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231.
  • Zhang, Songen, et al. (författare)
  • Targeting CD162 protects against streptococcal M1 protein-evoked neutrophil recruitment and lung injury
  • 2013
  • Ingår i: American Journal of Physiology: Lung Cellular and Molecular Physiology. - American Physiological Society. - 1522-1504. ; 305:10, s. 756-763
  • Tidskriftsartikel (refereegranskat)abstract
    • Streptococcus pyogenes of the M1 serotype can cause streptococcal toxic shock syndrome and acute lung damage. CD162 is an adhesion molecule that has been reported to mediate neutrophil recruitment in acute inflammatory reactions. In this study, the purpose was to investigate the role of CD162 in M1 protein-provoked lung injury. Male C57BL/6 mice were treated with monoclonal antibody directed against CD162 or a control antibody before M1 protein challenge. Edema, neutrophil infiltration, and CXC chemokines were determined in the lung, 4 h after M1 protein administration. Fluorescence intravital microscopy was used to analyze leukocyte-endothelium interactions in the pulmonary microcirculation. Inhibition of CD162 reduced M1 protein-provoked accumulation of neutrophils, edema, and CXC chemokine formation in the lung by >54%. Moreover, immunoneutralization of CD162 abolished leukocyte rolling and firm adhesion in pulmonary venules of M1 protein-treated animals. In addition, inhibition of CD162 decreased M1 protein-induced capillary trapping of leukocytes in the lung microvasculature and improved microvascular perfusion in the lungs of M1 protein-treated animals. Our findings suggest that CD162 plays an important role in M1 protein-induced lung damage by regulating leukocyte rolling in pulmonary venules. Consequently, inhibition of CD162 attenuates M1 protein-evoked leukocyte adhesion and extravasation in the lung. Thus, our results suggest that targeting the CD162 might pave the way for novel opportunities to protect against pulmonary damage in streptococcal infections.
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232.
  • Zhang, Songen, et al. (författare)
  • Targeting rac1 signaling inhibits streptococcal m1 protein-induced CXC chemokine formation, neutrophil infiltration and lung injury.
  • 2013
  • Ingår i: PLoS ONE. - Public Library of Science. - 1932-6203. ; 8:8
  • Tidskriftsartikel (refereegranskat)abstract
    • Infections with Streptococcus pyogenes exhibit a wide spectrum of infections ranging from mild pharyngitis to severe Streptococcal toxic shock syndrome (STSS). The M1 serotype of Streptococcus pyogenes is most commonly associated with STSS. In the present study, we hypothesized that Rac1 signaling might regulate M1 protein-induced lung injury. We studied the effect of a Rac1 inhibitor (NSC23766) on M1 protein-provoked pulmonary injury. Male C57BL/6 mice received NSC23766 prior to M1 protein challenge. Bronchoalveolar fluid and lung tissue were harvested for quantification of neutrophil recruitment, edema and CXC chemokine formation. Neutrophil expression of Mac-1 was quantified by use of flow cytometry. Quantitative RT-PCR was used to determine gene expression of CXC chemokines in alveolar macrophages. Treatment with NSC23766 decreased M1 protein-induced neutrophil infiltration, edema formation and tissue injury in the lung. M1 protein challenge markedly enhanced Mac-1 expression on neutrophils and CXC chemokine levels in the lung. Inhibition of Rac1 activity had no effect on M1 protein-induced expression of Mac-1 on neutrophils. However, Rac1 inhibition markedly decreased M1 protein-evoked formation of CXC chemokines in the lung. Moreover, NSC23766 completely inhibited M1 protein-provoked gene expression of CXC chemokines in alveolar macrophages. We conclude that these novel results suggest that Rac1 signaling is a significant regulator of neutrophil infiltration and CXC chemokine production in the lung. Thus, targeting Rac1 activity might be a potent strategy to attenuate streptococcal M1 protein-triggered acute lung damage.
233.
  • Zhang, X.W., et al. (författare)
  • Inhibition of selectin function and leukocyte rolling protects against dextran sodium sulfate-induced murine colitis
  • 2001
  • Ingår i: Scandinavian Journal of Gastroenterology. - Taylor & Francis. - 1502-7708. ; 36:3, s. 270-275
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The selectin family of adhesion molecules (P-, E- and L-selectin) plays an important role in inflammatory reactions by mediating interactions between leukocytes and activated endothelial cells. However, a recent study using gene-targeted mice has suggested that adhesion molecules (P- and E-selectin and ICAM-1) may not be relevant targets in intestinal inflammation. The objective of the present study was to re-evaluate the potential role of selectins in experimental colitis in wild-type mice using the polysaccharide fucoidan, which inhibits the function of P- and L-selectin. Methods: For this purpose, Balb/c mice were exposed to 5% dextran sodium sulfate (DSS) in the drinking water for 5 days with and without daily administration of fucoidan (25 mg/kg, i.v.). In separate experiments, the effect of fucoidan on leukocyte-endothelium interactions was examined by use of intravital microscopy. Results: It was found that pretreatment with fucoidan (25 mg/kg/day) reduced mucosal damage and crypt destruction in the colon of DSS-treated mice. Moreover, this fucoidan treatment markedly reduced the colonic MPO activity in mice exposed to DSS. In vivo microscopy revealed that the dose of fucoidan used in the present study abolished TNF-alpha -induced venular leukocyte rolling and extravascular recruitment. Conclusions: These results suggest that selectins mediate leukocyte infiltration and tissue damage in experimental colitis. Moreover, our data support: the concept that functional interference with adhesion molecules of the selectin family may have a beneficial effect in the treatment of inflammatory bowel disease.
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234.
  • Zhao, Yilin, et al. (författare)
  • Radicicol, an Hsp90 inhibitor, inhibits intestinal inflammation and leakage in abdominal sepsis.
  • 2013
  • Ingår i: Journal of Surgical Research. - Elsevier. - 1095-8673. ; 182:2, s. 312-318
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Intestinal injury is a key feature in sepsis. Inhibitors of heat shock protein 90 (Hsp90) have been shown to exert protective effects in models of inflammation. Herein, we hypothesized that Hsp90 might regulate intestinal inflammation and leakage in abdominal sepsis. MATERIALS AND METHODS: Male C57BL/6 mice were pretreated with radicicol (60 mg/kg), which is a specific inhibitor of Hsp90, prior to cecal ligation and puncture (CLP). Intravital fluorescence microscopy was used to quantify leukocyte-endothelium interactions in the colonic microcirculation 6 h after CLP. Colonic tissue was harvested to determine levels of myeloperoxidase, tumor necrosis factor-α and CXC chemokines. Intestinal injury was examined by histology. Intestinal barrier function was quantified by leakage of fluorescein isothiocyanate-dextran from the vascular system out into the abdominal cavity after intravenous injection. RESULTS: We found that radicicol significantly decreased CLP-induced leukocyte rolling and adhesion in colonic venules. Inhibition of Hsp90 reduced colonic levels of myeloperoxidase by 24% in septic animals. Moreover, radicicol significantly decreased CLP-provoked formation of CXC chemokines but had no significant effect on tumor necrosis factor-α levels in the colon. Notably, Hsp90 inhibition significantly attenuated intestinal tissue injury evoked by CLP. Lastly, it was found that radicicol reduced sepsis-induced intestinal leakage by 43%. CONCLUSION: Our novel findings suggest that targeting Hsp90 protects against intestinal inflammation and leakage and might be a useful strategy to ameliorate intestinal failure in polymicrobial sepsis.
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