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      Role of Submandibular Salivary Glands in LPS-Induced Lung Inflammation in Rats

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          Objective: Literature data suggest that rodent salivary glands can exert a neuroimmunomodulatory influence on distant inflammatory events. The release of regulatory factors by salivary glands appears to be influenced by time-dependent factors. In this paper we examined this possibility directly by studying the role of submandibular salivary glands in the temporal profile of lypopolysaccharide (LPS)-induced lung inflammation in rats. Methods: The submandibular glands were removed (SMGx) or not (sham) and, 4 days later, the animals received an intravenous LPS injection ( Salmonella abortus equi, 1 mg/kg). Cells in peripheral blood and in bronchoalveolar and bone marrow lavages were quantified after 90 min, 1, 3 and 5 days. Tumor necrosis factor (TNF) activity and corticosterone concentrations in serum were also determined. Baseline values were determined in a group of naïve rats. Results: One day after the LPS injection, neutrophil counts in lungs and blood in both animal groups were elevated, but the SMGx rats presented a significantly lower response in comparison to the sham-operated controls. Five days after LPS treatment, however, SMGx rats had higher neutrophil counts in the lungs than did sham animals, but numbers of blood neutrophils were equal. Ninety minutes after LPS injection, a peak of serum TNF activity was detected in both groups compared with naïve levels. At this time point, TNF activity was about 135% higher in the serum of the SMGx group than in controls. Corticosterone levels of sham-operated controls rose only on the 5th day after LPS, whereas SMGx rats had significant peaks of corticosterone both on the 1st and the 5th day, but not on the 3rd day. Conclusion: Our data indicate that submandibular glands have a dual effect on inflammatory pulmonary response by differentially modulating the profile of lung neutrophil influx.

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          Comparison of in vitro cell cytotoxic assays for tumor necrosis factor.

          Four published in vitro assays which measure cell cytotoxicity were compared utilizing murine tumor necrosis factor. These included determination of residual cell number by crystal violet staining in the presence and absence of actinomycin D, lack of viability as determined by neutral red uptake, and [3H]thymidine release in cytotoxin treated L929 cells. Treatment of cells with actinomycin D followed by crystal violet staining was the most sensitive method measured. However, addition of actinomycin D to the neutral red uptake assay could be shown to be even more sensitive. Additionally, it was shown how actinomycin D dosage, cell seeding density and time of incubation affect TNF titer.
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            Social stress increases the susceptibility to endotoxic shock.

            The influence of social disruption stress (SDR) on the susceptibility to endotoxic shock was investigated. SDR was found to increase the mortality of mice when they were challenged with the bacterial endotoxin lipopolysaccharide (LPS). Histological examination of SDR animals after LPS injection revealed widespread disseminated intravascular coagulation in the brain and lung, extensive meningitis in the brain, severe hemorrhage in the lung, necrosis in the liver, and lymphoid hyperplasia in the spleen, indicating inflammatory organ damage. In situ hybridization histochemical analysis showed that the expression of the glucocorticoid receptor mRNA was down-regulated in the brain and spleen of SDR animals while the ratio of expression of AVP/CRH-the two adrenocorticotropic hormone secretagogue, increased. After LPS injection, the expression of pro-inflammatory cytokines, IL-1beta and TNF-alpha, was found significantly higher in the lung, liver, spleen, and brain of the SDR mice as compared with the LPS-injected home cage control animals. Taken together, these results show that SDR stress increases the susceptibility to endotoxic shock and suggest that the development of glucocorticoid resistance and increased production of pro-inflammatory cytokines are the mechanisms for this behavior-induced susceptibility to endotoxic shock.
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              Inhibition of Allergic Inflammation by C-Terminal Peptides of the Prohormone Submandibular Rat 1 (SMR-1)


                Author and article information

                S. Karger AG
                October 2002
                04 October 2002
                : 10
                : 2
                : 73-79
                aDepartment of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, bLaboratory of Anaerobic Bacteria, Institute Butantan, São Paulo, cDepartment of Clinical Analysis, Faculty of Pharmacy, University of São Paulo, São Paulo, Brazil; dDepartment of Physiology and Biophysics, UniversityofCalgary,Calgary,Canada
                65182 Neuroimmunomodulation 2002–03;10:73–79
                © 2002 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 1, References: 36, Pages: 7
                Original Paper


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