucosa lamina propria
 
potential risk
 
secondary infection
 
sinusoidal capillary
 
taurocholate-induced pancreatitis
 
TLR4
 
TLR4 expression
 
TLR4 staining
 
Toll-like receptor 4